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4th Year Surgery Block > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

Causes of sudden visual loss (7)

A
  • Acute angle closure glaucoma
  • Vascular – CRAO, CRVO, ION, amaurosis fugax
  • Retinal detachment
  • Optic neuritis
  • GCA
  • Wet ARMD
  • Vitreous haemorrhage
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2
Q

Causes of gradual visual loss (5)

A
  • Cataracts
  • Refractive errors
  • Dry ARMD
  • Open angle glaucoma
  • Diabetic retinopathy
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3
Q

Causes of painful sudden visual loss?

A
  • GCA
  • Optic neuritis
  • Acute angle closure glaucoma
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4
Q

Causes of painless sudden visual loss?

A
  • Wet ARMD
  • Retinal detachment
  • Vitreous haemorrhage
  • Vascular - CRAO, CRVO, ION, amaurosis fugax
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5
Q

What are cataracts and some causes?

A
  • Age related cataracts are very common and their treatment is the most common elective procedure
  • Clouding of the lens
  • Throughout life the lens becomes progressively cloudy and most cataracts are age related
  • Other causes include congenital cataracts, traumatic cataracts, metabolic e.g. diabetes, drug induced e.g. steroids, intrauterine infections e.g. rubella, CMV and toxoplasma
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6
Q

Three types of age related cataract?

A

nuclear sclerotic, cortical and posterior subcapsular

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7
Q

Symptoms of cataracts?

A
  • Gradual loss of vision and blurring
  • Problems with glare when driving etc
  • Increasing near sightedness
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8
Q

Examination/ investigation for cataracts?

A
  • Can see the clouding of the lens
  • Partial or full loss of red reflex
  • Check visual acuity
  • Look at eye with slit lamp
  • Ophthalmoscopy
  • May check pressure in eye
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9
Q

Management of cataracts?

A
  • Phaco-emulsification with intraocular lens implantation is now routine
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10
Q

What is the commonest cause of blindness in the developed world?

A

ARMD

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11
Q

What is dry ARMD?

A

Essentially wear and tear of the RPE
deposition of druses and hypo/ hyperpigmentation in areas

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12
Q

Presentation of dry ARMD?

A
  • Results in slow less of central visual acuity
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13
Q

Management of dry ARMD?

A
  • There is no active treatment - low visual aids, dietary smoking advice, Amsler grid, blind registration
  • Amsler grid can help patient detect if converting to wet ARMD by allowing to detect distortion e.g. wavy lines which is an early sign of wet ARMD
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14
Q

What is more common, dry or wet ARMD?

A

dry
wet much less common and it would be a dry that converted to a wet usually

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15
Q

What happens in wet ARMD?

A
  • The eye grows new blood vessels within the macula to try and repair dry ARMD damage
  • The vessels then leak fluid or bleed into retinal tissue
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16
Q

Presentation of wet ARMD?

A
  • Early sign is metamorphopsia – shapes of objects appear distorted
  • Get rapid central visual loss
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17
Q

Investigations for wet ARMD?

A
  • OCT can be used to diagnose it, and differentiate it from dry ARMD and other pathologies, fluoroscene angiograms can also be helpful in diagnosis
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18
Q

Management of wet ARMD?

A
  • Anti VEGF therapy e.g. ranibizumab is treatment, this is a monoclonal antibody injection that inhibits growth factor that is stimulating the growth of new vessels, initially monthly injections then as required
  • Essentially converts wet ARMD to dry ARMD again – doesn’t cure it
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19
Q

What is CRAO?

A
  • Occlusion of the central retinal artery that supplies the inner 2/3 of retina
  • It is a type of stroke (basically a stroke of the eye)
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20
Q

Causes of CRAO?

A
  • It is a type of stroke (basically a stroke of the eye)
  • It is association with atherosclerosis and hypertension
  • Can also be caused by GCA so should rule this out!
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21
Q

Presentation of CRAO?

A
  • Sudden profound visual loss (<6/60)
  • 94% will only be able to count fingers at presentation
  • RAPD present
  • Pale swollen retina with cherry red spot at macula
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22
Q

Swollen retina with cherry red spot?

A

CRAO

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23
Q

Explain what is meant by RAPD positive?

A

RAPD test is relative afferent pupillary defect, and involves swinging a light from eye to eye, if the pupil dilates in response to the light then it is positive, this is because the pupil is perceiving less light when the light is shone directly into the eye vs when it is constricting due to consensual reflex from the other non-damaged eye.

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24
Q

Explain why you get a cherry red spot?

A

occurs in CRAO
cherry red spot – basically you are seeing underlying choroidal circulation shining through at the thinnest bit of the pale retina (retina is pale because it is ischaemic because the artery is blocked)

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25
Q

Management of CRAO?

