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!Final Year > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What is a cataract?

A

A common eye condition where the lens of the eye gradually opacifies (becomes cloudy)

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2
Q

What is the leading cause of curable blindness worldwide?

A

Cataracts

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3
Q

What is the main feature of cataracts?

A

Reduced/ blurred vision
This is due to the cloudiness which makes it more difficult for light to reach the back of the eye

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4
Q

What is the epidemiology of cataracts?

A
  1. More common in women
  2. Incidence increases with age
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5
Q

What is the most common cause of cataracts?

A

Normal ageing process

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6
Q

What are some of the other causes of cataracts?

A
  1. Smoking
  2. Increased alcohol consumption
  3. Trauma
  4. DM
  5. Long-term corticosteroids
  6. Radiation exposure
  7. Myotonic dystrophy
  8. Metabolic disorders: hypocalcaemia
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7
Q

What are the features of cataracts?

A
  1. Reduced vision
  2. Faded colour vision: more difficult to distinguish colours
  3. Glare: lights appear brighter than usual
  4. Halos around lights
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8
Q

What is the sign of cataracts on examination?

A

Defect in red reflex:
1. Red-reflex is the reddish-orange reflection when a light is shone on the retina by an ophthalmoscope
2. Cataracts prevent light from reaching the retina
3. Therefore there will be a defect in the red reflex

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9
Q

What are the investigations of cataracts?

A
  1. Ophthalmoscopy: (after pupil dilation) shows a normal fundus and optic nerve, defect in red reflex
  2. Slit-lamp examination: shows a visible cataract
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10
Q

What is the classification for cataracts?

A
  1. Nuclear: change lens refractive index, common in old age
  2. Polar: localized, commonly inherited, lie in the visual axis
  3. Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
  4. Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
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11
Q

What is the general management for cataracts?

A
  1. Conservative
  2. Surgical
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12
Q

What is the conservative management of cataracts?

A
  1. Prescribing stronger glasses/contact lens
  2. Encourage the use of brighter lighting
    (these only help optimise vision rather than slow down progression, surgery will eventually be needed)
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13
Q

What is the surgical management of cataracts?

A
  1. Only effective treatment
  2. Removing the cloudy lens and replacing with an artificial one
  3. Patients should be advised on the use of eye drops and eyewear
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14
Q

What is the success rate of surgical management of cataracts?

A

High success rate with 85-90% of patients achieving 6/12 corrected vision (on a Snellen chart) postoperatively

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15
Q

What should the referral for surgical management for cataracts be dependent on?

A
  1. Whether a visual impairment is present
  2. Impact on quality of life
  3. Patient choice
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16
Q

What are some of the complications following surgical management of cataracts?

A
  1. Posterior capsule opacification: thickening of the lens capsule
  2. Retinal detachment
  3. Posterior capsule rupture
  4. Endophthalmitis: inflammation of aqueous and/or vitreous humour
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17
Q

What is central retinal artery occlusion?

A

A relatively rare cause of sudden unilateral visual loss

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18
Q

What are the two causes of central retinal artery occlusion?

A
  1. Thromboembolism: from atherosclerosis
  2. Arteritis e.g. temporal arteritis
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19
Q

What are the features of central retinal artery occlusion?

A
  1. Sudden, painless unilateral visual loss
  2. Relative afferent pupillary defect
  3. ‘cherry red’ spot on pale retina
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20
Q

What are the investigations for central retinal artery occlusion?

A

*ESR for temporal arteritis
1. Identification of classic symptoms: sudden painless visual loss on one side
2. Relative afferent pupillary defect on examination
3. Fundoscopy: ‘cherry red’ spot on the background of a pale retina which is indicative of retinal hypo perfusion
4. Imaging if suspecting thromboembolism? MR?

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21
Q

What is the management of central retinal artery occlusion?

A
  1. Identify and treat any underlying condition e.g. IV prednisolone for temporal arteritis
  2. If acute presentation, intra-arterial thrombolysis may be attempted
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22
Q

What is the main concern with managing central retinal artery occlusion?

A

Management is difficult and prognosis is poor

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23
Q

What is central retinal vein occlusion?

A

A cause for sudden painless loss of vision, usually unilaterally

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24
Q

What are the risk factors for central retinal vein occlusion?

A
  1. Increasing age
  2. Hypertension
  3. Cardiovascular disease
  4. Glaucoma
  5. Polycythaemia
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25
Q

What are the features of central retinal vein occlusion?

A
  1. Sudden painless reduction or loss of vision, usually unilaterally
  2. Fundoscopy findings: widespread hyperaemia, severe retinal haemorrhages - ‘stormy sunset’
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26
Q

What are the main differences in fundoscopy between central retinal vein and artery occlusion?

