Ophthalmology Flashcards

Conditions and presentations

1
Q

What is glaucoma

A

Glaucoma is a group of disorders characterised by optic neuropathy due, in the majority of patients, to raised intraocular pressure (IOP).

Not all patients with raised I have glaucoma and vice versa

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2
Q

Factors which predispose to AACG (Acutely angle-closure glaucoma)

A

hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age

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3
Q

Features of AACG

A
  • severe pain: may be ocular or headache
  • decreased visual acuity
  • symptoms worse with mydriasis (e.g. watching TV in a dark room)
  • hard, red-eye
  • haloes around lights
  • semi-dilated non-reacting pupil
  • corneal oedema results in dull or hazy cornea
  • systemic upset may be seen, such as nausea and vomiting and even abdominal pain
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4
Q

Investigations of AACG

A

tonometry to assess for elevated IOP
gonioscopy (literally looking, oscopy, at the angle, gonio): a special lens for the slit lamp that allows visualisation of the angle

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5
Q

Management of AACG

A
  • typically an emergency and should prompt urgent referral to ophthalmology

Emergency medical treatment is required to lower the IOP with more definitive surgical treatment given once the acute attack has settled.

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6
Q

Example regime of managing AACG

A

combination of eye drops, for example:
a direct parasympathomimetic (e.g. pilocarpine, causes contraction of the ciliary muscle → opening the trabecular meshwork → increased outflow of the aqueous humour)
a beta-blocker (e.g. timolol, decreases aqueous humour production)
an alpha-2 agonist (e.g. apraclonidine, dual mechanism, decreasing aqueous humour production and increasing uveoscleral outflow)
intravenous acetazolamide
reduces aqueous secretions
some guidelines also recommend the use of topical steroids to reduce inflammation

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7
Q

Definitive management of AACG

A

laser peripheral iridotomy
creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle

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8
Q

Age-related macular degeneration

A

most common cause of blindness in the UK

Degeneration of the central retina (macula) is the key feature with changes usually bilateral.

ARMD is characterised by degeneration of retinal photoreceptors that results in the formation of drusen which can be seen on fundoscopy and retinal photography

It is more common with advancing age and is more common in females.

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9
Q

Risk factors of ARMD

A
  • advancing age (greatest risk)
  • smoking
  • current smokers are twice as likely as non-smokers
  • family history
  • ischaemic cardiovascular disease
  • hypertension
  • dyslipidaemia
  • diabetes mellitus.
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10
Q

Investigation of ARMD

A
  • slit-lamp microscopy (any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD)
    This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.
    fluorescein angiography is utilised if neovascular ARMD is suspected,
    optical coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren’t visible using microscopy alone.
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11
Q

Signs of ARMD during investigation

A

distortion of line perception may be noted on Amsler grid testing
fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.

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12
Q

Clinic features of ARMD

A

Patients typically present with a subacute onset of visual loss with:
a reduction in visual acuity, particularly for near field objects
gradual in dry ARMD
subacute in wet ARMD
difficulties in dark adaptation with an overall deterioration in vision at night
fluctuations in visual disturbance which may vary significantly from day to day
they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects
visual hallucinations may also occur resulting in Charles-Bonnet syndrome

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13
Q

Treatment of ARMD

A

combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.

vascular endothelial growth factor (VEGF)
VEGR is a potent mitogen and drives increased vascular permeability in patients with wet ARMD
a number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss
evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible
examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.

laser photocoagulation does slow progression of ARMD

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14
Q

Risk of laser photocoagulation

A

risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.

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15
Q

Allergic conjunctivitis features

A

Bilateral symptoms conjunctival erythema, conjunctival swelling (chemosis)
Itch is prominent
the eyelids may also be swollen
May be a history of atopy
May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)

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16
Q

Management of allergic conjunctivitis

A

first-line: topical or systemic antihistamines
second-line: topical mast-cell stabilisers, e.g. Sodium cromoglicate and nedocromil

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17
Q

Anterior uveitis

A

important differentials of a red eye

also referred to as iritis.

inflammation of the anterior portion of the uvea - iris and ciliary body.

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18
Q

What genes is associated with anterior uveitis

A

HLA-B27

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19
Q

Features of anterior uveitis

A

acute onset
ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
visual acuity initially normal → impaired

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20
Q

Associated conditions with anterior uveitis

A

ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen

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21
Q

Management of anterior uveitis

A

urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops

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22
Q

Argyll-Robertson pupil

A

Argyll-Robertson pupil is one of the classic pupillary syndrome. It is sometimes seen in neurosyphilis.

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23
Q

What conditions are associated with HLA-B27

A
  • Ankylosing spondylitis
  • Reactive arthritis (Reiter’s syndrome)
    -psoriatic arthritis
    -enteropathic arthritis (associated with IBD)
    Juvenile idiopathic arthritis
    Acute anterior uveitis
    Axial spondyloarthritis
    Behçet’s disease (in some populations)
    Reactive arthritis following certain infections, such as Chlamydia trachomatis or Salmonella spp.
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24
Q

Argyll-Robertson pupil ARP—>PRA

A

Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)

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25
Q

Features of Argyll-Robertson pupil

A

small, irregular pupils
no response to light but there is a response to accommodate

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26
Q

Causes of Argyll-Robertson pupil

A

diabetes mellitus
syphilis

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27
Q

Blepharitis

A

Blepharitis is inflammation of the eyelid margins. It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).

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28
Q

What condition is most associated with blepharitis

A

Rosacea

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29
Q

Function of the meibomian gland

A

The meibomian glands secrete oil on to the eye surface to prevent rapid evaporation of the tear film.

