Ophthalmology - Acute visual disturbance Flashcards
What differentials should be considered in acute painless loss of vision?
Central retinal artery occlusion Branch retinal artery occlusion Central retinal vein occlusion Branch retinal vein occlusion Anterior ischaemic optic neuropathy Vitreous haemorrhage Retinal detachment ARMD (wet type)
What is the pathogenesis of retinal vein occlusion?
Thrombosis occurs within the lumen of the vessel. In branch occlusions, this is frequently seen at an arteriovenous crossing point. Abnormalities of blood constituents may promote thrombus formation. Clotting tendency can be increased in:
- hyperviscosity states
- smoking
- oral contraceptive pill
- pregnancy
What is the clinical presentation of retinal vein occlusion?
Patients are typically middle aged or elderly. Sudden painless loss of central vision occurs when the involved segment of retina includes the macula, as is the case with central and some branch occlusions. The severity of the initial fall in visual acuity varies considerably from case to case, commonly ranging from 6/9 to hand movements. There may be a relative afferent pupillary defect. On fundoscopy, flame, dot and blot haemorrhages, cotton wool spots, a swollen optic disc and macular oedema may be seen.
The condition is usually unilateral.
What are the important complications of retinal vein occlusion?
The two major complications are macular oedema and neovascularisation of the iris and retina. Iris neovascularisation (rubeosis) can lead to severe, painful glaucoma which is difficult to control.
How should a patient be assessed with retinal vein occlusion?
Common systemic associations include hypertension and diabetes. Rarely, blood dyscrasias or vasculitis may be the cause. The major ocular association is elevated intraocular pressure. The diagnosis is clinical. Investigations are directed primarily at excluding treatable associations.
What is the treatment of retinal vein occlusion?
Treatment is of the disease and of any systemic associations.
Macular oedema - laser treatment to reduce oedema and improve vision may be successful in branch retinal vein occlusion
Neovascularisation - as with proliferative diabetic retinopathy, laser of ischaemic areas can reverse neovascularisation. The case for prophylactic laser after vein occlusion but before the development of neovascularisation is not yet proven
Neovascular glaucoma - a variety of treatment, including laser and surgery are used, but the outcome is usually poor. A painful, blind eye may need to be removed
What is the pathogenesis of retinal artery occlusion?
Arterial occlusions typically lead to more severe visual loss than venous occlusions. As with venous disease, arterial occlusion can involve the central artery itself or one of its branches.
The commonest cause of aterial occlusion is embolisation, the emobolus originated most frequently from a source in a carotid artery, consisting of cholesterol, calcific plaques or fibrinoplatelet material. Emboli may pass through the retinal vascular system cause transient rather than permanent visual loss. Inflammation within the vessel wall, arteritis, may also cause occlusion.
Systemic conditions associated with retinal artery occlusion are hypertension, diabetes, IHD and CAD.
How does retinal artery occlusion present?
A branch retinal arteriolar occlusion may not give symptoms if the area affected is away from the macula. Central artery occlusions usually present with the sudden onset of severe monocular loss of vision, often to “counting fingers”or worse. The patient may report having experienced similar but transient episodes previously (amaurosis fugax). A marked relative afferent pupillary defect is usually present in central occlusions and frequently in branch occlusions.
What are the key features of retinal artery occlusion?
History of amaurosis fugax
Retinal pallor, cherry red spot (recedes after 6 weeks)
Narrow truncated arteries
Emboli visible within arterioles
Note that unlike ischaemic optic neuropathy, the optic disc is not usually pale or swollen.
How should patients with retinal artery occlusion be assessed?
Patients often have systemic conditions associated with microvascular disease, particularly hypertension, diabetes mellitus, IHD and peripheral vascular disease. Giant cell arteritis, although usually causing ischaemic optic neuropathy rather than embolic retinal artery occlusion, should always be considered.
Key features are pain and tenderness along the superficial temporal artery and elevated ESR and CRP. Other investigations may be performed to detect occult cardiovascular disease and potential sources of embolisation - i.e. carotid Doppler.
What is the treatment for retinal artery occlusion?
There is no specific treatment which reliably restores vision, but urgent referral to confirm the diagnosis is necessary, especially if a diagnosis of giant cell arteritis, which is treatable is not to be missed.
Regular prophylactic aspirin is prescribed, if not contraindicated, since it is likely to have a protective effect against arterial occlusion in the other eye and against stroke.
What are the clinical features of anterior ischaemic optic neuropathy (AION)?
Sudden onset sight loss, usually unilateral at first, may be preceded by transient episodes of visual loss. There is a relative afferent pupillary defect and a swollen optic disc, with haemorrhage and cotton wool spots. Field loss is usually altitudinal, in which the upper and lower half of the uniocular field is affected. In a young patient, optic neuritis is more likely, although this usually causes pain exacerbated by eye movement. Other causes of optic disc swelling are much less likely.
What are the different types of AION?
Two types are recognised: arteritis and nonarteritic.
The arteritic form is caused by giant cell (temporal) arteritis. Urgent diagnosis and treatment with systemic steroids is necessary to prevent bilateral blindness. Key features are scalp tenderness with inflammatory swelling of the temporal arteries, jaw claudication and an elevated ESR and CRP.
Nonarteritic ischaemic optic neuropathy has no sign of inflammation and is associated with atherosclerosis, hypertension, smoking and diabetes mellitus.
How many layers are there in the retina?
The retina comprises two layers:
1) the neurosensory retina, including photoreceptors and the ganglion cell layer
2) the retinal pigment epithelium
What are the 2 main types of retinal detachment?
Retinal detachment is a cleavage in the plane between the neurosensory retina and the retinal pigment epithelium (the subretinal space). Most cases of retinal detachment are rhegmatogenous, cause by a tear or hole in the neurosensory retina, which allows fluid from the vitreous humour to pass through into the subretinal space. Degenerative changes in the vitreous are important in the pathogenesis of rhegmatogenous retinal detachment.
Retinal detachment without a retinal break (nonrhegmatogenous) may also occur:
- tractional, when the retina is pulled off by membranes growing across its surface (e.g. advanced diabetic eye disease)
- exudative, caused by breakdown of the blood-retinal barrier allowing fluid to accumulate in the subretinal space (e.g. choroidal tumour, uveitis)
How does rhegmatogenous retinal detachment present?
This can present in a number of ways. Clinical features include:
- floaters/ flashing lights
- peripheral field loss
- loss of central vision
- loss of red reflex
- detached retina
Usually there is an antecedent history of vitreous detachment, but the importance of the symptom may go unnoticed, so that presentation with visual loss is usual.
Key differentiating features are:
- dense shadow that starts peripherally and progresses towards central vision
- a veil or curtain over the field of vision
- straight lines appear curved
How is rhegmatogenous retinal detachment detected clinically?
The peripheral field loss can be detected by simple confrontational testing. On fundal examination, detached retina is grey and the normal red reflex is lost. The grey retina seems to balloon forwards, requiring examination with “plus” lenses in the ophthalmoscope. Retinal blood vessels are seen on the surface.