A

Artery occlusion: ‘cherry red’ spot on a pale (hypoxic) retina
Vein occlusion: widespread hyperaemia, severe retinal haemorrhages, ‘stormy sunset’

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27
Q

What is branch retinal vein occlusion (as opposed to central)?

A
  1. Occurs when a vein in the retinal venous system is occluded
  2. Thought to be due to a blockage of retinal veins at arteriovenous crossings
  3. Results in a more limited area of the funds being affected
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28
Q

What is the management of central retinal vein occlusion?

A
  1. Majority of patients managed conservatively
  2. Management includes intravitreal anti-vascular endothelial growth factor (VEGF) agents and laser photocoagulation
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29
Q

What is the indication for intravitreal anti-vascular endothelial growth factor management in central retinal vein occlusion?

A

Macular oedema

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30
Q

What is the indication for laser photocoagulation in the management of central retinal vein occlusion?

A

Retinal neovascularization

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31
Q

What are the most common causes of sudden, painless loss of vision?

A
  1. Ischaemic/ vascular (referred to as ‘amaurosis fugax’) e.g. TIA, central retinal artery/ vein occlusion
  2. Vitreous haemorrhage
  3. Retinal detachment
  4. Retinal migraine
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32
Q

Which is more common, central retinal artery occlusion or central retinal vein occlusion?

A

Central retinal vein occlusion

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33
Q

What is conjunctivitis?

A

Inflammation of the lining of the eyelids and eyeball
The most common eye problem presenting to primary care

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34
Q

What is conjunctivitis characterised by?

A

Sore, red eyes associated with a sticky discharge

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35
Q

What are the two types of conjunctivitis?

A
  1. Infective (bacterial and viral)
  2. Allergic
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36
Q

1What are the features of bacterial conjunctivitis?

A
  1. Purulent discharge
  2. Eyes may be ‘stuck together’ in the morning
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37
Q

What are the features of viral conjunctivitis?

A
  1. Serous discharge
  2. Recent URTI
  3. Preauricular lymph nodes
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38
Q

What are the investigations for infective conjunctivitis?

A

Usually clinical
Can consider:
1. Rapid adenovirus immunoassay- 2 visible lines equal positive
2. Cell culture/ Gram stain/ PCR- isolate viral or bacterial strains, amplify DNA

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39
Q

What is the management for infective conjunctivitis?

A
  1. Normally a self-limiting condition, should settle without treatment within 1-2 weeks
  2. Can offer chloramphenicol (topical antibiotics), given 2-3 hours initially
  3. Topical fusidic acid is an alternative, used for pregnancy women, BD
  4. For contact lens users:
    a. Do not wear during the infection
    b. Topical fluoresceins should be used to identify any corneal staining
    c. Offer topical antibiotics e.g. chloramphenicol
  5. Give advice to not share towels
  6. School exclusion is not necessary
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40
Q

What is allergic conjunctivitis?

A

Inflammation of the lining of the eyelids and eyeball in response to an irritant
Usually seen in the context of hayfever

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41
Q

What are the features of allergic conjunctivitis?

A
  1. Bilateral symptoms: conjunctival erythema, conjunctival swelling (chemosis)
  2. Itch is prominent
  3. Eyelids may be swollen
  4. PH of atopy
  5. May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)
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42
Q

What is the management of allergic conjunctivitis?

A
  1. First line = topical or systemic anti-histamines
  2. Topical mast-cell stabilisers e.g. Sodium cromoglicate and nedocromil
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43
Q

What is atopy?

A

IgE mediated atopic conditions:
1. Asthma
2. Allergic dermatitis e.g. eczema
3. Allergic rhinitis e.g. hay fever

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44
Q

What is glaucoma?

A

A group of disorders characterised by optic neuropathy due to raised intraocular pressure

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45
Q

What are the different types of glaucoma?

A
  1. Acute closed-angle glaucoma
  2. Primary opened-angle glaucoma
  3. Chronic closed-angle glaucoma
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46
Q

What are some of the secondary causes of glaucoma?

A
  1. Trauma
  2. Uveitis
  3. Steroid use
  4. Rubeosis iridis: DM, central retinal vein occlusion
  5. Congenital e.g. Buphthalmos: enlargement of the eyelid
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47
Q

What is the uvea?

A
  1. The vascular coat of the eyeball
  2. Lies between the sclera and retina
  3. Composed of 3 parts:
    a. Iris
    b. Ciliary body
    c. Choroid
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48
Q

What is the anterior chamber?

A

The area between the cornea and lens, filled with clear aqueous fluid which is nutrient-rich

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49
Q

What is the role of the ciliary body?

A

To secrete aqueous fluid into the anterior chamber

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50
Q

What structure drains the aqueous fluid out of the eye?

