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Transcript
Ophthalmic Emergencies
How to avoid missing a serious and
treatable condition
Hong Woon
SJUH, Leeds
Ophthalmic Emergencies
• Ophthalmic emergencies with
obvious clinical signs
• Ophthalmic emergencies
without obvious clinical signs
Alkali burns
• Fertilizers and cleaning products/ drain and oven cleaners/ cement
• Must treat immediately with irrigation before referring on.
• Irrigate with copious amounts of water/ buffer solution until pH normal
• Untreated can become blind due to stromal damage and ischaemia
Beware infection in CL
wearer of if recent operation
• Painful red eye: - may
indicate infective keratitis/
endophthalmitis
• Urgent treatment required
Dendritic ulcers
• Self limiting
• Problem occurs if treated
with topical steroids
Ophthalmic emergencies
without obvious clinical signs
Choices:
1.
Make diagnosis from examination
– Become competent at slit lamp and fundus
examination
2.
Make diagnosis from symptoms
– Learn to take a good history
What to ask for when taking a history of visual loss?
• Character of visual loss may help identify location of disease:
–
–
–
–
Extent of visual loss: sharpness / darkness / field loss
Blurred vision: Out of focus / Distorted vision
Floater
Glare / Halos
• Timing: onset / progressive / transient
• Associated factors: pain / headache
Extent of visual loss
• Very important clue about severity of problem
• Ask about vision of each eye
• Vision of less than CF is indicative of serious
disease
• But remember serious disease can also be present
if vision is good
Quantify extent of visual loss with vision test
• Sit patient at correct distance from
chart
• Test each eye individually
• Ask patients to use distance
glasses
• Use pinhole if no glasses
• If unable to see any letters
– ? CF, ?HM, ?PL
• Compare with previous vision
Blurred vision
• Out of focus / not sharp
• No distortion
• Refractive problem
– Cornea
– Lens
– Shape of eye
• Macular problem
Distortion of vision
(Metamorphopsia)
• Things look wavy, jumbled up.
Lines not straight. Kink in lines
• Condition affecting retina
– Wet macular degeneration
– Macular hole
– Macular pucker
– Retinal detachment
Field defect
• Curtain, bit missing, bump
into things
• Always a sign of serious
problem
• If homonymous: -same visual
field both eyes
– Defect of visual pathways
• Not hononymous
– Retinal
– Optic nerve
Shadow in the eye
• Retinal detachment
• Glaucoma
• Vitreous haemorrhage
• Vascular lesion
• Optic nerve disorder
• Visual pathway problem
Floater
• Due to opacity in vitreous
• Fly/spider, blob, haze
• Movement
Floaters
• PVD
– May notice Weiss’ ring
• Syneresis
• Vitreous haemorrhage
– Rain drops
– Black streaks
• Posterior uveitis
Flashes
• PVD
– Moores lightening streak
– Peripheral scintillation with
eye movement
• Migraine
– Scintillating scotoma
– Fortification spectrum
• Mass lesion
• Retinal ischaemia
Glare
• Difficulty seeing in bright light
– Low sun
– Driving at night
– Fluorescent light in
supermarkets
• Corneal or lens problem
– Often due to cataract
• Vision may be good otherwise
“Halos” in acute glaucoma
• Not strictly a halo – diffraction
of light by ice crystals
• Coloured rings around lights
due to refraction by water
droplets
• Not to be confused with glare
due to scatter by corneal or
lens opacities
Reduced colour
sensitivity
• Things look darker / less
colour
• Optic nerve disease
– Optic neuritis
– Compressive optic nerve
disease
• Condition affecting retina
– Wet macular
degeneration
– Central serous
retinopathy
Timing of visual loss
• Recent or chronic
• Static or progressive
• Transient or persistent
• Very important in determining urgency of situation
Conditions causing sudden visual loss
• Vascular occlusion
– Central retinal artery occlusion
– Central retinal vein occclusion
– Anterior ischaemic optic neuropathy
• Vitreous haemorrhage
• Acute glaucoma
Conditions causing rapid progressive visual loss
• Retinal detachment
• Wet macular degeneration
Causes of transient visual loss
• Amaurosis fugax
• Subacute angle closure glaucoma
• Visual obscuration due to papilloedema
• Giant cell arteritis
• Floaters
• Ocular surface problem
Symptoms suggestive of urgent condition
•
•
•
•
•
Marked visual loss
Field loss
Floaters/Photopsia
