Ophthalmology - high yield Flashcards

(116 cards)

1
Q

What is glaucoma?

A

optic nerve damage caused by a rise in intra-ocular pressure by blockage in aqueous humour trying to escape eye
*peripheral vision loss then total

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2
Q

What is the path of travel for aqueous humour?

A
  • produced by ciliary body
  • flows through posterior chamber and around iris into anterior
  • drain through trabecular meshwork to canal of schlemm
  • eventually entering general circulation
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3
Q

What is the normal intra ocular pressure?

A

10-21 mmHg

*created by resistance to flow through trabecular meshwork

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4
Q

What is the pathophysiology of acute angle-closure glaucoma?

A

iris bulges forward and seals off trabecular meshwork from anterior chamber, preventing aqueous drainage

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5
Q

What is the pathophysiology of open angle glaucoma?

A

gradual increase in resistance to flow through the trabecular meshwork, pressure slowly builds up

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6
Q

What are some risk factors of open angle glaucoma?

A

ncreasing age
family history
black ethnic origin
myopia

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7
Q

What are some risk factors of close-angle glaucoma?

A

increasing age
family history
Chinese and was asian ethnic origin
shallow anterior chambers
female

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8
Q

What medications might precipitate acute angle-closure?

A

adrenergic eg: noradrenaline
anticholinergic eg: oxybutynin and solifenacin
tricyclic eg: amitriptyline

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9
Q

How does closed angle closure present?

A

severely painful red eye
blurred vision
halos around lights
associated headaches, N+V

o/e - red eye, hazy cornea, decreased visual acuity, mid-dilated pupil not reactive to light, hard eye on gentle palpation

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10
Q

How does open angle present?

A

luctuating pain, headaches, blurred vision, halos around lights, particularly at night

*peripheral loss of vision, arcuate scotomoa, nasal step

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11
Q

What are some secondary causes of glaucoma?

A

iatrogenic, lens relates issues like cataracts, medicine related like steroids, neovascular, pigment related

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12
Q

How would you investigate suspected glaucoma?

A

measure intra-ocular pressure with non-contact tonometry or Goldmann
slit lamp for cup-disk ratio and angle
visual field
gonioscopy

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13
Q

How do you manage open-angle glaucoma?

A

360 degree selective laser trabeculoplasty
prostaglandin analogue - latanoprost
beta blocker - timolol
carbonic anhydrase inhibitor - dorzolamide
sympathomimetics
trabeculectomy

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14
Q

How do you manage closed angle glaucoma?

A

*>24 pressure first line laser trabeculoplasty
*second latanoprost, then others as needed

initial - pilocarpine, acetazolamide, other like timolol, latanoprost, analgesia

secondary - pilocarpine, acetazolamide, timolol, brimonidine

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15
Q

What is uveitis?

A

inflammation of uveal tract, comprising iris, ciliary body and choroid
*commonly uveitis

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16
Q

What is anterior uveitis?

A

iritis - which only affects the iris and iridocyclitis affects iris and ciliary body

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17
Q

What are some causes of iritis?

A

HLA-B27 conditions - AS, reactive arthritis, IBD
autoimmune - sarcoidosis, vasculitis
infection - herpes, herpes zoster
traumatic
iatrogenic - surgery, bisphosphonates
cancer - leukaemia, malignant melanoma

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18
Q
A
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19
Q

What is posterior uveitis?

A

inflammation of back of eye - retina or choroid

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20
Q

How does anterior uveitis present?

A

*over few hours or gradually over several

bilateral presentation - systemic conditions
unilateral - idiopathic or herpetic
painful, red eye with blurring of vision
photophobia
tearing
systemic - joint pain, back pain, flare up of IBD, infective sx

*chronic or intermediate and posterior - painless and decreased vision

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21
Q

How is anterior uveitis investigated?