A

Treatment only really effective if presentation within 12-24 hrs
Treatment aims at dislodging blockage and restoring circulation
- Ocular massage
- Paper bag breathing (increases PCO2, causes vasodilation and may dislodge blockage)
- IV Diamox (acetazolamide to rapidly lower pressure to try and dislodge)
- Anterior chamber paracentesis (hypodermic needle into anterior chamber to take out aqueous humor to try and drop pressure in the eye)

94% Counting fingers at presentation, less than 1/3 show any improvement with or without treatment

Also got to consider that this is a type of stroke and investigate why and get them on long term stroke risk management

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26
Q

What is more common CRAO or CRVO?

A

CRVO much more common

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27
Q

What is CRVO? Predisposing factors?

A
  • Occlusion of central retinal vein causing obstruction in outflow of blood leading to a rise in intravascular pressure
  • Predisposing factors – age, hypertension, CV disease, glaucoma, blood disorders
  • This is a lot more common than CRAO
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28
Q

Presentation of CRVO?

A
  • Sudden, painless moderate to severe visual loss
  • RAPD present if severe enough
  • On fundoscopy: retinal flame haemorrhages (stormy sunset), dilated torturous veins, swollen disc and macula (there’s this build up/ back flow which increases pressure leading to haemorrhages and causes the veins to dilate as the blood can’t flow normally vs in CRAO where the retina is pale because no blood is getting to it)
  • Can sometimes get neovascularisation if long standing
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29
Q

Retinal flame haemorrhages (stormy sunset) and dilated torturous veins?

A

CRVO

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30
Q

If only part of eye looks like CRVO?

A

could be a branch vein occlusion

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31
Q

Management of CRVO?

A
  • Find underlying cause
  • Refer to ophthalmology for monitoring
  • If no signs of ischaemia observe (every 3 months then less frequently)
  • If ischaemic but no neovascularisation observe closely (every 4-6 weeks)
  • If ischaemic with neovascularisation patient requires urgent argon laser pan-retinal photocoagulation
  • They may do photocoagulation or anti-VEGF intravitreal injection is there is neovascularization
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32
Q

What is the retina?

A

The retina is the light-sensitive layer of tissue at the back of the eyeball. Images that come through the eye’s lens are focused on the retina. The retina then converts these images to electric signals and sends them along the optic nerve to the brain

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33
Q

What is a retinal detachment?

A
  • This occurs when there is separation of the 2 embryonic layers of the retina (the neuroretina from the retinal pigment epithelium)
  • The pigment epithelium layer is the layer that nourishes retinal visual cells and the neuroretina is the layer with photoreceptors
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34
Q

Risk factors for retinal detachment?

A
  • Can occur following trauma but more commonly following separation of vitreous gel from retina, this traction can lead to retinal tear which can then progress to retinal detachment, this is more common in myopes
  • Retinal detachment is more common with in older people
  • Previous cataract surgery can increase risk
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35
Q

Presentation of retinal detachment?

A
  • Persisting flashing lights, burst of new floaters
  • Then, painless loss of vision – depends on where the detachment affects first, there is usually a primary shadow and increases
  • On fundoscopy: the detached retina is elevated and grey in colour
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36
Q

Management of retinal detachment?

A
  • If picked up as early retinal tear can be lasered to prevent progression to detachment
  • If retina detached it requires surgery
  • Prognosis is generally good if caught early
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37
Q

What is glaucoma?

A
  • A group of diseases characterised by progressive optic nerve damage and visual field loss with raised intra-ocular pressure as a prominent risk factor
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38
Q

Pathogenesis of glaucoma?

A
  • Usually, blockage to aqueous outflow caused by raised intra-ocular pressure
  • There is damage and loss of retinal nerve fibres at optic disc with visual field loss
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39
Q

Explain IOP in glaucoma?

A

tends to be raised but can get normotensive
can be on high side but not have glaucoma and can be on high side of normal and still get glaucoma

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40
Q

Presentation of POAG?

A
  • It causes insidious painless loss of peripheral vision, patients tend not to notice as the brain compensates
  • Generally picked up on routine ophthalmic exam
  • the optic disc shows an enlarged cup with a thin retinal rim
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41
Q

Risk factors for POAG?

A

age, raised IOP, afro-Caribbean origin, family history

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42
Q

Fundoscopy of glaucoma?

A

the optic disc shows an enlarged cup with a thin retinal rim

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42
Q

Fundoscopy of glaucoma?

A

the optic disc shows an enlarged cup with a thin retinal rim

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43
Q

Objective of POAG treatment?

A

Lower IOP to a level that prevents further nerve damage, target IOP will vary between patients

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44
Q

5 classes of medications for POAG?

A
  • There are 5 classes of medication which are designed to turn off the tap (reduce aqueous production) or open up the drain (increase aqueous drainage)
  • 5 medicines: beta blockers, carbonic anhydrase inhibitors, prostaglandins, parasympathominetics, sympathomimetics
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45
Q

Describe prostaglandin eye drops for glaucoma?

