Download Problem 24 – Visual Disturbance

Core clinical problem – Visual Disturbance
Anatomy of the eye
Visual pathway diagram:
If loss of vision is sudden and painless:
Ischaemic optic neuropathy –
Optic nerve is damaged through blockage of ciliary arteries
(inflammation/atheroma)
Giant cell arteritis – the ophthalmic artery is involved, can affect one or both eyes. If
one eye, the other eye is at risk until steroids are given (prednisolone 80mg/24hrs.
Vitreous haemorrhage:
One of the most common causes of loss of vision
Floaters are a symptom
Bleeding occurs whenever sensory retina is torn
Urgent investigation is required incase retinal detachment occurs
Central retina artery occlusion:
Visual loss within seconds of occlusion
Afferent pupil defect in seconds
Visual acuity decreased
Retina appears white with red spot at the macula
Look for signs of atherosclerosis
No reliable treatments but try and lower intraocular pressure
If occlusion lasts for >1hr optic nerve will atrophy and sight loss will be permanent
Central vein occlusion:
Commoner than central artery occlusion
Incidence increases with age
Causes (chronic simple glaucoma, arteriosclerosis)
Fundus is like ‘stormy sunset’
Gradual loss of vision:
Age related macular degeneration –
-
Chief cause of blindness in the U.K.
Loss of central vision
Deposition of colloid bodies (drusen) in the
retina
-
When they reach a particular size and number
they give rise to macular degeneration
Main risk factors – smoking, non-healthy diet,
genetic factor, hypertension increases risk.
Signs and symptoms:
May be incidental finding
Trouble with daily tasks e.g. driving, recognising faces etc.
Yellow deposits in the macular area on fundoscopy
Decreased visual acuity
Scar in the macular area
Bleeding in the macular area
Investigations – slit lamp examination, optical coherence tomography
Management- often rehab and life modification mainstays of management e.g.
large print books, optician involvement to make sure sight is best possible for
them. Laser photocoagulation and anti-VEGF’s (ranibizumab) can be used in
some cases of AMD.
Diabetic retinopathy:
Pathogenesis: capillary endothelial change  vascular leak  microaneurysms
 capillary occlusion  local hypoxia + ischaemia
Background retinopathy
Microaneurysms (dots)
Haemorrhages (blots)
Hard exudates (lipid deposits)
Pre-proliferative retinopathy
Cotton wool spots (infarcts)
Haemorrhages
Venous bleeding
Signs of retinal ischaemia
Proliferative retinopathy
New vessels form (URGENT REFERRAL)
Cataracts:
Opacity and gradual thickening of the crystalline lens or its capsule resulting in
decreased vision
Risk factors:
Diabetes
UV exposure
Smoking
Eye trauma
Steroid use
Uveitis
Divided into the segment of lens that is affected –
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Nuclear (new layers of fibres compress lens
nucleus)
-
Cortical (new layers are added to the outside of
the lens)
-
Subcapsular (opacities in the central posterior
cortex)
Presents with gradual loss of vision, failure to recognise faces, difficulty in reading
Can sometimes see halos in the eye, loss of red reflex
Treat with cataract surgery – Phacoemulsification
Congenital cataracts caused by: hypoglycaemia, trisomy (down’s syndrome, patau’s,
Edwards), myotonic dystrophy, intrauterine infections (rubella, toxoplasmosis,
cytomegalovirus, herpes simplex) and prematurity. Treat with cataract surgery
before baby is 17 weeks old preferably.
Glaucoma:
Disease of optic nerve
Neuropathy associated with an increase in intraocular pressure (IOP) – mean IOP is
15-16mmhg; upper limit of normal is 21mmhg. This can be measured by tonometry.
About 5% of individuals have increased IOP (>21mmhg) without any signs of
glaucoma – approx. 9% of these will develop glaucoma, they should therefore be
treated with IOP-lowering drugs.
Cup to disc ratio is also increased.
Open angle – painless and silently progressive (90% of glaucoma)
There is an increased resistance to aqueous outflow in the trabecular meshwork in
the irodocorneal angle. Approx 90% of the nerve is damaged when visual loss
becomes symptomatic.
Risk factors
–
–
–
–
Family history
Ocular hypertension
Age
Race (afro-Caribbean)
Treatment:
First drugs that lower IOP
-
Beta blockers
Prostaglandin analogues
Carbonic anhydrase analogues
Miotics
Laser and surgical treatments second line
Closed angle – painful and acute (10% of glaucoma)
Iris is not as wide and open as it should be – outer edge of iris bunches up over
drainage canals and blocks the drainage of aqueous outflow.
It presents with pain, headache, blurred vision and systemic malaise
(nausea/vomiting). Red eye (ciliary flush), non or mildly reactive, dilated pupil.
Management:
Refer immediately
Lie patient supine
Treat with topical agents e.g. beta-blockers, steroids (prednisolone), apraclonidine
And also give IV acetazolamide (carbonic anhydrase)
Definitive surgical treatment – peripheral iridotomy
Nerve Palsies:
3rd nerve palsy (oculomotor)
ptosis, proptosis, fixed pupil dilatation, eye
down and out.
Causes – cavernous sinus lesions, superior orbital fissure syndrome, diabetes
mellitus, posterior communicating artery aneurysm.
4th nerve palsy (trochlear)
Diplopia, eye looks upwards adduction, and
cannot look down and in (superior oblique paralysed).
Causes – trauma (30%), Diabetes (30%), tumour, idiopathic.
6th nerve palsy (abducens)
Diplopia in horizontal plane. Eye medially
deviated cannot move laterally. (lateral rectus is paralysed)
Causes – tumour causing increased intracranial pressure, trauma to base of skull,
vascular, MS.
Horner’s syndrome:
Sympathetic fibres are disrupted
-
miosis
ptosis
facial anhydosis
causes of horner’s – posterior inferior cerebellar or basilar artery occlusion, MS,
cavernous sinus thrombosis, pancoast’s tumour, mediastinal mass.
Papilloedema:
A result of raised intracranial pressure.
Usually bilateral and comes on over a few hours or weeks.
A symptom of underlying pathology – if papilloedema is seen on fundoscopy further
evaluation is needed, usually a CT/MRI scan.
If papilloedema is unilateral it suggests an orbital cause, for example, optic nerve
glioma.
Signs/symptoms –
Headache
Blurring of vision
Venous engorgement
Loss of venous pulsation
Haemorrhages over optic disc
Blurring of optic margins
Elevation of optic disc
Ambylopia:
Visual disturbance usually in childhood where the eye is physically normal but visual
stimulation is poorly transmitted or fails to transmit through the optic nerve.
Developmental problem.
3 types –
Strabismic
Refractive
Occlusive
Treat with glasses or force patient to use amblyopic eye by using a patch over the
normal eye.
Strabismus (squint):
The eyes are not correctly aligned. Lack of coordination between extraocular
muscles and depth perception/ binocular vision is disturbed.
Types of squint:
Non-paralytic – one muscle has increased tone compared to the other, the eye
movements are all normal when tested separately. To manage use spectacles,
occlude good eye and use optical exercises.
Paralytic – usually acquired, the innervation to or the extraocular muscles are
damaged. Will usually spontaneously resolve after underlying condition is treated. If
no improvement in 6 months think about surgery.
Miscellaneous
Retinitis pigmentosa:
Triad of
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Night blindness
Peripheral vision loss
Pigmentary retinopathy
Inherited degenerative condition – retinal pigment epithelium become damaged.
No cure but vitamin A supplementation can postpone blindness by approx. 10yrs
Other things that cause visual loss/disturbance:
Tumours
Infections
Hysterical visual loss