A

general - ciliary injection, irregular pupil, cloudy cornea, hypopyon
slit lamp - ciliary flush, inflammatory cells in anterior chamber, flare, adhesions between lens and pupil
lab - bloods for HLA-B27, ANA, infectious diseases screen
OCT - macular oedema, CXR, spinal XR for AS

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22
Q

How is anterior uveitis managed?

A

*can be self limiting

ophthalmologist referral 24h assessment
aim to control inflammation, prevent visual loss, minimise long term complications
topical steroid drops to reduce inflammation
pupil dilating drops (cyclopentolate) to alleviate sx
treat underlying
systemic in severe - steroids and immunosuppressants

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23
Q

What are the complications of anterior uveitis?

A

severe - vision loss
macular oedema
secondary cataract
rise in intra-ocular pressure by inflammation of trabecular meshwork

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24
Q

What is age related macular degeneration?

A

progressive loss of central vision associated with formation of drusen or angiogenesis and changes in retinal pigmentary epithelium
*dry or wet

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25
What is characteristic of dry macular degeneration?
drusen in buch’s membrane - undigested cellular debris from degeneration of RPE (retinal pigment epithelium) cells as a part of normal ageing process *accumulation leads to atrophy of retinal epithelium
26
What characterises wet macular age degeneration?
characterised by choroidal neovascularisation - VEGF (vascular endothelial growth factor) is a protein molecule that has critical role in angiogenesis so in wet AMD causes abnormal angiogenesis and vessel leakage *fibrous scar tissue and central vision loss and leads to scotoma
27
What are some RF for AMD?
age smoking Caucasian ethnicity high fat diet drugs like aspirin co-morbidities like CVS and HTN ocular characteristics light coloured iris hyperopia genetics complement factor H gene variant Y402H (drusen formation link)
28
How would you classify AMD?
early - few medium sized druse, mild pigmentary abnormalities intermediate - >1 large drusen advanced - gradual vision loss or advanced wet is rapid vision loss
29
How does dry AMD present?
visual changes unilateral with gradual loss of central vision reduced visual acuity crooked or wavy appearance to straight lines (metamorphopsia) gradually worsening ability to read small text
30
How does wet AMD present?
wet AMD - more acutely visual loss within days and progress to complete within 2-3 years often progresses to bilateral disease
31
How is AMD investigated?
- pinhole worsens - reduced visual acuity - snellen chart - scotoma - enlarged central area of vision loss - amsler grid test - assess for distortion of straight lines seen in AMD - drusen - fundoscopy - slit lamp - detailed view of retina and macula - optical coherence tomography - cross sectional view of retina - fluorescein angiography - fluorescein contrast and photographing the retina to assess the blood supply, oedema neovascularisation in wet AMD
32
How is dry AMD managed?
no cure, ambler to monitor vitamin supplements in early disease registration with national centre for blind social work involvement, OT, psychology involvement informing DVLA if visual acuity poor
33
How is wet AMD managed?
*no cure - maintain functional sight, amsler grid to monitor 2w referral for wet AMD intravitreal anti-VEGF therapy - monthly registration with national centre for blind social work involvement, OT, psychology involvement informing DVLA if visual acuity poor
34
What may cause gradual vision loss?
corneal abrasion chemical injury cataracts diabetic eye disease presbyopia
35
What is a cataract?
progressively opaque eye lens which reduces light entering eye and visual acuity *can be congenital or progressive
36
What are some causes of cataracts?
age related pre-senile steroids DM trauma uveitis congenital
37
What are some risk factors of developing cataracts?
increasing age smoking alcohol DM steroids hypocalcaemia
38
How does cataracts present?
*asymmetrical - change in glasses prescription - myopic shift with short sighted first as light converges as cataract hardens - slow reduction in visual acuity - progressive blurring of vision - colours more faded - brown or yellow - starbursts around lights at night especially *loss of red reflex