A

Trabecular meshwork through the canal of Schlemm

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51
Q

What is the normal intraocular pressure?

A

12-21 mmHg

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52
Q

What is acute angle-closure glaucoma (AACG)?

A

A type of glaucoma where there is a rise in IOP secondary due to an impairment in the aqueous fluid outflow (trabecular meshwork dysfunction)

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53
Q

What are the factors that predisposed to acute angle-closure glaucoma (AACG)?

A
  1. Hypermetropia (long-sightedness)
  2. Pupillary dilatation
  3. Lens growth associated with age
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54
Q

What are the features of acute angle-closure glaucoma (AACG)?

A
  1. Severe pain: either ocular or headache
  2. Decreased visual acuity
  3. Symptoms worse with mydriasis (e.g. watching TV in a dark room)
  4. Hard, red-eye
  5. Haloes around lights
  6. Semi-dilated non-reacting pupil
  7. Corneal oedema leads to dull or hazy cornea
  8. Systemic upset e.g. nausea, vomiting, abdominal pain
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55
Q

What is the management for acute angle-closure glaucoma (AACG)?

A

EMERGENCY - urgent referral to ophthalmology
Emergency medical treatment is required to lower the IOP with more definitive surgical treatment once the acute attack has settled

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56
Q

What is the initial medical treatment used in the management of acute angle closure glaucoma (AACG)?

A
  1. Combination of eyedrops:
    a. Direct parasympathomimetic e.g. pilocarpine, opens the trabecular meshwork therefore allowing drainage of the aqueous humour
    b. Beta-blocker e.g. timolol, decreases aqueous humour production
    c. alpha-2- agonist e.g. apraclonidine, decreases aqueous humour production and increases outflow
  2. IV acetazolamide: reduces aqueous secretions
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57
Q

What is the definitive surgical management for acute angle-closure glaucoma (AACG)?

A

Laser peripheral irirdotomy
Creates a tiny hole in the peripheral iris which drains the aqueous humour (alternative drainage pathway)

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58
Q

What is the cause of acute angle-closure glaucoma?

A

Rise in IOP due to an impairment in the aqueous humour outflow/ drainage

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59
Q

What is primary open-angle glaucoma (POAG)?

A

An insidious onset of optic neuropathy due to raised IOP, usually detected on routine optometry

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60
Q

What are the risk factors for primary open-angle glaucoma (POAG)?

A
  1. Increasing age
  2. Genetics
  3. Afro-Carribean ethnicity
  4. Myopia
  5. Hypertension
  6. DM
  7. Corticosteroids
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61
Q

What are the features of primary open angle glaucoma (POAG)?

A

Often symptomatic and detected during routine optometry appointments:
1. Peripheral visual field loss: nasal scotomas progressing to ‘tunnel vision’
2. Decreased visual acuity
3. Optic disc cupping

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62
Q

What are the signs of primary open-angle glaucoma (POAG) on fundoscopy?

A
  1. Optic disc cupping (due to loss of disc substance), cup: disc ratio > 0.7
  2. Optic disc pallor: due to atrophy
  3. Bayonetting of vessels: disappear into the deep optic disc cup and re-appear at the base
  4. Additional features: cup notching (where vessels enter disc inferiorly), disc haemorrhages
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63
Q

How is the diagnosis of primary open-angle glaucoma (POAG) made?

A
  1. Found and provisionally made by optometrist
  2. Referred to ophthalmology via GP who carry out a set of investigations
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64
Q

What are the investigations for primary open-angle glaucoma (POAG)?

A
  1. Automated perimetry: assess visual fields
  2. Slit lamp examination with pupil dilation: assess optic nerve and fundus
  3. Application tonometry: measure IOP
  4. Central corneal thickness measurement
  5. Gonioscopy: assess peripheral anterior chamber configuration and depth
    Using this and risk factors, assess risk of future visual impairment
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65
Q

What is are the two main differences between acute angle-closure and primary open-angle glaucoma (AACG vs POAG)?

A
  1. Trabecular meshwork dysfunction: in AACG there is an impairment in aqueous outflow due to this leading to rise in IOP
  2. Features: AACG is an acute presentation of painful red eye, impaired vision and haloes around eyes. In POAG, often asymptomatic with a slow rise in IOP causing peripheral visual field loss and optic disc cupping
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66
Q

What is the management of primary open-angle glaucoma (POAG)?

A
  1. First line: prostaglandin analogue eyedrops
  2. Second: beta blocker, carbonic anhydrase inhibitor or sympathomimetic eyedrop
  3. If more advanced, surgery or laser treatment can be tried
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67
Q

What is the aim of eyedrops in the management of primary open-angle glaucoma (POAG)?

A

Aim to lower the IOP which in turn prevents progressive loss of visual fields

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68
Q

What is the surgical management of primary open-angle glaucoma (POAG)?

