24. Visual disturbance/impairment Flashcards
differentials for sudden vision loss
ischaemic/vascular
- retinal vein occlusion
- retinal artery occlusion: TIA/stroke/giant cell arteritis
- anterior ischaemic optic neuropathy: TIA/stroke/giant cell arteritis
- vitreous haemorrhage
- retinal detachment
- acute angle closure glaucoma
- optic neuritis
differential for gradual vision loss?
Refractive error
Cataracts
Macular degeneration
Chronic (open angle) glaucoma
Diabetic retinopathy
Hypertensice retinopathy
differentials for diplopia
eye muscle problem:
- myasthenia gravis
- graves
- strabismus
neurological:
- head injury
- stroke
- migraine
- tumour
- wernikes
Nerve problem (eg 3rd CN, 4th CN or 6th CN)
- diabetes
- congenital
- raised ICP
- MS
- guilian barre
examination vision loss
Inspection: is it RED (acute angle closure)
Optic nerve: acuity, visual fields, attention, accommodation, pupils, colour vision
- Pupil unreactive/not responding/ well to light/RAPD suggests optic nerve dysfunction therefore could be due to anterior optic neuropathy (GCA or TIA), optic neuritis etc
Eye movements: H test, any double vision? any pain on movement? (any CN palsys?)
To complete…
Opthalmoscopy
HbA1c, BP
Referral for slit lamp examination
what should you be able to label on fundoscopy
optic disc
optic cup
macula
fovea
retinal vein
retinal artery (thinner than veins)
history taking vision loss/disturbance
PC: onset? sudden? is the vision loss in one portion of your vision? eg the sides or the middle etc. floaters/flashes?
HoPC: PAIN?? - suggests acute angle closure glaucoma. pain on eye movement? (optic neuritis), do colours look the same? (loss of red in optic neurtis)
Associated symptoms: headache especially near temples?(GCA) weakness?
SHx:
eye trauma e.g. boxing, ask about occupation and hobbies
what is amaurosis fugax? causes
Amaurosis fugax describes a temporary loss of vision caused by a temporary interruption to the blood supply - like a curtain coming down…
causes of amaurosis fugax?
ischaemic/vascualr causes of sudden vision loss eg
Retinal vein occlusion
Retinal artery occlusion: TIA/stroke/GCA
Anterior ischaemic optic neuropathy: TIA/stroke/GCA
Giant-cell arteritis
As this may represent a TIA, 300mg aspirin is given
central retinal vein occlusion
presentation
causes
examination
fundoscopy
management
presentation: sudden, painless, reduction or loss in visual acuity, unilateral
causes:
Risk factors
increasing age
hypertension
cardiovascular disease
glaucoma
polycythaemia
examination: reduced visual acuity
fundoscopy:
“stormy sunset” multiple haemorrhages
management:
majority conservative
if macualr oedema, consider VGEF
central retinal artery occlusion
presentation
examination
fundoscopy
management
presentation:
sudden, painless, unilateral vision loss
examiantion: RAPD
causes:
TIA/stroke/GCA
fundoscopy
‘cherry red’ spot on a pale retina
management:
think of it as TIA/stroke/GCA
–> any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)
Anterior ischaemic optic neuropathy
presentation
causes
examination
fundoscopy
management
presentation: loss of vision
causes: TIA/stroke/GCA
examination: RAPD
fundoscopy: swollen pale disc and blurred margins
management:
think of it as TIA/stroke/GCA
–> any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)
vessel occluded in AION
posterior ciliary artery
cherry red spot
central retinal artery
blood supply optic nerve
central retinal artery
“stormy sunset” multiple haemorrhages
central retinal vein occlusion
Giant cell arteritis causing visual symptoms
presentation
examination
fundoscopy
management
PC: decreased visual acuity, temporal headache
examination: reduced visual acuity, tenderness over temple
fundoscopy: Retinal splinter haemorrhages or disc oedema. AION swollen pale disc and blurred margins.