39
How are cataracts managed?
phacoemulsification - if vision 6/12 with sub-tenon block *important to treat as prevents detection of other pathology like AMD, DM retinopathy etc
40
What is a complication of cataracts?
post-surgery endophthalmitis - inflammation of vitreous and aqeous humour mx: intravitreal abx seondary glaucoma
41
What is the blood supply to the retina?
carotid → ophthalmic → central retinal and posterior ciliary artery
42
What is the pathophysiology of diabetic retinopathy?
chronic hypoglycaemia damages retinal small vessels and endothelial cells increases vascular permeability -> leaks and blot haemorrhages + hard exudates neovascularisation etc
43
What are some characteristic features of diabetic retinopathy?
hard exudates micro-aneurysms and venous beading cotton wool spots intra-retinal microvascular abnormalities neovascularisation
44
What are the stages of diabetic retinopathy?
background retinopathy pre-proliferative proliferative diabetic maculopathy ischaemic diabetic maculopathy
45
What is background diabetic retinopathy? and what does this mean for management?
micro-aneurysms dot and blot haemorrhages cotton wool spots hard exudates *no tx indicated, annual screening with digital photography
46
What is pre-proliferative stage and what’s the management?
extensive blot haemorrhages and intra-retinal microvascular abnormalities (ischaemia) *4-6m follow up with digital fundus colour photos + retinal laser tx
47
what is proliferative stage and what is the management?
neovasuclarisation and vitreous haemorrhages *pan retinal photocoagulation targeting new vessels, retinal laser, anti-VEGF
48
Differentiate between diabetic maculopathy and ischaemic diabetic maculopathy and what is the management?
diabetic - exudates within macula and macular oedema! ischaemic - angio needed to diagnose, occlusions within vessels *mx - anti-VEGF bevacizumab, ranibizumab, intravitreal dexamethasone implant to reduce macular oedema
49
What are some risk factors for diabetic retinopathy?
duration of diabetes - 50% at 7 years duration and 90% at 17-50 poor glycaemic control hypertension dyslipidaemia obesity pregnancy
50
How might diabetic retinopathy present?
asymptomatic and most present with severe disease floaters blurred vision and distortion if macula affected decreased visual acuity - gradual, painless reduction in quality loss of vision - severe haemorrhage in results in sudden complete and painless vision loss blindness in untreated and uncontrolled
51
What is the diabetic eye screening programme?
for anyone with diabetes every 1-2 years depends on previous 2 scans
52
How is diabetic retinopathy investigated?
visual acuity - logMAR gold: fundoscopy with slit lamp or through fundus photography OCT: non invasive and infrared Fundus fluorescein angiography dye into arm to see retinal blood vessels
53
What is the general management options available for non-proliferative diabetic retinopathy?
close monitoring and careful diabetic control pre-proliferative: 4-6m follow up with digital fundus colour photos retinal laser treatment given if, only one good eye left attendance to clinic poor prior cataract surgery
54
What is the management for proliferative DM retinopathy?
Pan-retinal photocoagulation (PRP) - extensive laser treatment across the retina to suppress new vessels aim to kill ischaemic retina so hypoxic drive and oxygen demand is lessened and supply focused to central retina *complications - visual field defects, impaired night vision, accidental macular burn anti VEGF - medication intravitreal injection bevacizumab, ranibizumab surgery - vitrectomy in severe disease macular oedema intravitreal implant containing dexamethasone
55
what conditions cause sudden loss of vision?
retinal detachment central retinal artery occlusion central retinal vein occlusion vitreous haemorrhage (due to diabetic retinopathy)
56
what causes amaurosis fugax?
temporary loss of vision caused by a temporary interruption to the blood supply
57
what is the pathophysiology of central retinal artery occlusion?
obstruction to blood flow through the central retinal artery, which was a brach of ophthalmic artery which is a brach of ICA *cause atherosclerosis, GCA, vasculitis hence CVS RF