A

Prostaglandins (eye drops) end in “prost” e.g. lantanoprost
* These increase uveoscleral outflow and make iris vessels more leaky
* They have very few side effects, occasionally tachycardia, lashes grow more, increase pigmentation in iris i.e. blue eyes may go darker
* Once daily dosing (which is better than some which need 4 daily doses!)

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46
Q

Describe beta blocker eye drops for POAG?

A

Beta blockers (eye drops) end in “lol” e.g. timoptol, laevobutanol
* Reduce aqueous secretion
* Twice daily dosing
* Have systemic side effect e.g. bradycardia and hypotension
* Can reduce systemic side effects by shutting eyes for a few minutes
* There are few topical side effects

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47
Q

Describe carbonic anhydrase inhibitors for POAG?

A

Acetazolamide (oral)
* This is very effective at lowering IOP
* But because it is oral get systemic side effects of paraesthesia, peri-oral tingling, renal calculi
* Should be used short term only

Dorzolamide (topical)
* This has no systemic side effects but causes local irritation (stinging) and some patients can develop an allergy
* Much less effective and second line to prostaglandins

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48
Q

Describe parasympathominetics for POAG?

A
  • Increases outflow
  • Few systemic side effects
  • Many local side effects – pupil constriction, pain, dimming of vision, problems at night
  • 4 times a day
  • Tend not to use much
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49
Q

Describe sympathomimetics for POAG?

A

e.g. adrenaline, propine, alphagan
* Increase outflow
* Dilate pupil
* Local irritation, hyperaemia, can develop a late allergy
* Cardiovascular side effects
* Long term use reduces the success of surgery

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50
Q

General treatment order for POAG?

A
  • Prostaglandin
  • Beta blocker/ carbonic anhydrase inhibitor
  • Sympathomimetic/ parasympathomimetics
  • Surgery
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51
Q

Describe surgery for POAG?

A

trabeculectomy

  • Aims to make a guarded fistula into anterior chamber
  • Downside makes it open system from a closed system which means more susceptible to infections (endophthalmitis risk with trabeculectomy – but low risk)
  • Surgery is most effective esp due to compliance with eye drops
  • But leaves eye at risk of infection and does result in cataracts (which can be treated)
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52
Q

Explain what secondary open angle glaucoma is?

A
  • This can be caused secondarily by things blocking the drain e.g. blood or inflammatory cells
  • e.g. uveitis, trauma etc
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53
Q

What causes acute angle closure glaucoma?

A
  • Sudden rise in intraocular pressure due to reduced aqueous drainage when the lens pushes the iris forward against the trabecular meshwork
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54
Q

acute angle closure glaucoma is more common in ?

A

hypermetropics (long sighted)

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55
Q

Presentation of acute angle closure glaucoma ?

A
  • This presents acutely as a red eye, sudden vision loss, headache, nausea, vomiting, cloudy cornea (due to water logging), fixed mid-dilated pupil (iris sphincter can’t work properly)
  • This can sometimes present vaguely with the GI symptoms before realising it is actually glaucoma causing the issue
  • This is a medical emergency
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56
Q

Management of acute angle closure glaucoma?

A
  • Refer to ophthalmology
  • Should start by reducing IOP medically: Acetazolamide IV
  • Definitive treatment involves making a hole in the periphery of the iris by lazer or surgical means (peripheral iridotomy) meaning the chamber is always open
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57
Q

What is conjunctivitis?

A
  • Inflammation of the conjunctiva generally caused by infection
  • Conjunctiva = protective mucous membrane over the sclera)
  • Can be bacterial or viral
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58
Q

Importance of establishing visual loss in red eye?

A

Establish if visual loss – mild to moderate visual loss is common especially if there is watering or discharge but if there is severe visual loss then need an urgent referral

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59
Q

Importance of establishing pain in red eye?

A

Scratchy/ gritty pain/ discomfort indicates external or surface problem, therefore examine lids, conjunctiva and cornea e.g. conjunctivitis, foreign body

Severe/ deep/ aching pain more likely to indicate an intra-ocular or orbital problem e.g. iritis, scleritis, angle closure glaucoma

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60
Q

Importance of establishing distribution of redness in red eye?

A

If greatest in the conjunctival fornices (inside lids) likely to indicate surface infection or lid disease
If greatest around the cornea (circumcorneal injection) likely to indicate an intra-ocular problem

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61
Q

Explain what the conjunctiva, sclera and cornea are?

A

The conjunctiva is the clear, thin membrane that covers part of the front surface of the eye and the inner surface of the eyelids.
The sclera is a thick layer that forms the white of the eye, a dense connective tissue of the eyeball.
The cornea is the transparent connective tissue part of the eye that covers the iris and pupil and allows light to enter the inside

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62
Q

Describe examination of the cornea in a red eye patient?