management:
medical emergency due to risk of
- stroke
- blindness (a strple affecting the retinal vessels, optic nerve) - 90% AION (Anterior Ischemic Optic Neuropathy)
phone rheum on-call
Should have confirmatory test: USS halo sign or temporal artery biopsy
Initial
1. High dose oral glucocorticoids eg oral methylprednisolone
With visual loss:
1. IV methylprednisolone
+ Urgent ophthalmology review
+ Bone protection for steroids
refractory/relapsing : tocilizumab
vitreous haemorrhage
presentation
causes
examination
fundoscopy
management
presentation: painless vision loss, dark spots obscuring vision with a red hue
causes:
- DIABETES, bleeding disorders, anticoagulants
examination: decreased visual acuity, visual field defect if severe haemorrhage
dilated fundoscopy: may show haemorrhage in the vitreous cavity
if new onset rf urgently (<24hrs) for slit-lamp examination,
other stuff may be used eg:
ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
fluorescein angiography: to identify neovascularization
orbital CT: used if open globe injury
retinal detachment
presentation
causes
examination
fundoscopy
management
PC: vision loss, curtain or shaddow progressing to the centre from the periphery, floaters or flashes,
risk factors
diabetes mellitus
myopia
age
previous surgery for cataracts
eye trauma e.g. boxing
examination
fundoscopy
the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms
if the break is small, however, it may appear normal.
It is a reversible cause of visual loss, provided it is recognised and treated before the macula is affected.
rf urgently
plan pt with new onset flashes and floaters
Arrange immediate referral to an ophthalmologist with retinal surgery expertise to be seen on the same day, if there are signs of sight-threatening disease, such as:
- Visual field loss or changes in visual acuity.
- Fundoscopic signs of retinal detachment or vitreous haemorrhage.
any patients with new onset flashes and floaters WITHOUT VISUAL/FUNDOSCOPY CHANGES should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for:
pigment cells
vitreous haemorrhage
posterior vitreous detachment
presentation
causes
examination
fundoscopy
management
presentation: no vision loss, floaters, flashes, blurred vision, cobwebs
causes:
ageing
myopia
fundoscopy: weiss ring
Investigations:
All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.
Management:
Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this.
optic neuritis
presentation
causes
examination
fundoscopy
management
PC: unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
central scotoma
causes:
multiple sclerosis: the commonest associated disease
diabetes
syphilis
examiantion: relative afferent pupillary defect
Mangement
MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases
high-dose steroids
recovery usually takes 4-6 weeks
most common cause of blindness in the UK
Age-related macular degeneration
what is age related macualr degenertaion
Degeneration of the central retina (macula) is the key feature with changes usually bilateral.
ARMD is characterised by degeneration of retinal photoreceptors that results in the formation of drusen which can be seen on fundoscopy and retinal photography. It is more common with advancing age and is more common in females.
fundoscopy how is wet AMD different to dry? pathophysiology
In wet AMD, new vessels develop from the choroid layer and grow into the retina (neovascularisation). These vessels can leak fluid or blood, causing oedema and faster vision loss. A key chemical that stimulates the development of new vessels is vascular endothelial growth factor (VEGF). This is the target of medications to treat wet AMD.
which is more common wet or dry AMD?
dry = 90%
risk factors macualr degeneration
Older age
Smoking
Family history
Cardiovascular disease (e.g., hypertension)
Obesity
Poor diet (low in vitamins and high in fat)
dry and wet AMD
compare presentation
Presentation:
both:
- vision loss- reduction in visual acuity particualrly for close objects
- difficulties in dark adaptation
- fluctuations in visual disturbance
- visual hallucinations may also occur resulting in Charles-Bonnet syndrome
- photopsia, (a perception of flickering or flashing lights), and glare around objects
gradual in dry ARMD
subacute in wet ARMD
Wet AMD presents more acutely than dry AMD. Vision loss can develop within days and progress to complete vision loss within 2-3 years. It often progresses to bilateral disease.
differentiating AMD and glaucoma presentation
Glaucoma is associated with peripheral vision loss and halos around lights. AMD is associated with central vision loss and a wavy appearance to straight lines. This helps you tell them apart in exams
examination and fundoscopy ARMD
Reduced visual acuity using a Snellen chart
Scotoma (an enlarged central area of vision loss)
Amsler grid test can be used to assess for the distortion of straight lines seen in AMD
Drusen may be seen during fundoscopy
what invetsigation is useful for wet
ARMD
Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to assess the blood supply, showing oedema and neovascularisation in wet AMD.
management wet ARMD
Anti-VEGF medications
laser photocoagulation but is more risky
management dry ARMD
Management involves monitoring and reducing the risk of progression by:
Avoiding smoking
Controlling blood pressure
Vitamin supplementation has some evidence in slowing progression
what are cataracts
A cataract is a common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy. This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision
causes of cataracts
Normal ageing process: most common cause
Other possible causes
Smoking
Increased alcohol consumption
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders: HYPOCALCAEMIA
presentation cataracts
Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights
o/e cataracts
A Defect in the red reflex: the red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex.