58
how does central artery occlusion present?
sudden painless loss of vision: curtain coming down RAPD
59
what is relative afferent pupillary defect?
pupil in affected eye constricts more when light shone in other eye than when shone in itself, hence appears to dilate when shone on affected when swung from non-affected input not sensed by ischaemic retina when testing direct but sensed in consensual
60
how is retinal artery occlusion investigated?
fundoscopy: pale retina with cherry red spot (fovea) due to lack of perfusion GCA: ESR, temporal artery biopsy *refer immediately
61
how is central artery occlusion managed?
GCA: potentially reversible so high dose prednisolone +/- IV Methylpred attempt to dislodge blockage: ocular massage, anterior chamber paracentesis, inhaled carbogen, IV acetazolamide+mannitol etc secondary prevention of CVS, treat reversible RF
62
what is the pathophysiology of central vein occlusion?
thrombus forms in retinal veins and obstructs the venous drainage from retina central retinal vein run through the optic nerve - responsible for draining retinal capillaries atherosclerotic thickening of central retinal artery leading to vein compression causes retinal tissue ischaemia, infarction, vessel leakage and neovascularisation
63
what are some risk factors for central vein occlusion?
age FHx of vascular atherosclerosis open angle glaucoma inflammatory: sarcoidosis, Lyme hyper coagulable state myeloproliferative states
64
what is the presentation of central vein occlusion?
sudden, painless unilateral visual loss (more gradual than artery occlusion) relative afferent pupillary defect - ischaemia visual field defect
65
what is a differential for CRVO?
branch retinal vein occlusion (BRVO) - this occurs when a vein in the distal retinal venous system is occluded
66
how is retinal venous occlusion investigated?
fundoscopy: widespread hyperaemia, severe retinal haemorrhages, macular oedema, cotton wool spots BP FBC, glucose, ESR fundal photo fundus fluorescein angio
67
how is CRVO managed?
immediate ophthal referral control BP treatment aim to control complications macular oedema: anti-VEGF, intravitreal steroid implant, laser neovascular complications: pan-retinal photocoagulation
68
what is a complication of CRVO?
Ischaemic carries poorer prognosis retinal non-perfusion, capillary closure, retinal hypoxia which increases neovascularisation risk may resolve spontaneously, cause vitreous haemorrhages or cystoid macular oedema
69
what is retinal detachment?
involves the neurosensory layer of retina (containing photoreceptors and nerves) separating from the retinal pigment epithelium (base later attached to choroid) *resulting in fluid accumulation in between
70
what is the consequence of a retinal detachment?
due to retinal tear -> vitreous fluid to get under the neurosensory retina and fill the space neurosensory retina relies on blood vessels of the choroid for its blood supply detachment disrupts this causing permanent damage to photoreceptors -> sight threat
71
what are some RF for retinal detachment?
lattice degeneration (thinning of retina) posterior vitreous detachment trauma diabetic retinopathy retinal malignancy family history
72
how does retinal detachment present?
painless peripheral vision loss - sudden, shadow coming across vision blurred vision or distorted vision flashes and floaters RAPD if optic nerve involved fundoscopy: red reflex might be lost
73
how is retinal detachment managed?
aim to create adhesions between retina and choroid with laser and cryo aim to reattach retina: vitrectomy, scleral buckle, pneumatic retinoplexy
74
what is optic neuritis?
inflammatory condition of the optic nerve that leads to acute, unilateral, central loss of vision (over hours to days) common in females 20-40
75
what is the pathophysiology of optic neuritis?
immune-mediated demyelination of the optic nerve as an isolated incident or part of wider disorder acute version of MS also associated with DM, syphillis
76
what is the presentation of optic neuritis?
acute, central vision loss - unilateral over hours to days poor discrimination of colours - red desaturation pain worse of eye movement photopsia - flashes of light relative afferent pupillary defect visual field defects - central scotoma optic atrophy - chronic
77