A

Trabeculectomy- similar surgery to AACG to create a new pathway for aqueous humour drainage

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69
Q

What is an important consideration in the management of primary open-angle glaucoma?

A

Reassessment:
1. To exclude progression and visual field loss
2. Needs to be more frequent if IOP uncontrolled or if the patient is high risk

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70
Q

What is a raised IOP?

A

> 24 mmHG

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71
Q

What is closed angle glaucoma?

A
  1. Where increased IOP pushes the iris/lens complex forwards
  2. This blocks the trabecular meshwork which drains the aqueous fluid- exacerbates the problem increasing pressure further
  3. Can be acute or chronic
72
Q

What is the epidemiology of glaucoma?

A

Prevalence 1 % in over 40 years, 10 % in over 80 years (POAG)
Third most common cause of blindness worldwide

73
Q

What is keratitis?

A

Inflammation of the cornea
Potentially sight threatening and therefore should be urgently evaluated and treated

74
Q

What is the aetiology of keratitis?

A
  1. Bacterial: usually staphylococcus aureus, pseudomonas aerugionosa in contact lens users
  2. Fungal
  3. Amoebic:
    a. Acanthamoebic keratitis
    b. Accounts for 5% of cases
    c. Increased incidence if eye exposure to soil or contaminated water
    d. Pain is classically out of proportion to the findings
  4. Parasitic: onchocercal keratitis ‘river blindness’
75
Q

What are some of the other causes of keratitis?

A
  1. Viral = herpes simplex keratitis
  2. Environmental = photokeratitis e.g. welder’s arc eye
  3. Environmental = exposure keratitis
  4. Environmental = contact lens acute red eye (CLARE)
76
Q

What are the features of keratitis?

A
  1. Red eye: pain and erythema
  2. Photophobia
  3. Foreign body, gritty sensation
  4. Hypopyon may be seen (white layer of fluid in lower part of anterior chamber from WBC)
77
Q

When should patients be referred to an eye specialist for keratitis?

A
  1. If they are contact lens wearers and they present with a painful red eye
  2. Require a slit-lamp examination to rule out microbial keratitis (usually from pseudomonas aeruginosa)
78
Q

What is the management of keratitis?

A
  1. Stop using contact lens until the symptoms have fully resolved
  2. Topical antibiotics = first choice are quinolones
  3. Cycloplegic for pain relief e.g. cyclopentolate
79
Q

What are the complications for keratitis?

A
  1. Corneal scarring
  2. Perforation
  3. Enophthalmitis (spread of infection into the eye)
  4. Visual loss
80
Q

What is herpes simplex keratitis?

A
  1. Commonly presents with a dendritic corneal ulcer
  2. Red painful eye
  3. Photophobia
  4. Epiphora: excess tear production
  5. Visual acuity may be decreased
  6. Fluorscein staining = epithelial ulcer
81
Q

What is the management of herpes simplex keratitis?

A
  1. Immediate referral to an ophthalmologist
  2. Topical aciclovir
82
Q

What is macular degeneration?

A

Degeneration of the central retina (macular) with changes usually bilaterally

83
Q

What is age-related macular degeneration?

A

The most common cause of blindness in the UK due to the degeneration of retinal photoreceptors in the central retina (macula)

84
Q

What is formed in age-related macular degeneration?

A
  1. Drusen
  2. Due to the degeneration of retinal photoreceptors
  3. Yellow areas of pigment deposition in the macular area which may later form a scar
  4. Visualised on fundoscopy and retinal photography
85
Q

What is the epidemiology of age-related macular degeneration?

A
  1. Most common cause of blindness in the UK
  2. More common with advancing age
  3. More common in females
86
Q

What are the risk factors for age-related macular degeneration?

A
  1. Age = greatest risk factor (inverses 3-fold for >75 years)
  2. Smoking
  3. Family history (4 times as likely if there is a first degree relative with it)
  4. Co-morbidities e.g. ischaemic CVD: HTN, dyslipidaemia, DM
87
Q

What are the two forms of macular degeneration?

A
  1. Dry macular degeneration (atrophic):
    a. 90% of cases
    b. Drusen: yellow round sports in Bruch’s membrane
  2. Wet macular degeneration:
    a. 10% of cases
    b. Also known as exudative or neovascular
    c. Choroidal neovacularisation
    d. Leakage of serous fluid and blood results in rapid loss of vision
    e. Worst prognosis
88
Q

What is the classification for macular degeneration?

A
  1. Early age-related macular degeneration = atrophic, non-exudative
  2. Late age-related macular degeneration = neovascularisation, exudative
89
Q

What are the clinical features of macular degeneration?