invetsigations catracts
Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract
management cataracts
conservative: stronger glassess, use brighter lights
surgical
This involves removing the cloudy lens and replacing this with an artificial one. NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice
complications post-cataracts surgery
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour
define glaucoma
Glaucoma refers to the optic nerve damage caused by a rise in intraocular pressure.
risk factors for open-angle glaucoma
Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)
presentation open angle glaucoma
Glaucoma affects the peripheral vision first, resulting in a gradual onset of peripheral vision loss (tunnel vision). It can also cause:
Fluctuating pain
Headaches
Blurred vision
Halos around lights, particularly at night
gold standard way to measure intraocualr pressure
Goldmann applanation tonometry
It involves a device mounted on a slip lamp that makes contact with the cornea and applies various pressures.
investgations open angle glacuoma
Goldmann applanation tonometry for the intraocular pressure
Slit lamp assessment for the cup-disk ratio and optic nerve health
Visual field assessment for peripheral vision loss
Gonioscopy to assess the angle between the iris and cornea
Central corneal thickness assessment
when is treatment indicated for open angle closure glaucoma
intraocular pressure of 24 mmHg or above.
management open angle closure glaucoma
- 360° selective laser trabeculoplasty (lazer hole to improve drainage of aqueous humour…delays need for eye drops)
- Prostaglandin analogue eyedrops (e.g., latanoprost) are the first-line medical treatment. They increase uveoscleral outflow. Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning).
the next line of treatments includes:
beta-blocker eye drops
carbonic anhydrase inhibitor eye drops
sympathomimetic eye drops
surgery in the form of a trabeculectomy may be considered in refractory cases.
adverse effects of miotics such as pilocarpine
constricted pupil, headache and blurred vision
adverse effects of prostaglandin analogues eg latanoprost
brown pigmentation of the iris, increased eyelash length
who shouldn’t get beta blocker eye drops (e.g. timolol, betaxolol)
Should be avoided in asthmatics and patients with heart block
most common cause of blindness in adults adults aged 35-65 years-old?
diabetic retinopathy
types ofclassification of dianetic retinopathy
non-proliferative diabetic retinopathy (NPDR)
proliferative retinopathy (PDR)
Maculopathy.
characteristics of non-proliferative diabetic retinopathy - fundoscopy
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots
venous bleeding
Intraretinal microvascular abnormalities (precursor to neovascularisation)
characteristics of proliferative diabetic retinopathy - fundoscopy
retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
what type of diabetic retinopathy is more common in type 1 DM
PROLIFERATIVE
more common in Type I DM, 50% blind in 5 years
characteristics of maculopathy in diabetic retinopathy
hard exudates and other ‘background’ changes on macula
check visual acuity
management diabetic retinopathy for all patients
All patients:
optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology
managemet maculopathy diabetic retinopathy
if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors
management non-prolifertaive diabetic retinopathy
non-prolifertive:
regular observation
if severe/very severe consider panretinal laser photocoagulation
management prolifertaive dianetoc retinopathy
prolifertaive:
panretinal laser photocoagulation
+/- intravitreal VEGF inhibitors
complications panretinal laser photocoagulation
following treatment around 50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue
other complications include a decrease in night vision (rods are predominantly responsible for vision in low light conditions, the majority of rod cells are located in the peripheral retina), a generalised decrease in visual acuity and macular oedema
example of intravitreal VGEF inhibitor
ranibizumab
stages of hypertensive retinopathy
SAC papilloedema
Stages:
1. S = silver wiring (increased light reflex) and arteriolar narrowing
2. A = arteriovenous nipping
3. C = cotton wool exudates and flame and blot haemorrhages
4. Papilloedema
Contralateral hemiparesis and sensory loss, upper extremity > lower, Contralateral homonymous hemianopia, Aphasia
Middle cerebral artery
Contralateral homonymous hemianopia with macular sparing, Visual agnosia
Posterior cerebral artery
contralateral hemiparesis/hemisensory loss of face arma dn leg, higher cog dysfunction such as aphasia, homonymous hemianopia
total anteroir ciruclation infact, if only 2 = partial
Bitemporal hemianopia
Midline lesion at chiasm
upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
Right nasal hemianopia
Lesion involving right perichaismal area
Left homonymous hemianopia
Lesion or pressure on right optic tract (posterior to chiasm, before optic radiations)
Lesion or pressure across all right optic radiations
Left homonymous hemianopia with macular sparing
Lesion in right occipital lobe (both banks of calcarine fissure) posterior cerebral artery
Left superior homonymous quadrantanopia
PITS = parietal inferior, temporal superior therefore;
Temporal as superior
Right sided tract
Lesion to the right inferior optic radiations in the temporal lobe (meyer’s loop)
Right inferior homonymous quadrantanopia
PITS = parietal inferior, temporal superior therefore;
Parietal as inferior
Right visual field so left optic tract
Lesion to the left superior optic radiations in the parietal lobe
How do patients with pituitary adenoma present?