how is optic neuritis investigated?
swinging light test: RAPD visual acuity ishihara colour test ophthalmoscopy: mildly swollen disc MRI brain and orbits with contrast: confirm demyelinating optic neuritis LP: elevated protein, lymphocytes,oligoclonal bands
78
how is optic neuritis managed?
high dose IV steroids - methylprednisolone disease modifying therapies - MS? recovery usually 4-6w
79
what is the significance of thyroid diseases in relation to ophthalmology?
autoimmune condition resulting in inflammation and swelling of extra-ocular muscle, fatty tissue and connective tissue within orbit *follows acute phase for 6m to 2y where damage happens, inactive phase when sx remain
80
how might thyroid related eye disease present?
excessive watering ‘gritty’ sensation photophobia eye pain ask - red eye, blurred vision, pressure sensation systemic - pretibial myxoedema, goitre, acropachy
81
what might thyroid eye disease examination show?
eye lid retraction proptosis lig lag - von Graefe’s sign lid oedema diplopia due to restriction of inferior rectus incomplete eyelid closure strabismus
82
what investigations are carried out for thyroid related eye disease?
measure proptosis assess optic disc visual acuity, colour vision, RAPD TFT antibody test anti-thyroid peroxidase, anti-TSH USS extra-ocular muscles CT orbit - nerve involvement MRI orbits
83
how is thyroid related eye disease managed?
compressive optic neuropathy - Urgent IV methylprednisolone Ophthal + endo review correct thyroid hormone levels smoking cessation steroids to reduce swelling
84
what are some complications of thyroid related eye disease?
*compressive optic neuropathy - reduced visual acuity, colour vision → sight-threatening globe subluxation gaze abnormalities raised IOP → glaucoma
85
what is the pathophysiology of amaurosis fugax?
result of ischaemia to the retina, choroid, or optic nerve from an arterial embolus, usually in the retinal artery (from ipsilateral carotid artery disease)
86
what are some RF for amaurosis fugax?
over 50 vascular RF HTN, HPL, smoking, previous TIA or stroke
87
how does amaurosis fugax present?
transient vision loss in one or both eyes abrupt, maximum severity within seconds lasting to minutes full recovery negative visual phenomenon - blackout or ‘greying out’ of vision normal ophthal exam
88
how is amaurosis fugax investigated?
inflammatory markers - rule out GCA carotid imaging for stenosis cardiac investigations - AF other stroke RF neuro-imaging is needed
89
how is amaurosis fugax managed?
300mg of aspirin unless contraindicated urgent TIA referral within 24h secondary prevention - statin, antiplt, optimising BP etc
90
what is blepharitis?
inflammation of the eyelid margins - due to meibomian gland dysfunction (common, posterior bleph), or seborrhoeic dermatitis/ staphylococcal infection (less common, anterior bleph)
91
how does blepharitis present?
bilateral symptoms grittiness and burning discomfort - around lid margins eyes sticky in the morning results in dry eye which could cause redness foreign body sensation margins may be red - swollen in staphylococcal blepharitis styes and chalazions common in these secondary conjunctivitis
92
what does blepharitis look like on examination?
anterior - eyelash deformity and depigmentation and loss posterior - dilated and obstructed Meibomian glands
93
how is blepharitis managed?
diagnosis - history, examination - slit lamp - swabs maybe done for cultures hot compress lid hygiene artificial tears abx ophthal referral if painful
94
how is lid hygiene done for blepharitis?
lid hygiene - mechanical removal of debris from margins cotton wool buds dipped in mix of cooled boiled water and baby shampoo often used alternative is sodium bicarb, teaspoonful in cup of cooled water recently boiled
95
what is the pathophysiology of posterior vitreous detachment?
vitreous body comes away from retina - common in older age vitreous humour is gel inside the vitreous chamber of eye, maintain structure of eyeball and keeps retina pressed on choroid with age, less firm and less able to maintain shape
96
How is posterior vitreous detachment managed?
*exclude retinal detachement brain adjusts overtime safety net for retinal detachment as predisposes
96
how does posterior vitreous detachment present?
painless can be asymptomatic floaters flashing lights blurred vision