A
  1. Subacute onset of visual loss
  2. Reduction in visual acuity, particularly for near field objects
    a. gradual in dry degeneration
    b. subacute in wet degeneration
  3. Difficulties in dark adaptation - overall deterioration in night vision
  4. Fluctuations in visual disturbance
  5. Photopsia: perception of flickering or flashing lights, glare around objects
  6. Visual hallucinations resulting in Charles-Bonnet syndrome
90
Q

What is Charles Bonnet syndrome?

A
  1. persistent or recurrent complex hallucinations occurring in clear consciousness
  2. Generally against a background of visual impairment
  3. Insight is usually preserved
91
Q

What are the signs of macular degeneration on examination?

A

Fundoscopy:
1. Dry degeneration shows presence of drusen, yellow areas of pigment deposition, can become a macular scar in later disease
2. Wet degeneration shows well demarcated red patches which represent intra-retinal or sub-retinal fluid leakage or haemorrhage
Amsler grid testing:
1. distortion of line perception

92
Q

What are the investigations for macular degeneration?

A
  1. Initial investigation of choice: slit lamp microscopy
    a. Identifies any pigmentary, exudative or haemorrhagic changes affecting the retina
    b. Usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time
  2. Fluorescein angiography: if wet (neovascular) degeneration is suspected
    a. Can guide intervention with anti-VEGF therapy
    b. Complemented with indocyanine green angiography to visualise any changes in the choroidal circulation
  3. Ocular coherence tomography: used to visualise the retina in 3D to reveal areas not visible using microscopy alone
93
Q

What is the management of macular degeneration?

A
  1. Dry degeneration (90% of cases): combination of zinc with anti-oxidant vitamins A,C and E to reduce progression of disease
  2. Wet degeneration: anti- vascular endothelial growth factor (anti-VEGF) is the definitive treatment
94
Q

What is the mechanism of anti-VEGF agents in the management of wet macular degeneration?

A
  1. Vascular endothelial growth factor (VEGF) is a potent mitogen and drives increased vascular permeability in patients with wet degeneration
  2. Therefore anti-VEGF agents can limit progression of degeneration and stabilise or reverse visual loss
  3. E.g. ranibizumab, bevacizumab and pegaptanib, usually administered by 4 weekly injection
95
Q

What is a less preferred management option for wet macular degeneration?

A
  1. Laser photocoagulation
  2. Does slow progression of age-related macular degeneration where there is new vessel formation, although there is a risk of acute visual loss after treatment
96
Q

What is orbital cellulitis?

A
  1. Medical emergency
  2. The result of an infection affecting the fat and muscles posterior to the orbital septum
  3. Usually caused by a spreading URTI from the sinuses
  4. Carriers a high mortality rate
97
Q

What is the common cause of orbital cellulitis?

A

A spreading upper respiratory tract infection from the sinuses

98
Q

What is periorbital cellulitis?

A
  1. A less serious superficial infection anterior to the orbital septum
  2. Resulting from a superficial tissue injury e.g. chalazion (painless lump on eyelid) or insect bite
  3. Can progress to orbital cellulitis
99
Q

What are the risk factors for orbital cellulitis?

A
  1. Childhood (mean age of hospitalisation is 7-12 years)
  2. Previous sinus infection
  3. Lack of Haemophilus influenzae type b (Hib) vaccination
  4. Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
  5. Ear or facial infection
100
Q

What is the presentation of orbital cellulitis?

A
  1. Redness and swelling around the eye
  2. Severe ocular pain
  3. Visual disturbance
  4. Proptosis (bulging of eye)
  5. Ophthalmoplegia/ pain with eye movements
  6. Eyelid oedema and ptosis
  7. Drowsiness ± nausea and vomiting in meningeal involvement (RARE)
101
Q

What are the main differences in periorbital cellulitis and orbital cellulitis on examination?

A
  1. Perioribtal cellulitis mainly presents with redness, swelling and ocular pain
  2. Orbital cellulitis has reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements which are not seen in periorbital
102
Q

What are the investigations for orbital cellulitis?

A
  1. Medical emergency - A to E approach, involve seniors/ ophthalmology
  2. Clinical examination with complete ophthalmological assessment: Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema
  3. Bloods:
    a. Elevated WBC and inflammatory markers
    b. Blood culture (plus microbiological swab) to determine organism
  4. CT with contrast: Inflammation of the orbital tissues deep to the septum, sinusitis
103
Q

What are the most common bacterial organisms in orbital cellulitis?

A

Streptococcus, Staphylococcus aureus and Haemophilus influenzae B

104
Q

What is the management of orbital cellulitis?

A

A to E approach and refer to ophthalmology
Admission to hospital for IV antibiotics due to high mortality rate

105
Q

Why is a CT with contrast a useful investigation in orbital cellulitis?

