Blurred Vision Flashcards
Painful acute, red-eye, blurred vision
Corneal ulcer
Uveitis
Glaucoma (AACG)
See red eye deck
Chronic blurred vision
Diabetic retinopathy/maculopathy --> see systemic diseases deck Glaucoma (POAG) Cataract Dry age-related macula degeneration See gradual loss of vision deck
Painless acute, white-eye, blurred vision
Central retinal artery occlusion/Central retinal vein occlusion
Wet age-related macula degeneration –> gradual vision loss deck
Non-arteritic Anterior ischemic optic neuropathy
Giant cell arteritis (arteritic anterior ischemic optic neuropathy)
Retinal detachment
Retinal vein occlusion
Blockage of a central or peripheral retinal vein -> peripheral may show local haemorrhage
Second most common retinal vascular disorder, more common in people over 65yrs
May be due to thrombus formation or compression by adjacent arterioles
Central Retinal vein occlusion - risk factors
Atherosclerotic -> age, diabetes, raised cholesterol and hypertension, smoking and obesity
Raised IOP
Inflammatory/coagulative diseases –> sarcoidosis or myeloma, protein C or S deficiencies
Central Retinal vein occlusion - complications
Backlog of blood and hypoxia causes leakage of blood contents.
Ischemic damage leads to VEGF - causing new vessel growth which can cause haemorrhage or neovascular/’90 day’ glaucoma if they clog the trabecular meshwork
Permanent macula or optic atrophy
Central Retinal vein occlusion - Non-ischaemic
Milder, 75%, may resolve fully with good outcomes or progress to ischaemic type
Mild or absent afferent pupillary defect
Widespread dot-blot and flame haemorrhages throughout the fundus - some disc oedema
Central Retinal vein occlusion - Ischaemic
Rarer and more severe - can lead to a painful blind eye or neovascular glaucoma –> rarely linked to retinal detachment
Severe visual impairment and afferent pupillary defect
Similar fundus appearance to non-ischaemic but disc oedema is more severe - haemorrhage scattered in ‘blood-storm’ pattern with cotton wool spots
Central Retinal artery occlusion - management
No proven treatment options
Identify and modify risk factors
Recognise and treat complications
Ischaemic CRVO observation and panretinal photo coagulation therapy if they show signs of neovacularization near the iris
Non-ischaemic central Retinal artery occlusion - outcome
<10% recover normal vision, 50% have persistent impairment of 6/60 or worse
1/3 develop ischaemic type within 3 years
Presentation acuity predicts acuity outcome
Ischaemic central Retinal artery occlusion - outcome
Very poor due to macula oedema and ischaemia
>90% have impaired vision of 6/60 or worse
60% develop neovascularisation and 50% develop it around the iris (rubeosis iris) - usually between 2-4 months later
Require monitoring, may need panretinal photocoagulation (PRP)
Branch/peripheral retinal artery occlusion
3x as common as CRVO,
Presentation and prognosis depends on occlusion location and affect on macula drainage - a hemiretinal occlusion is proximal enough to affect half of retinal drainage
Fundoscopy will show vessel dilation/tortuousity + haemorrhage
Treatment for Branch/peripheral retinal artery occlusion
Refer to ophthalmologist
Some benefit from PRP treatment if there is macula oedema
Triamcinolone treatment has anatomical and functional benefits in reducing macula oedema but increases the risk of glaucoma/cataracts etc
Dexamethasone implants can be used to treat macula oedema
RPE
Retinal pigment epithelium
Retinal artery occlusions - anatomy
Outer layer of RPE, photoreceptors and overlying tissue are supplied by the choroid –> supplied by various cillary arteries, branches of the ophthalmic artery
The inner neural retina is supplied by the central retinal artery directly from the ophthalmic, which divides into 4, superior and inferior nasal and temporal branches
Retinal artery occlusions - causes
80% - atherosclerosis related thrombus, hypertension accounts for 60% of these, diabetes is co-morbid in 25%
Embolism - from carotid, cardiac or aorta
Inflammatory - giant cell arteritis, wegener’s, SLE
Rarely infectious, pharmacological or ophthalmic causes
Central retinal artery occlusion
Blockage before it branches incidence 8.5/million/year
Mostly in elderly pts, in young it is usually due to valve disease
Presents as sudden, unilateral, painless vision loss –> close to total blindness - Hx of amaurosis fugax in 10% of pts
Bilateral in 1-2% of cases, not necessarily symmetrical
Amaurosis fugax
A transient monocular visual loss usually due to a temporary reduction in retinal artery blood flow
Central Retinal artery occlusions - signs
Afferent pupillary defect
Pale retina with attenuation of vessels
Centre of the macula is supplied from the underlying choroid and so stands out as a ‘cherry red spot’
Central Retinal artery occlusions - management
Investigate to exclude underlying disease - carotid endartectomy
If patient presents within 90-100mins of event firm ocular massage or reducing IOP can be tried with variable results
Referral to ophthalmology is essential but even with early treatment prognosis is poor
Central Retinal artery occlusions - outcomes
Inner neural layer becomes atrophic and all useful vision is lost
1/3 patients show some improvement, in 1-15% of patients there is spontaneous resolution of symptoms –> these must be monitored for neovascular changes
CRAO counts as H/O IHD and has a 3x increased mortality rate
Branch retinal artery occlusion
Like CRAO but defect is only altitudinal or sectoral
Retinal pallor corresponds to the area affected
Occasionally embolus is seen->cotton wool spots in the area later
As with CRAO treatment is investigation for underlying disease, prognosis is better with most pts achieving 6/12 or better vision