A
  • Is it clear or hazy? Are there any foreign bodies abrasions or ulcers?
  • Use fluorescein dye and blue light – stains any epithelial defect and fluoresces under blue light
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63
Q

Overview of specific causes of red eye?

A
  • Infection – conjunctivitis, corneal ulcers
  • Trauma – corneal foreign body, chemical injury
  • Inflammatory – episcleritis, scleritis, iritis
  • Raised intra-ocular pressure – acute angle closure glaucoma
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64
Q

What is more common, bacterial or viral conjunctivitis?

A

viral

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65
Q

What organisms are generally involved in bacterial conjunctivitis?

A

staph A, strep pneumonia and haemophilus influenzae

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66
Q

Presentation of bacterial conjunctivitis?

A

usually bilateral but sequential
Purulent discharge
Mild chemosis (oedema of conjunctiva)
Gritty discomfort

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67
Q

Management of bacterial conjunctivitis?

A
  • Can delay treatment as sometimes resolve but if not resolving or need resolution – prescribe antibiotic – topical chloramphenicol drops
  • Should note that it is contagious – advice on hand washing, don’t share towels etc
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68
Q

Viral conjunctivitis is generally what virus? and generally occurs

A

adenovirus - generally occurs after a cold

69
Q

Presentation of viral conjunctivitis?

A
  • Often bilateral
  • Watery discharge
  • Moderate chemosis
  • Gritty discomfort/ burning
  • Often associated with pre-auricular lymph nodes (good way to differentiate viral vs bacterial)
70
Q

Management of viral conjunctivitis?

A
  • Generally self limiting and should give advice re self care such as eye flannels etc
71
Q

Chlamydia conjunctivitis is caused by what serovars?

A

chlamydia serovars A-C

72
Q

Describe presentation of chlamydia conjunctivitis?

A
  • This often has a slow onset with discomfort over weeks
  • There is scanty non-purulent discharge
  • Can get follicular reactions – multiple slightly elevated lesions with appearances of rice grains in the fornices
73
Q

Management of chlamydia conjunctivitis?

A
  • Needs treated to prevent scarring of the lids
  • Might need treated with oral antibiotics
74
Q

What is keratitis and what are common symptoms?

A
  • Corneal inflammation which can be caused by infection
  • Symptoms: sensation of foreign body or pain, photophobia and lacrimation
75
Q

Dendritic corneal ulcer ?

A

herpes simplex keratitis

76
Q

How can you diagnose herpes simplex keratitis?

A
  • The ulcer stains with fluorescein dye and can be observed with a blue light
77
Q

Why should you be v cautious in prescribing steroids in red eye case?

A

if it is herpes simplex keratitis it can cause corneal perforation
so only prescribe if this is definitely ruled out

78
Q

Management of herpes simplex keratitis?

A
  • Herpes simplex keratitis needs hospital referral and ganciclovir or acyclovir hourly eye drops
79
Q

Risk factors for bacterial corneal ulcers?

A

corneal abrasion, Contact lens wearer, dry eye, iatrogenic

80
Q

How to identify causative organism in bacterial keratitis? What is common?

A
  • Corneal scrape to determine causative organism, staph and strep are common
81
Q

Management of bacterial keratitis?

A
  • Usually treated with topical ofloxacin hourly then taper down
82
Q

2 contact lens specific associated infections?

A
  • In contact lens wearers acanthamoeba which is a parasite infection can occur and so can pseudomonas (bacterial)
83
Q

Pseudomonas keratitis is treated with?

A

topical ofloxacin hourly then taper down

84
Q

Acanthomoeba keratitis is treated with?

A

generally antiseptic drops e.g. chlorhexidine with or without diamidine (chemical group that seems to be used against parasites)

85
Q

Explain what episcleritis is vs scleritis?

A

episcleritis - inflammation of only the outer layer of the sclera
scerlitis - inflammation of the sclera - severe ocular inflammation

86
Q

What is more common, episcerlitis or scleritis?

A

episcleritis much more common, scleritis relatively rare

87
Q

Causes of episcleritis and scleritis?

A

episcleritis * Cause is mostly unknown can flare up with fatigue, staring at screens, dry dusty environments – not really associated with systemic conditions so does not need further investigation

scleritis - * It is associated with many connective tissue diseases so need investigation to see if patient has one of these

88
Q

Presentation of scleritis vs episcleritis?

A

Episcleritis: Mild discomfort, Causes localised, superficial injection that blanches with topical phenylephrine (dilating pupil drops)

Scleritis: Moderate to severe pain
Causes a diffuse, deep redness with “violaceous hue”
Not a diagnostic test but less likely to blanch with topical phenylephrine

89
Q

Management of scleritis vs episcleritis?