Patients will present with the consequences of hormone excess (e.g. Cushing’s due to ACTH, or acromegaly due to GH) or depletion.
Compression of the optic chiasm will cause a bitemporal hemianopia due to the crossing nasal fibers.
Most common paediatric supratentorial tumour? how does it present?
Craniopharyngioma
hormonal disturbance, symptoms of hydrocephalus or bitemporal hemianopia.
features of third nerve palsy
eye is deviated ‘down and out’
ptosis
if surgical:
pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)
painful
causes of third nerve palsy
consider surgical :
eg posterior communicating artery aneurysm
other serious:
- false localizing sign* due to uncal herniation through tentorium if raised ICP
- Weber’s syndrome stroke
other:
diabetes mellitus
vasculitis e.g. temporal arteritis, SLE
features of fourth nereve palsy
Trochlear nerve
LR6SO4
Defective downward gaze –> vertical diplopia
Nasal upshoot is how it looks!!!!
head tilted to the other side
causes of 4th nerve palsy
- CONGENITAL (esp if head tilted)
Vasculopathy (htn, diabetes)
Tumour
Congenital (esp if head tilt)
Trauma
features of 6th nerve palsy
defective lateral gaze
appear cross-eyed
causes of 6th nerve palsy
think RAISED ICP eg IIH
Vasculopathic
Tumour
types of strabismus
Manifest strabismus = there all the time
Latent = underlying - picked up with cover test - may be symptomatic
Intermittent exotropia = strabismus when looking far
Esotropia - inwards towards nose
Exotropia - outwards
Hypertropia - upwards
Hypotropia - downwards
causes strabismus
non-paralytic squint (excess tone in one muscle compared to other)
- Hereditary
- Refractive error - most common is long sighted - associated with esophoria -need glasses
Paralytic squint
- disease of the III, IV and VI cranial nerves
pseudostrabismus cuases
Broad epicanthus as not much sleral showing medially
Narrow or wide interpupillary distance
Facial asymmetry
Unilateral ptosis
examination ?diplopia ?strabismus
Cover/uncover : shows manifest strabismus (when other eye is covered, the squint corrects itself)
Alternate cover test : shows latent strabismus (squint present when covers so when uncovered it moves in opposite direction)
Fundoscopy (or red reflex) to rule out retinoblastoma, cataracts and other retinal pathology
Visual acuity
differentiating features non-paryltic vs paryltic squint
non-paralytic
- usually congenital
- no diplopia
- full movement in both eyes if tested separately
- extraocular muscles and nerves are grossly normal
what is amblyopia
Defective visual acuity which persists after correction of the refractive error and removal of any pathology
the brain will cope with this misalignment by reducing the signal from the less dominant eye. This results in one eye they use to see (the dominant eye) and one eye they ignore (the “lazy eye”). If this is not treated, this “lazy eye” becomes progressively more disconnected from the brain and over time the problem becomes worse. This is called amblyopia.
management of ambylopia
- Wear appropriate glasses for 16-18 weeks
- Occlusion of better seeing eye (patching/atropine)
management of strabismus
Aim:
- To restore comfortable binocular single vision (BSV)
- To achieve good alignment
- To eliminate diplopia
Conservative:
Optical - glasses/contact lenses
Prisms
Orthoptic exercise
Surgery:
Resection of muscles to shorten
Botulinum toxin
Injecting into muscle to temporarily paralyse muscle
why should you always check red reflex in children especially with strabismus
RETINOBLASTOMA
absence of red-reflex, replaced by a white pupil (leukocoria) - the most common presenting symptom
pathophysiology retinoblastoma
autosomal dominant
caused by a loss of function of the retinoblastoma tumour suppressor gene on chromosome 13
around 10% of cases are hereditary
presentation retinoblastoma
absence of red-reflex, replaced by a white pupil (leukocoria) - the most common presenting symptom
strabismus
visual problems
management of retinoblastoma
classically enucleation
other options now available: external beam radiation therapy, chemotherapy and photocoagulation
how to interpret snellen chart?
6/6 is normal eg 20/20 in america
1st number is what pt can see
2nd number is average number
6 metres from snellen chart
therefore
9/6 is rly good
2/6 is bad
how to use a snellen chart
pt stood at 6 metres the whole time. cover one eye and test separetly
interpret it off the chart
which metre they land on is first number