Cilloretinal artery occlusion
Supply posterior pole of the globe
Occlusion of these artery may occur in up to 30% of the population, usually young people and will often be associated with other oculo-vascular problems
Reasonable prognosis except giant cell arteritis associated
Non-arteritic anterior ischemic optic neuropathy
Caused by occlusion of the short posterior cillary arteries
This causes infarction of the optic nerve head
Non-arteritic anterior ischemic optic neuropathy (NAAION) - risk factors
Male Systemic arteriopathy 40-60yro Small, hypermetropic optic discs Hypertension and diabetes
Non-arteritic anterior ischemic optic neuropathy - history
Establish when vision was lost and in which eye
Assess cardiovascular RFs - exclude giant cell arteritis (palpate temporal artery)
Measure acuity and RAPD - typically a unilateral altitudinal hemianopia
Examine the optic discs using dilated fundoscopy
Visual field defects in Non-arteritic anterior ischemic optic neuropathy
Usually altitudinal
Bottom or top half of the vision in one eye is gone
Inferior altitudinal most common
Non-arteritic anterior ischemic optic neuropathy - symptoms & signs
Symptoms - Painless, monocular sudden onset loss of vision
May be asymptomatic if good vision in other eye
Signs - moderate/severe reduction in visual acuity in affected eye (6/12-6/60) - RAPD
Some or all of the optic disc may be swollen with flame or splinter haemorrhages - visual field defect will correspond
Non-arteritic anterior ischemic optic neuropathy - management
Refer to ophthalmology - exclude giant cell arteritis with examination/CRP/ESR
Review and treat cardiovascular risk factors - consider starting aspirin
Non-arteritic anterior ischemic optic neuropathy - prognosis
30% will improve 3 or more lines on a Snellen chart
15-30% risk to fellow eye
Optic disc swelling will resolve leading optic disc pallor due to loss of nerve fibres
Giant cell arteritis
A rare but important disease - aka temporal arteritis or arteritic anterior ischaemic optic neuropathy
Giant cell arteritis is a vasculitis of the medium and large arteries and often affects arteries in the scalp/head/neck compromising optic nerve head blood supply
Giant cell arteritis - symptoms
a sudden, painless, monocular vision loss - may be preceded by transient episodes of visual loss
similar to NAAION but with raised CRP/ESR and pain
Headache and scalp tenderness
Jaw claudication, loss of appetite and weight loss
Giant cell arteritis - signs
Severe reductions in visual acuity
Non-pulsatile and tender temporal arteries
Swollen optic disc and RAPD
May have flame haemorrhages & cotton wool spots indicating retinal nerve fibre layer infarction
Giant cell arteritis - investigations
Examine temporal artery for welling and feel for pulsation
Measure acuity - test for field defect and RAPD
fundoscopy for optic disc swelling
Giant cell arteritis - management
Inflammatory markers (ESR/CRP) High dose systemic steroids Temporal artery biopsy within a couple of days of starting steroids to confirm giant cell
Anatomy of retinal tears
Tears occur when the inner neurosensory retina is separated from the outer RPE
Posterior vitreous detachment (PVD)
As people age the vitreous humour shrinks and detaches from the retina - normally this doesn’t cause a problem but if there is abnormal adhesion between the retina and the humour then this can tear (rhegma) the retina
Rhegmatogenous retinal detachment
Occurs if vitreous fluid passes through a tear caused by PVD and separates the NS retina from the RPE
Most common form of retinal detachment
Retinal detachment - presentation
Painless loss of visual field - flashing lights (photopsia) most commonly in the peripheral temporal field
Increased number of floaters
There isn’t any loss of visual acuity unless the fovea detaches (macula-off retinal detachment)
Floaters
Blood, RPE cells or condensed vitreous fibres which have entered the vitreous cavity
They move around as the pt moves their eye
A small number are not worrying but lots with photopsia is serious and requires investigation
Retinal detachment - examination
Check RAPD & acuity - check fellow eye
Often difficult to exclude a retinal tear using dilated ophthalmoscopy
Early detachments usually occur in the periphery so you must investigate the quadrants
Risk factors for retinal tears
Myopia
Previous retinal detachment or detachment in fellow eye
Trauma
Poorly controlled Diabetics –> tractional retinal detachment
pts with inflammatory eye disorders –>serous retinal detachment
Tractional retinal detachment
Occur when retinal scar tissue contracts and pulls the retina off the RPE, causing a detachment without formation of a tear
Occurs in conditions causing retinal damage and scarring
Particularly poorly controlled diabetics
Serous retinal detachment
Exudative fluid collects between the neurosensory retina and the RPE, causing detachment without a tear
Occurs in conditions causing inflammation and oedema of the retina
Retinal detachment - management
A medical emergency
If a pt reports flashes, field defects and floaters refer immediately
Aim to treat before the macula detaches to preserve vision
Surgery - cryobiology surgery or pars plana vitrectomy
Cryobuckle surgery
A treatment for retinal detachment
A silicone explant is used to indent the sclera from the outside of the globe, pushing the RPE back against the retina and a cryotherapy probe is used to create a scar that seals the retinal break
Pars plana vitrectomy
A three port procedure which is the most common treatment of retinal detachment
Involves removal of the vitreous humour and use of cryotherapy or a laser to seal the retinal tear
A bubble of gas is then used to push the retina against the RPE
