Painless Loss of Vision Flashcards
(36 cards)
What acronym can be used to help differentiate the cause of painless loss of vision
5 quick questions to differentiate causes – HELLP
Headache – do an ESR and CRP in all cases urgently for GCA
Eye movement hurting – optic neuritis
Light flashing preceding visual loss – retinal detachment
Like a curtain descending – Amaurosis fugax may precede permanent visual loss – GCA or emboli
Poorly controlled DM – vitreous haemorrhage
What are optic neuropathies?
Optic Neuropathies – damage to the optic nerve that results in monocular blindness with a central scotoma, afferent pupillary defects, dyschromatopsia (colour blindness) and papillitis on fundoscopy which progresses to optic atrophy (pale disc indicates long term damage)
What is anterior ischaemic optic neuropathy (AION)?
Most common cause in older patients. Posterior blood supply to the optic nerve is blocked by inflammation or atheroma. Fundoscopy – pale swollen optic disc. Two types, either arteritic AION or non-arteritic AION.
What is the most common type of AION?
Giant Cell (temporal) Arteritis (GCA) Most common type of arteritic AION. It is a medium to large vessel vasculitis in patients typically over 70 years and very rarely occurring before 50yrs.
What are the risk factors for GCA?
Twice as common in women as men. Strong association with polymyalgia rheumatica, hip and shoulder girdle aching and morning stiffness.
Describe the clinical features of GCA?
New onset headache
Malaise
Jaw claudication (chewing pain)
Tender scalp and temporal arteries (thickened and pulseless)
Neck pain
Monocular visual loss (can be transient – amaurosis fugax)
Diplopia
Pulseless temporal artery
Skip lesions on biopsy
Features of PMR – aching, morning stiffness, lethargy, depression, low grade fever, anorexia and night sweats
How should suspected GCA be investigated?
ESR and CRP (before steroids)
Temporal artery biopsy within a week (but may miss affected section – skip lesions)
How is GCA managed?
Give steroids asap as other eye is at risk – prednisolone PO STAT – should see a rapid response, if not then reconsider diagnosis
Tail off steroid as ESR and symptoms settle but this may take over a year
1 in 5 left with partial or complete blindness
What is optic neuritis?
Demyelinating inflammation of the optic nerve. Full recovery usually takes place over 2-6 weeks, but a very large number go on to develop multiple sclerosis in the next 15 years.
Other than MS what other causes are there for optic neuropathy?
Syphilis
Leber’s optic atrophy
Diabetes
Vitamin deficiency
What are the clinical features of optic neuropathy?
Unilateral loss of vision occurring over hours or days
Colour vision affected first with red appearing less red (red desaturation)
Eye movements hurt
Afferent pupillary defect
Central scotoma
How is optic neuropahty managed?
High dose methylprednisolone for 72 hours
Followed by prednisolone for 11 days
On MRI if >3 white matter lesions then 5-year risk of developing MS is 50%
What is retinal vein occlusion?
Incidence increases with age and is the 2nd most common cause of blindness from retinal vascular disease. If whole central retinal vein is occluded there is complete visual loss in that eye resulting in ischaemia and macular oedema. CRVO can be ischaemic or non-ischaemic. Non-ischaemic is more common and has a better prognosis and may even have normal vision but may progress to ischaemic.
What can cause retinal vein occlusion?
Arteriosclerosis Hypertension Diabetes Polycythaemia Glaucoma
What are the clinical features of central retinal vein occlusion?
Note branch retinal vein occlusion can be asymptomatic if it doesn’t affect the macula
Occurs less suddenly than central retinal artery occlusion
Non-Ischaemic
Decrease in visual acuity to >20/200, RAPD mild or absent, macular oedema, haemorrhage, cotton wool spot, venous tortuosity, and dilation
Ischaemic
Cotton wool spots, swollen optic nerve, maula oedema, severe venous tortuosity and dilation and risk of neovascularisation.
How should retinal vein occlusion be investigated?
Acuity
Retinal imaging
Fundus fluorescein angiogram – determines extend of the ischaemia
How is retinal vein occlusion managed?
Refer to on call ophthalmologist
Non-Ischaemic – follow up after 3 months after exploring causes and managing this
Ischaemic – follow up monthly for 6 months
Intravitreal anti-VEGF
Dexamethasone implants or intravitreal triamcinolone
Photocoagulation if new vessels have begun to form
What is central retinal artery occlusion?
A lot less common than retinal vein occlusion but considered a stroke and should be treated as such. Most commonly it is thromboembolic from AF or carotid disease. Look for heart valve disease diabetes, BP.
How does retinal artery occlusion present?
Afferent pupillary defect appears within seconds and may precede retinal changes. Retina appears white with a cherry red spot at the macula.
How should retinal artery occlusion be managed from the ophthalmic point of view?
Extra ophthalmic management
Attempt to increase blood flow if within 100mins
Reduce intraocular pressure with ocular massage, surgical removal of aqueous or use of intraocular hypotensive treatment.
What is a vitreous haemorrhage?
This occurs after retinal revascularisation, retinal tears, retinal detachment or trauma. Small extravasation of blood results in vitreous floaters. Very common causes of painless loss of vision. After bleeding stops typically absorbed at a rate of 1% per day.
What investigations should be done in vitreous haemorrhage?
Dilated fundoscopy
Slit lamp examination – red blood cells in the anterior vitreous
If retina not seen then B-scan USS – can detect retinal tear/detachment
Fluorescein angiography to identify neovascularisation
Orbital CT if globe injury
How does a vitreous haemorrhage present and can it be treated?
Painless loss of vision or visual haze (more common)
Red hue in the vision
Floaters or shadows/dark spots in the vision
Visual field defect if severe haemorrhage
If bleed is large enough to obscure vision, there will be no red reflex and the retina may not be seen. In this case a B-scan US can be used to located a cause.
Usually the blood undergoes spontaneous absorption. However, in extensive and dense a vitrectomy is done to remove the blood if the retina is torn/detached.
What is a retinal detachment?
Holes/tears in the retina allow fluid to separate the sensory retina from the pigment epithelium. If macula involved may not recover even after fixation.