A

May help to differentiate between periorbital and orbital cellulitis
Therefore should be performed in all patients suspected to have orbital cellulitis

106
Q

What is the management of periorbital cellulitis?

A
  1. All cases referred to secondary care for assessment
  2. Oral antibiotics are frequently sufficient - usually co-amoxiclav
  3. Children may require admission for observation
107
Q

What is the main concern with periorbital cellulitis?

A

The bacterial infection may spread into the orbit and evolve in orbital cellulitis

108
Q

What is retinal detachment?

A
  1. Occurs when the neurosensory tissue that lines the back of the eye comes away from it’s underlying pigment epithelium
  2. Reversible cause of visual loss - if untreated will inevitably lead to permanent visual loss
109
Q

Why is retinal detachment a reversible cause of visual loss (if treated)?

A

If recognised and treated early, the macula will not be affected

110
Q

What are the risk factors for retinal detachment?

A
  1. Diabetes mellitus: occurs as a result of breaks in the retina due to traction by the vitreous humour which may proceed to detachment if left untreated
  2. Myopia (short-sightedness)
  3. Age
  4. Previous surgery for cataracts = accelerate posterior vitreous detachment
  5. Eye trauma e.g. boxing
111
Q

What are the features of retinal detachment?

A
  1. New onset of floaters or flashes
  2. Sudden onset, painless and progressive visual field loss (described as a curtain or shadow progressing to the centre of the visual field)
  3. If the macula is affected = central visual acuity becomes much worse
112
Q

Why is there a new onset of flashes or floaters in retinal detachment?

A

Indicate pigment cells entering the vitreous space (floater) or traction on the retina (flashes)

113
Q

What is a sign of macula detachment on examination?

A

Peripheral fields reduced PLUS central acuity reduced to hand movements

114
Q

What are the signs of retinal detachment on examination?

A
  1. Peripheral visual field loss (central acuity if macula involvement)
  2. Swinging light test: relative afferent pupillary defect if optic nerve is involved
  3. Fundoscopy:
    a. Red reflex is lost
    b. Retinal folds may appear as pale, opaque or wrinkled forms
    c. If the retinal detachment is small, it may appear normal
115
Q

What is the management of retinal detachment?

A
  1. Any patients with new onset of floater or flashes should be referred urgently to an ophthalmologist (<24 hours)
  2. Assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage
  3. Either scleral buckle or vitrectomy: to seal the retinal breaks
116
Q

What two conditions present with a defect in the red reflex?

A
  1. Cataracts: defect in the reflex, opacification prevents light going to the retina
  2. Retinal detachment: red reflex is lost
117
Q

What is Strabismus?

A
  1. Also known as squint
  2. Characterised by misalignment of the visual axes
  3. May be concomitant (common) and paralytic (rare)
118
Q

Why is it important to detect strabismus?

A

If left uncorrected then it may lead to amblyopia: where the brain fails to fully process inputs from one eye and over time favours the other eye

119
Q

What is concomitant strabismus?

A
  1. Due to imbalance in extra ocular muscles
  2. Convergent is more common than divergent
120
Q

What is paralytic strabismus?

A

Due to paralysis of extra ocular muscles

121
Q

How can strabismus be investigated/ detected?

A

Made by the corneal light reflection test:
Holding a light source 30cm away from the child’s face to see if the light reflects symmetrically on the pupils

122
Q

What is the cover test for strabismus?

A

Used to identify the nature of the squint:
1. Ask the child to focus on an object
2. Cover one eye
3. Observe the movement of the uncovered eye
4. Cover the other eye and repeat the test
No movement = normal

123
Q

What are the investigations for strabismus?

A
  1. Cover test
  2. Simultaneous prism and cover test
124
Q

What are the features of strabismus?

A
  1. Diplopia (double vision)
  2. Visual confusion in adults (seeing different objects in the same place)
  3. Amblyopia in children: decreased vision in an anatomically normal eye caused by failure of processing inputs
125
Q

What is the management of strabismus?

A
  1. Referral to secondary care
  2. Correction of refractive errors using glasses or contact lenses
  3. Treatment of amblyopia: eyepatches/ occlusion of the good eye
126
Q

What disease could strabismus be a presenting feature of?

A

Retinoblastoma:
1. Most common ocular malignancy in children
2. Most common feature is absence of red-reflex replaces by a white pupil
3. Could also present with a squint and visual problems

127
Q

What is uveitis?

A

The broad term for inflammation of one or all parts of the uvea

128
Q

What is anterior uveitis?

A

Involves inflammation of the iris and the ciliary body

129
Q

What is intermediate uveitis?

A

Involves the posterior ciliary body and pars plana

130
Q

What is posterior uveitis?

A

Involves the posterior vitreous, retina, choroid, retinal vasculature and optic nerve

131
Q

What is panuveitis?