A

Episcleritis: Can be treated with topical lubricants or NSAIDs
Scleritis: Treatment with oral NSAIDs or systemic steroids/ immunosuppression if necrosis - need to investigate for an underlying cause

90
Q

What is the uvea?

A

middle layer of the eye - iris ciliary body and choroid

91
Q

What is anterior uveitis / iritis?

A

inflammation of the iris plus minus the ciliary body

92
Q

Causes of anterior uveitis/ iritis?

A
  • 50-60% are idiopathic, the remainder are related to inflammation of other body systems
  • HLAB27 are the most common systemic causes
93
Q

Presentation of anterior uveitis?

A
  • Red eye
  • Ache
  • Photophobia
  • Lacrimation
  • Blurred visual acuity
  • Circumcorneal redness
  • Can get hypopyon if severe (accumulation of WBC in anterior chamber)
  • Synechiae – adhesion of posterior surface of the iris to the lens capsules
94
Q

Hyphaema vs hypopyon?

A

Hypopyon = WBC in anterior chamber – sign of serious inflammation
Hyphaema = RBC in anterior chamber – sign of trauma

both should be referred to ophthalmology

95
Q

Management of anterior uveitis?

A
  • Topical steroids (hourly with gradual taper) and topical mydriatic (this helps break up the synechiae and also helps with photosensitivity caused by ciliary body spasm)
  • If it is a one-off episode tend not to investigate
  • However, if it is bilateral, severe or recurs frequently then usually start investigations for an underlying cause
96
Q

Brief overview of the visual pathway?

A
  • Optic Nerve
  • Optic chiasm – where nasal retina crosses over
    (remember nasal retina is getting vision from your temporal field and vice versa)
  • Optic tract
  • Optic radiations – where upper goes with the temporal lobe, lower goes with parietal
  • Occipital cortex – left occipital cortex is for right visual field, right occipital cortex is for left visual field
97
Q

Monocular vs binocular double vision?

A
  • All eye movement defects caused by cranial nerve palsies will cause binocular double vision
  • Binocular diplopia occurs when both eyes are open and can be corrected by covering either eye – caused by conditions affecting carnial nerves that control eye movements
  • Monocular diplopia persists in one eye despite covering the other eye – this is a problem with the eye itself – e.g. cataracts causing weird scattering of light
98
Q

Causes of 6th nerve palsy?

A

Increased ICP, infiltration of the nerve sheath by tumours, microvascular ischaemia (occurs in diabetes), basal skull fracture

99
Q

Describe presentation of a sixth nerve palsy?

A
  • The patient will be unable to abduct the eye and have medial deviation of the eye when looking straight on
  • They will have double vision which occurs mainly when looking far away or in the direction of the affected eye
  • Diplopia is horizontal
100
Q

Causes of a fourth nerve palsy?

A

congenital or can be caused by trauma

101
Q

Presentation of a fourth nerve palsy?

A
  • Trochlear nerve palsy affects the superior oblique muscle which primary action is intorsion but also helps with depression and abduction
  • The patient will have torsional diplopia (double vision is at an angle)
  • When asked to gaze to the right, their eye moves superior as well as medial
102
Q

Causes of a 3rd nerve palsy?

A

Microvascular (pupil sparing), trauma, aneurysm

103
Q

Presentation of a 3rd nerve palsy?

A
  • Oculomotor palsy affects all eye muscles except SO and LR, sphincter pupillae and LPS are also paralysed
  • Only actions left are abduction and depression so the eye has a down and out appearance
  • There is ptosis of the eyelid due to LPS paralysis
  • Pupil may be dilated as sphincter pupillae can be affected
104
Q

Pupil sparing or not spared in 3rd nerve palsy?

A
  • If the pupil is involved this suggests a compressive lesion as parasympathetics run on the outside of the nerve
  • If the pupil is spared this could indicate a microvascular infarction affection the middle inside part of the nerve
105
Q

Painful 3rd nerve palsy that does not spare the pupil?

A

aneurysm

106
Q

Optic nerve lesion causes

A

unilateral visual loss (right nerve causes right visual loss and vice versa)

107
Q

Causes of optic nerve lesions?

A

optic neuritis, trauma or compression, ischaemic optic neuropathy, infection, papilloedema

108
Q

Optic chiasm lesions cause?

A

bitemporal hemianopia
The optic chiasm is nasal retina which carries temporal visual field information crosses over, hence you lose temporal fields on both sides

109
Q

Causes of bitemporal hemianopia?

A

pituitary tumours, meningiomas and craniopharyngiomas

110
Q

Optic tract lesions cause?

A

homonymous hemianopia
After the optic chiasm, the right half of the brain has your left vision and the left half has your right vision – hence homonymous hemianopia

111
Q

Causes of optic tract lesions?

A

tumours, demyelination or vascular anomalies

112
Q

Optic radiation lesions?