Distortion of vision
Transient marked loss of vision
• Recent change
• Rapidly progressive change
Ophthalmic emergencies without obvious clinical signs
•
•
•
•
•
•
•
Subacute angle closure glaucoma
CRAO
AION
Wet macular degeneration
PVD with retinal tear/detachment
Retinal detachment
Trauma
• CRVO
• Neurological conditions presenting with eye
signs/symptoms
Subacute angle closure glaucoma
• Acute angle closure glaucoma –
ophthalmic emergency with
obvious clinical signs
– Red eye
– Painful eye
– Severe visual loss in affected eye
• Often premonitory episodes of
subacute angle closure glaucoma
Subacute angle closure
glaucoma
• Angle closure develops in
evenings when pupil dilates
– Pressure increases to give pain and
corneal oedema
– Patient sees blurred vision and
haloes around lights
•
Patient goes to bed
– Sleep induced miosis aborts attack
of glaucoma
– Normal eye next day
• Should be referred urgently
before established AACG
develops
Treatment of to prevent
angle closure glaucoma
• YAG PI
• Laser treatment
• PI prevents build up of
aqueous behind pupil
Central retinal artery occlusion
• Sudden severe visual loss
• Visual loss may not be total
due to cilioretinal artery
• Usually embolic, rarely due
to GCA
• Attempt to reperfuse artery if
within 24 hours of onset
• Should be seen urgently to
exclude GCA and identify
cause
• No recovery of vision
• Often premonitory symptoms
Amaurosis fugax
• Transient visual loss due to passage of emboli
through central retinal artery
• Recovery to normal vision unless permanent central
retinal artery occlusion develops
• Often no emboli visible on clinical examination
• Total or altitudinal visual loss in one eye for a few
minutes
• Visual recovery often described like a curtain lifting
• Aspirin very effective in preventing CRAO
Cause of CRAO is usually carotid disease
• Risk factors:
– Hypertension, Smoking, Diabetes, High Cholesterol
•
•
•
•
Risk of further emboli to eye or brain
Reduce risk factors
Antiplatelet agents
Carotid endarectomy if greater than 70% stenosis
Anterior ischaemic optic neuropathy
• Infarction of optic nerve head - pale swollen disc with visual loss.
• Sudden severe visual loss if entire disc affected, altitudinal defect if only one
short posterior ciliary artery occluded
Anterior ischaemic optic neuropathy
• No treatment for affected eye
• 75% due to atherosclerosis in
middle aged smokers
• 25% due to Giant cell arteritis headache, tenderness of temporal
arteries, malaise, raised ESR .
• AION due to GCA is emergency high risk of developing AION in
fellow eye
Wet macular degeneration
1. Serous elevation of retina or PED
2. Blurred vision and distorted vision
3. Usually progressive over weeks
4. Difficult to see with ophthalmoscope
5. Initial vision may be very good
Wet ARMD
• Highly likely to progress to
severe visual loss if untreated
• Recovery of vision best if treated
before chronic changes have
developed
• Treatment not recommended for
late cases
Treatment of CNM with intravitreal injection of
antiVEGF
• VEGF (vascular endothelial growth factor) stimuates growth of
choroidal neovascular membrane
• antiVEGF binds to VEGF and prevents it acting on CNM
• Visual loss can be reversed if caught early
Incidence of PVD
Diagnosis of posterior
vitreous detachment
• Flashes and floaters
• Weiss’ ring
• Age, myopia, cataract
operation
• Examination
– Weiss’s ring
– Posterior hyaloid membrane
80
60
40
20
0
10-45
yrs
46-65
yrs
66-86
yrs
Symptomatic Posterior Vitreous Detachment
• Risk of developing retinal tear (8-22%)
• Risk of developing RD: 3 – 7% in symptomatic PVD
• If RD develops, it usually occurs within 6 weeks
Symptomatic Posterior Vitreous
Detachment
Indications for urgent referral
• Recent history (? Within 6weeks)
• Symptoms suggestive of vitreous
haemorrhage
• Symptom of retinal detachment
Reason for urgent referral
• To pick up retinal tear before retinal
detachment
• Early treatment of retinal detachment
Penetrating ocular injury
• Suspect if history of high velocity fragment – ie metal on
metal fragment
• May be minimal external eye signs.
Symptoms suggestive of urgent condition
•
•
•
•
•
Marked visual loss
Field loss
Floaters/Photopsia
Distortion of vision
Transient marked loss of vision
• Recent change
• Rapidly progressive change