A

Involves inflammation in the anterior, intermediate and posterior segments of the eye

132
Q

What is the difference between acute, recurrent or chronic uveitis?

A

Acute: sudden onset (over hours or days) and limited duration < 3 months
Recurrent: repeated episodes separated by disease inactivity > 3 months
Chronic: persistent uveitis >3 months duration, characterised by relapse within 3 months of therapy termination

133
Q

What is the diagnosis and management for all uveitis?

A

Diagnosis is clinical and all types of uveitis are potentially blinding conditions and so should be referred to and managed by an experienced ophthalmologist

134
Q

What is anterior uveitis and what is it associated with?

A
  1. Describes inflammation of the anterior part of the uvea: iris and ciliary body
  2. Associated with HLA-B27 diseases e.g. ankylosing spondylitis, reactive arthritis, IBD, Behcet’s disease and sarcoidosis
135
Q

What are the features of anterior uveitis?

A
  1. Acute onset of ocular discomfort and pain (may increase with use)
  2. Pupil may be small ± irregular, due to sphincter muscle contraction
  3. (intense) photophobia
  4. Blurred vision
  5. Red eye
  6. Lacrimation
  7. Ciliary flush: ring of red spreading outwards
  8. Hypopyon: pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
  9. Visual acuity initially normal and then later impaired
136
Q

What are the investigations of anterior uveitis?

A
  1. Usually clinical
  2. Offer Bloods: ESR, CRP, HLA-B27
  3. HLA-B27 and antibodies including andti-dsDNA, ANCA, anti-CCP
137
Q

What is the management of anterior uveitis?

A
  1. Urgent review by ophthalmology
  2. Cycloplegics: dilate the pupil which helps to relive pain and photophobia e.g. atropine, cyclopentolate
  3. Steroid eye drops
138
Q

What is the treatment of intermediate or posterior uveitis?

A

Usually requires injected local corticosteroids or systemic corticosteroids
May need other forms of immunosuppression

139
Q

What are the main differentials for a red eye?

A
  1. Acute angle closure glaucoma
  2. Anterior uveitis
  3. Scleritis
  4. Conjunctivitis
  5. Subconjunctival haemorrhage
  6. Endophthalmitis
140
Q

What is scleritis?

A
  1. Severe pain (may be worse on movement) and tenderness
  2. May be underlying autoimmune disease e.g. rheumatoid arthritis
141
Q

What does subconjunctival haemorrhage usually have a history of?

A

Trauma or coughing bouts

142
Q

What are the features of endophthalmitis?

A

Typically a red eye, with pain and visual loss following intraocular surgery

143
Q

What are the main features of anterior uveitis?

A
  1. Acute onset
  2. Red eye
  3. Pain
  4. Blurred vision and photophobia
  5. Small, fixed oval pupil with ciliary flush
144
Q

What is a vitreous haemorrhage?

A

Bleeding into the vitreous humour

145
Q

What is the aetiology of vitreous haemorrhage?

A
  1. The source of bleeding can be from disruption of any vessel in the retina as well as the extension through the retina from other areas
  2. Causes disruption to vision to a variable degree, ranging from floaters to complete visual loss
  3. Once the bleeding stops, the blood is typically cleared from the retina at an approximate rate of 1% per day
146
Q

What are the common causes of vitreous haemorrhage?

A
  1. Proliferative diabetic retinopathy (over 50%)
  2. Posterior vitreous detachment
  3. Ocular trauma: most common cause in children and young adults
147
Q

What is the most common cause of vitreous haemorrhage?

A

Proliferative diabetic retinopathy

148
Q

What are the main features of vitreous haemorrhage?

A

Acute or subacute onset of:
1. Painless visual loss or haze (commonest)
2. Red hue in the vision
3. Floated or shadows/ dark spots in the vision

149
Q

What are the signs of vitreous haemorrhage on examination?

A
  1. Decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
  2. Visual field defect (if severe haemorrhage)
150
Q

What is the biggest risk factor for vitreous haemorrhage?

A

Poorly controlled diabetes

151
Q

What are the investigations for vitreous haemorrhage?

A
  1. Dilated fundoscopy: may show haemorrhage in the vitreous cavity
  2. Slit lamp examination: red blood cells in the anterior vitreous
  3. Ultrasound: useful to rule out retinal tear/ detachment and if the haemorrhage obscures the retina
  4. Fluorescein angiography: to identify neovascularization
  5. Orbital CT: used if open globe injury (ocular trauma in children and YP)
152
Q

What is the management of vitreous haemorrhage?

A

Refer to specialist, ensure good DM control after
1. Panretinal photocoagulation
2. Vitrectomy

153
Q

What is posterior vitreous detachment?