A
  • Tracts form radiations which meet in the cortex
  • The parietal radiation takes information from the lower field so the lesion causes loss of inferior quadrant on the other side
  • Temporal radiation takes information from the upper field so the lesion causes loss of superior quadrant on the other side
113
Q

Occipital cortex lesions?

A
  • This causes an homonymous hemianopia but often with macular sparing as the information from the macular takes up such a large area of the cortex
  • Causes of this include stroke
114
Q

What is optic neuritis and what causes it?

A
  • Inflammation of the optic nerve
  • The most common cause is MS (argument for early MRI) but can be caused by viral illnesses
115
Q

Presentation of optic neuritis?

A
  • Variable loss of vision, usually over few days
  • Washed out colours
  • Dull ache on eye movements
  • Examination: decreased visual acuity, RAPD present, decreased colour vision, enlarged blind spot, optic disc swelling
116
Q

Management and prognosis of optic neuritis?

A
  • Good prognosis in 90% of cases
  • Vision drops rapidly initially then gradually improves
  • Can improve on own or may give steroids
  • Co-manage with neurology team – may be role for MS medications
117
Q

Ophthalmoscopy examination?

A

check if patient long or short sighted as need to correct ophthalmoscope (also need to correct it for your vision)
right eye examine with right hand on ophthalmoscope using your right eye

check for red reflex by standing arms length away on 0 lens
then go forward, look at front of eye with it dialled up to 10
then dial back slowly to look at back of eye

6 steps: view optic nerve (cup, colour, contour), 4 vascular regions (superotemporal, superonasal, inferotemporal, inferonasal), and macula

get patient to look in direction you are examining and you move in opposite direction

118
Q

Visual fields testing?

A

get patient to remove glasses – rims can create artificial defects
sit with knees almost touching at same height

Gross test for gross defects e.g., can you see my hands, are there only 2
Test the quadrants – in each quadrant how many fingers am I holding up
Subtle defects - using white pin
Blind spot - using red pin, start nasally and move temporally

119
Q

Visual acuity?

A

use snellen chart, 6 metres away
test unaided, with glasses and with pinhole
recorded as 6/6, 6/9 etc, can have plus and minuses if dont get whole line
if cant see snellen can move to 3 metres recorded as 3/60
if still cant do counting fingers
then test hand movement - what direction are my hands coming in
then test perception of light - what direction is the light coming from

120
Q

What is the anterior and posterior chamber?

A

Anterior chamber = cornea and iris
Posterior chamber = iris and lens

121
Q

What is a squint?

A
  • A squint is the term used when the two eyes are not pointing in the same direction. This means they are not working together as a pair, one eye may turn either inwards, outwards, downwards or upwards, whilst the other eye looks straight at the target of interest
122
Q

What is the cover test?

A
  • The purpose of the cover test is to detect a squint
  • The cover test detects a manifest squint and the uncover cover test detects a latent squint
  • Should be carried out near and at distance
  • You should get the patient to focus on a target
  • As you cover one eye you should watch the other eye for movement
  • If the opposite eye moves to fix on the target then a manifest squint is present
123
Q

Describe the types of manifest squint?

A
  • Esotropia/ convergent squint: outwards movement of the eye (the eye started inwards and moves out to fixate on target)
  • Exotropia/ divergent squint: inwards movement of the eye (the eye started outwards and moved in to fixate on the target)
  • Hypotropia/ low eye: upwards movement of the eye (eye started low down and moved up to fixate on the target)
  • Hypertropia/ high eye: downwards movement of the eye (eye started high and moved down to fixate on the target)
124
Q

Explain latent and manifest squints?

A

LATENT (PHORIA)
* Symmetric corneal reflections
* Binocular vision
* Underlying deviation in both eyes i.e. cannot have a left exophoria
* You only get deviation when eye covered as you have stopped them working as a pair
* Generally normal – quite a lot of the population have this, your eyes just don’t quite rest straight

MANIFEST (TROPIA)
* Asymmetric corneal reflections
* No/ poor binocular vision
* Squint only in one eye at a time
* Record the manifest eye

125
Q

Management of a paediatric squint?

A

Maximise visual acuity:
* Correct refractive error
* Treat amblyopia

Amblyopia should always be treated first before considering surgery

Then if needed squint surgery (for cosmetic reasons if binocular vision not possible) or for functional reasons

126
Q

Management of an adult squint?

A

First aims:
* Preserve/ improve BSV (binocular single vision)
* Fresnel prisms on glasses
* Orthoptic exercises

Next steps:
* Botulinum toxin (BTXA) Used to temporarily paralyse extra ocular muscle - Can be used for patients not suitable for surgery
* Extraocular muscle surgery – functional or cosmetic

127
Q

Explain what amblyopia is?