97
How is red eyes assessed?
history of symptoms and onset - pain - visual loss - serious - gritty - conjunctivitits, dry eyes, foreign body - itching - allergic, blepharitis examination of both eyes - visual acuity with snellen - evidence of trauma, discharge, swelling - pattern on redness - perform fluorescein examination - assess pupils, RAPD? - BP
98
what are some red flags for a red eye?
reduced visual acuity severe pain, headache, photophobia significant ciliary injection, fluorescein staining unequal pupils and abnormal reactions pain on pupillary constriction, loss of red eye, corneal haze, hyphaema or hypopyon (blood and pus in anterior chamber)
99
what are some differentials for a painful red eye?
acute angle-closure glaucoma anterior uveitis scleritis corneal ulcerations keratitis foreign body trauma or chemical injury endophthalmitis
100
what are some differentials for a painless red eye?
conjunctivitis episcleritis subconjuctival haemorrhage dry eye episcleritis
101
what is anisocoria?
difference in pupil size physiological is ≤2mm and difference same in all light levels
102
what is the pupillary light reflex anatomy?
light activates retinal ganglion cells → axons through optic nerve → chiasm → optic tract → synapse at EWN → efferent parasympathetic fibres travel with CN3 → cilairy ganglion iris contains 2 muscles - constricting sphincter innervated by parasympathetic and dilating by sympathetic (which starts at ipsilateral hypothalamus)
103
what is the significance of anisocoria in dark or light?
greater anisocoria in dark → impaired dilation in small pupil (sympathetic dysfunction) greater anisocoria in light → impaired constriction in large pupil (parasympathetic dysfunction)
104
what are some differentials for a large pupil?
Adie’s tonic pupil post viral denervation of the sphincter pupillae and ciliary muscle dilator drops 3rd nerve palsy traumatic mydriasis
105
what are some differentials of a small pupil?
horners syndrome pilocarpine drops uveitis
106
what is your understanding of positive or negative phenomenon in terms of vision loss?
positive - brightness, shimmering, hallucinations → migraine aura, seizure negative - blackness, greyness, shade-obscuring vision → TIA, stroke
107
how do you assess visual loss?
visual acuity and colour vision snellen, pinhole, fingers, movement ishihara, red saturation swing test for RAPD visual fields ophthalmoscopy
108
what are some differentials for acute loss of vision?
amaurosis fugax central venous occlusion central arterial occlusion vitreous haemorrhage retinal detachment optic neuritis GCA
109
what is strabismus?
misalignment of the two eyes when focusing on one object which could be persistent (manifest or tropia) or latent (phoria)(discovered with cover test)
110
what could cause strabismus?
**Primary** - idiopathic - congenital **Secondary** - cranial nerve palsies of EOM - intracranial infection - intracranial, intraorbital and intraocular masses - orbital # or other trauma - myopathies - MG - endocrine - DM, graves - heavy metals and toxins
111
what are some risk factors for developing strabismus?
- family history - low birth weight - premature birth - maternal smoking
112
what are some red flags associated with strabismus?
- recent trauma - symptoms of raised ICP - new strabismus in school age child
113
how might strabismus present?
- onset, reduced visual acuity, diplopia, asthenopia, decreased socialisation, behavioural problems, maladjustment at home or school - other - developmental history, obstetric, previous medical, previous visual acuity
114
how would you examine strabismus?
- corneal light reflex - Deflection of the corneal light reflex in one eye suggests a misalignment - Brüchner test - asymmetry of red reflexes suggest ocular disorder - cover test - determine heterotropia (latent stabismus) - cover-uncover test - check covered eye for refixation movement, if phoria present eye will shift back to being orthopic or straight - prism cover test
115
how would you manage strabismus?
- orthoptics - measure visual acuity, assess eye movement, assess binocular vision, monitors amblyopia with patching to encourage use of amblyopic eye - patch unsuccessful after age of 7 - refraction to correct deviation and improve acuity - strabismus surgery - EOM operated on