A
  1. Separation of the vitreous membrane from the retina
  2. This occurs due to natural changes to the vitreous fluid of the eye with ageing
  3. Does not cause any pain or vision loss
154
Q

What is a complication of posterior vitreous detachment?

A

Rarely the separation of the vitreous membrane can lead to tears and detachment of the retina: important to rule these out due to the risk of permanent loss of vision

155
Q

What is the epidemiology of posterior vitreous detachment?

A
  1. Occur in over 75% of people over 65
  2. More common in females
156
Q

What is the pathophysiology of posterior vitreous detachment?

A
  1. As people age, the vitreous fluid in the eye becomes less viscous, and thus, does not hold its shape as well
  2. Therefore, it pulls the vitreous membrane away from the retina towards the centre of the eye
157
Q

Which group of people are at a greater risk of developing posterior vitreous detachment earlier?

A
  1. Highly myopic (short-sighted) patients
  2. Because the myopic eye has a longer axial length than an emmetropic eye
158
Q

What are the symptoms of posterior vitreous detachment?

A
  1. Sudden appearance of floaters
  2. Flashes of light in vision
  3. Blurred vision
  4. Cobweb across vision
  5. Appearance of a dark curtain descending down - presence of retinal detachment
159
Q

What are the signs of posterior vitreous detachment?

A

Weiss ring on ophthalmoscopy: detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater

160
Q

What are the investigations for posterior vitreous detachment?

A

All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or retinal detachment

161
Q

What is the management of posterior vitreous detachment?

A
  1. Alone it does not cause any permanent loss of vision
  2. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary
  3. If there is an associated retinal tear or detachment the patient will require surgery to fix this
162
Q

What is diabetic retinopathy?

A

Most common cause of blindness in adults aged 35-65 years old

163
Q

What is the pathophysiology of diabetic retinopathy?

A
  1. Hyperglycaemia is thought to increase retinal blood flow and abnormal metabolism of the retinal vessel walls
  2. This precipitates damage to endothelial cells and pericytes
  3. Endothelial damage results in increased vascular permeability which causes characteristic exudates on fundoscopy
  4. Pericyte damage predisposes to the formation of micro aneurysms
  5. Neovascularisation is caused by the production of growth factors in response to retinal ischaemia
164
Q

What are the three broad groups of diabetic retinopathy?

A
  1. Non-proliferative retinopathy
  2. Proliferative retinopathy
  3. Maculopathy
165
Q

What is non-proliferative diabetic retinopathy divided into?

A
  1. Mild
  2. Moderate
  3. Severe
166
Q

What is mild non-proliferative diabetic retinopathy?

A

One or more micro aneurysm

167
Q

What is moderate non-proliferative diabetic retinopathy?

A
  1. Microaneurysms
  2. Blot haemorrhages
  3. Hard exudates
  4. Cotton wool spots - ‘soft exudates’: represent areas of retinal infarction
168
Q

What is severe non-proliferative diabetic retinopathy?

A
  1. Blot haemorrhages and micro aneurysms in 4 quadrants
  2. Venous beading in at least 2 quadrants
  3. Intraretinal microvascular abnormalities in at least 1 quadrant
169
Q

What are the key features of proliferative diabetic retinopathy?

A
  1. Retinal neovascularisation- may lead to vitreous haemorrhage
  2. Fibrous tissue forming anterior to retinal disc
170
Q

What group is proliferative diabetic retinopathy more common in?

A

Type 1 diabetes patients- 50% become blind in 5 years

171
Q

What are the key features of maculopathy?

A
  1. Based on location rather than severity as anything is potentially serious
  2. Hard exudates and other ‘background’ changes on macula
  3. Important to check for changes in visual acuity
172
Q

What group is maculopathy more common in?

A

Type 2 diabetics

173
Q

What is the management for all patients with diabetic retinopathy?

A
  1. Optimise glycemic control, BP and hyperlipidaemia
  2. Regular reviews by ophthalmology
174
Q

What is the management of maculopathy?

A

If there is a change in visual acuity: intravitreal vascular endothelial growth (VEGF) inhibitors/ anti-VEGF agents

175
Q

What is the management of non-proliferative retinopathy?

A
  1. Regular reviews/ observation
  2. If severe, consider pan retinal laser photocoagulation
176
Q

What is the management of proliferative retinopathy?

A
  1. Panretinal laser photocoagulation
  2. Intravitreal VEGF inhibitors/ anti-VEGF agents e.g. ranibizumab
    * often 1 and 2 are used in combination as they both slow progression of proliferative diabetic retinopathy and improve visual acuity
  3. If severe or vitreous haemorrhage: vitreoretinal surgery
177
Q

What is a complication of pan retinal laser photocoagulation therapy in the management of proliferative diabetic retinopathy?

A

50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue

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