A
  • The child’s visual system is constantly developing from birth until around 6 years of age
  • So if vision is not used properly by age 6 it will never be used properly
  • Amblyopia is a vision development disorder in which an eye fails to achieve normal visual acuity even with prescription glasses
  • This is essentially because you have something causing a degraded image that stops the development of your visual pathway i.e. if as a child you have a squint or uneven refractive error your brain stops using your bad eye and the binocular visual pathway never develops properly
128
Q

What are some causes of amblyopia?

A
  • Strabismic – squinting eye is “suppressed” (brain ignores eye not moving properly – binocular vision doesn’t develop properly)
  • Anisometropic – unequal refractive error (brain ignores eye with worse refractive error and looks only out better eye so double vision does not develop)
  • Stimulus deprivation – congenital cataract/ ptosis (something physical in one eye stops vision in one eye)
  • Ametropic – bilateral uncorrected refractive error (vision doesn’t develop properly in both eyes due to such bad refractive error)
129
Q

Management of amblyopia?

A
  • First step is to correct any refractive errors – get both eyes seeing the same thing
  • If needed will then go on to further treatment, this involves occlusion treatment where the bad eye is forced to work in order to ensure visual development
  • Start with total occlusion – patching treatment (maximum is 6 hours a day)
  • Partial occlusion – pharmaceutical penalisation: atropine 1% in good eye stops accommodative ability which makes you use bad eye, this can be a second choice in children who don’t tolerate total occlusion
130
Q

Infants with abnormal red reflexes?

A
  • Infants with abnormal red reflexes need referred urgently to ophthalmology
  • Loss of red reflex does not mean it needs to be black or white, can simply be asymmetrical red reflexes where one is more red than other etc
131
Q

Explain some causes of abnormal red reflexes in infants?

A

Alteration in colour (pale yellow):
* Most commonly caused by asymmetrical camera shot – which is obviously completely benign
* Worrying cause however is retinoblastoma
* Coloboma is another cause which is failure of the eye to fuse in a complete circle, the effect on a child’s vision depends on where the defect is

Opacities in red reflex:
* Usually caused by congenital cataracts (these may be present from birth or come up as late as 14-16months)

No or black red reflex:
* Worried about retinoblastoma again
* Or retinal detachment or dysplasia

132
Q

What is diabetic retinopathy?

A
  • Damage to retina caused by hyperglycaemia in diabetes
  • After 20yrs 95% type 1 will have some form and 60% of type 2
  • Basically, hyperglycaemia damages vessels, you get reduced oxygen transport, so get tissue hypoxia, then get Vaso formative factors being produced and then neo-vascularisation, then get haemorrhage and scarring
133
Q

Risk factors for diabetic retinopathy?

A
  • Duration of diabetes
  • Poor blood sugar control
  • Hypertension
  • Hypercholesterolaemia
  • Pregnancy
  • Dramatically improved diabetic control – in people who have had poor control will get temporary worsening
134
Q

Types of diabetic retinopathy?

A
  • Mild, moderate and severe non-proliferative
  • Then you get proliferative diabetic retinopathy which is characterised by new vessel growth
135
Q

Some words for diabetic retinopathy?

A
  • Dot and blot haemorrhages
  • Hard exudates
  • Flame haemorrhages
  • Cotton wool spots
  • In proliferative: new vessels at the disc, or in the periphery or on the posterior vitreous face
136
Q

Management of diabetic retinopathy?

A
  • Non-proliferative retinopathy is observed
  • Proliferative is treated by lasering the peripheral retina to preserve the centre (decrease oxygen demands by getting rid of the peripheries)
137
Q

Screening for diabetic retinopathy?

A
  • This is offered every year for those aged 12 and over with diabetes
138
Q

What is thyroid eye disease?

A
  • Most common extra-thyroidal manifestation of Grave’s disease
  • Auto-immune reaction to TSH results in infiltration of lymphocytes into orbital tissue stimulating release of cytokines, end result is oedema of the orbital fat and extraocular muscles which forces the eye ball forward resulting in exophthalmos
139
Q

Presentation of thyroid eye disease?

A

Generally, have concurrent hyperthyroidism symptoms

Initially symptoms due to the crowded orbit because of the oedema
- Ocular irritation
- Ache behind the eyes
- Red eyes
- Exophthalmos – eyes bulging forwards
- Diplopia
- Dry or watery eyes
- Mild photophobia
- Redness of lids and eyes
- Difficulty moving eyes

Then can progress to:
Lid retraction and lid lag
Conjunctival injection and chemosis
Orbital fat prolapse
Exposure keratopathy

Can also get acute progressive optic neuropathy where the tissues begin to compress the optic nerve and can cause visual loss if not treated quickly

140
Q

Management of thyroid eye disease?

A
  • Joint endocrine and ophthalmology treatment
  • Maintain euthyroid state
  • Many treatment options for eyes themself
141
Q

What is periorbital cellulitis?

A

Peri-orbital cellulitis is an infectious process occurring in the eylid tissues superficial to the orbital septum, it is usually due to a superficial tissue injury e.g. insect bites

142
Q

Symptoms of periorbital cellulitis?

A
  • Symptoms include swelling, redness, pain and tenderness to touch, the affected person can move eye in all directions without causing pain but may be difficulties in opening the eye often due to swelling
  • Vision is normal
143
Q

Treatment of periorbital cellulitis?

A
  • This can be treated with oral antibiotics e.g. co-amoxiclav
144
Q

Define orbital cellulitis?

A
  • Orbital cellulitis is an infectious process affecting the muscles and fat within the orbit, posterior or deep to the orbital septum, not involving the globe, this is usually due to underlying bacterial sinusitis
145
Q

Symptoms of orbital cellulitis?

A
  • Symptoms include swelling, redness, pain, tenderness to touch, often significant pain with movement of the eye
  • Double vision or blurriness may occur
  • May get proptosis
146
Q

Management of orbital cellulitis?

A
  • Orbital cellulitis is more serious and warrants hospital admission
  • Medical emergency
  • Treated with IV Ceftriaxone
147
Q

Define endophthalmitis?

A

This is a rare infection of the whole globe of the eye and almost always occurs post surgery because usually there is a brain retina barrier which stops the immune system accessing the eye and it is surgery that has broken this

148
Q

Symptoms of endophthalmitis?

A

very red eye, very systemically unwell, significantly reduced vision

149
Q

Management of endophthalmitis?

A
  • Medical emergency and needs admission to hospital
  • Need to send an intravitreal sample and then usually give intravitreal antibiotics (systemic antibiotics are of little value)
150
Q

What is blepharitis?

A
  • Common chronic inflammatory condition affecting the margins of the eyelids
151
Q

Presentation of blepharitis?

A

In eyelids:
- Burning
- Itching
- Erythema
- Crusting (worse in morning)

152
Q

Management of blepharitis?

A
  • Eyelid hygiene measures
  • Warm compresses
  • These can help control the condition although likely to get relapses every now and then
153
Q

What is a chalazion?

A
  • Red bump that forms on eyelid due to blockage of a meibomian gland
  • Meibomian glands sit along the edges of eyelids where eyelashes are found and produce an oil that is part of tears
154
Q

Chalazion vs stye

A

stye is essentially an infected chalazion
chalazion are painless although might be irritating
stye are painful

155
Q

Management of chalazion?

A
  • Most go away in a month or less, should use warm compresses, massage and eye hygiene
156
Q

What are stye?

A
  • Stye are bacterial infections of the meibomian glands
157
Q

Appearance of stye?

A
  • They appear as red painful lumps near the edge of the eyelids
  • They are usually filled with pus
158
Q

Management of stye?

A
  • They generally disappear on their own like chalazion and should use same techniques
  • Can also take paracetamol and ibuprofen for pain
  • If it does not get better over a few weeks, becomes very painful or affects vision GP may drain the stye with a sterilised needle, remove eyelashes close to the stye or refer to ophthalmology
  • May get antibiotics in persistent stye
159
Q

Congenital tear (lacrimal) duct obstruction describe?

A

is a cause of recurrent watery or sticky eye in neonates and usually, self-resolves by 1 year of age

160
Q

Mechanisms of sight loss in diabetic retinopathy?

A

retinal detachment and vitreous haemorrhage

161
Q

Describe an entropion?

A

causes a sore eye
in turning of eyelids due to scarring of lid or lid laxity
can cause corneal ulcers
definitive management is surgical

162
Q

Bilateral grittiness think

A

blepharitis

163
Q

Flashes or floaters that dont go away?

A

retinal or vitreous detachment

164
Q

How does ischaemic optic neuropathy appear on fundoscopy?

A

a pale and swollen disc with blurred margins

165
Q

Causes of ischaemic optic neuropathy

A

occlusion of the blood flow to the optic nerve
most commonly arterial disease e.g. high blood pressure, diabetes
but other important cause is GCA

166
Q

2 mechanisms by which GCA can cause loss of vision?

A

most common- ischaemic optic neuropathy
second most common- central retinal artery occlusion

167
Q

Presentation of ischaemic optic neuropathy?

A

sudden visual loss that is usually painless

168
Q

How does wet ARMD appear on fundoscopy?

A

bleeding but only really around the macula
which is how you differentiate from things like proliferative diabetic retinopathy where haemorrhages and new vessels are more spread out

169
Q

In diabetic retinopathy cotton wool spots represent?

A

areas of retinal infarction

170
Q

Any patient who presents with new-onset flashes or floaters?

A

should be referred urgently for ophthalmology assessment

4th Year Surgery Block (11 decks)

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