Any problem affecting the meibomian glands (as in blepharitis) can hence cause drying of the eyes which in turns leads to irritation

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30
Q

Features of blepharitis

A

symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur

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31
Q

Management of blepharitis

A

softening of the lid margin using hot compresses twice a day
‘lid hygiene’ - mechanical removal of the debris from lid margins
cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used
an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film

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32
Q

Blurred vision

A

Loss of clarity or sharpness of vision
Patients who have it will have long-term refractive errors
Make sure to assess for other symptoms such as visual loss, double vision and floaters

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33
Q

Causes of blurred vision (7)

A

refractive error: most common
cataracts
retinal detachment
age-related macular degeneration
acute angle closure glaucoma
optic neuritis
amaurosis fugax

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34
Q

Assessment of blurred vision

A

visual acuity with a Snellen chart
pinhole occluders are a useful way to check for whether the blurred vision is due to a refractive error or not
if the blurring improves with a pinhole occluder then likely cause is a refractive error
visual fields
fundoscopy

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35
Q

Management of blurred vision

A

depends on the suspected underlying cause
if gradual onset, corrected by pinhole occluder and no other associated symptoms then an optician review would be the next step
other patients should be seen by ophthalmology. If there are associated symptoms such as visual loss or pain this should be urgent

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36
Q

Thyroid eye disease

A

Grave’s disease

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37
Q

Pathophysiology of grave’s disease

A

it is thought to be caused by an autoimmune response against an autoantigen, possibly the TSH receptor → retro-orbital inflammation
the inflammation results in glycosaminoglycan and collagen deposition in the muscles

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38
Q

Prevention of grave’s eye disease

A
  • smoking
  • radioiodine treatment
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39
Q

Features of grave’s eye disease

A
  • eu/ hypo/ hyperthyroid at time of presentation
  • exophthalmos
    conjunctival oedema
    optic disc swelling
    ophthalmoplegia
    inability to close the eyelids
    Dry eye
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40
Q

Managment of grave’s eye disease

A

smoking cessation
topical lubricants may be needed to help prevent corneal inflammation caused by exposure
steroids
radiotherapy
surgery

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41
Q

Complications of grave’s eye disease

A
  • exposure kerathopathy
  • optic neuropathy
    -strabismus and dipolopia
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42
Q

Exposure kerathopathy

A
  • eye lid retraction and proptosis causes cornea to become excessively exposed

Causes dryness and imitation and corneal ulceration

Pt may report a foreign body experience

Photophobia

Can cause scarring and vision impairment as well

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43
Q

Optic neuropathy

A

enlarged extraocular muscles compress the optic nerve at the apex of the orbit → a reduction in visual acuity, colour vision deficits, and visual field defect
it requires urgent medical intervention to prevent permanent vision loss.

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44
Q

Strabismus and diplopia

A

fibrosis and enlargement of the extraocular muscles can result in restrictive strabismus → misalignment of the eyes → double vision (diplopia)
this not only affects visual function but can also significantly impair the quality of life.

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45
Q

When to urgently review someone with grave’s disease?

A

unexplained deterioration in vision
awareness of change in intensity or quality of colour vision in one or both eyes
history of eye suddenly ‘popping out’ (globe subluxation)
obvious corneal opacity
cornea still visible when the eyelids are closed
disc swelling
(EUGOGO guidelines)

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46
Q

Optic neuritis

A

Inflammation of the optic nerve

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47
Q

Causes of optic neuritis

A
  • MS
  • diabetes
    -syphilis
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48
Q

Features of ON

A

unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect
central scotoma

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49
Q

Investigation of ON

A

MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases

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50
Q

Managment of ON

A
  • high dose steroid (usually takes 4-6 weeks to recover )
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51
Q

Prognosis of ON

A

MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%

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52
Q

Scleritis

A

Full thickness inflammation of the sclera
Non- infective cause and associated with red painful eye

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53
Q

Risk factors for scleritis

A

rheumatoid arthritis: the most commonly associated condition
systemic lupus erythematosus
sarcoidosis
granulomatosis with polyangiitis

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54
Q

Features of scleritis

A

red eye
classically painful (in comparison to episcleritis), but sometimes only mild pain/discomfort is present
watering and photophobia are common
gradual decrease in vision

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55
Q

Managment of scleritis

A
  • same day assessment by ophalmologist

oral NSAIDs are typically used first-line
oral glucocorticoids may be used for more severe presentations
immunosuppressive drugs for resistant cases (and also to treat any underlying associated diseases)

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56
Q

Corneal abrasion

A

Defect of the corneal epithelium and usually has occurred due to recent local trauma

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57
Q

Feaures of corneal abrasion

A

eye pain
lacrimation
photophobia
foreign body sensation and conjunctival injection
decreased visual acuity in the affected eye

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58
Q

Investigation for corneal abrasion

A
  • fluorescein staining
  • visualisation can be enhanced using cobalt blue filter or a wood’s lamp
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59
Q

Managment of corneal abrasion

A

a topical antibiotic is recommended for these patients in order to prevent secondary bacterial infection.

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60
Q

Hyphema definition

A

Blood in the anterior chamber of the eye

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61
Q

Managment of hyphema

A
  • required urgent referral to opthlamic specialist for review and managment
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62
Q

Why do hyphema risk sight?

A
    • raised IOP
  • can cause blockage of the trabecular mesh work with erythrocytes
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63
Q

Managment of hyphema

A
  • strict bed rest and reduce excessive movements
  • high risk classes often require admission
  • assessment should also be made for orbital compartmental syndrome (e.g retrobulbar haemorrhage)
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64
Q

Features of orbital compartmental syndrome

A

eye pain/swelling
proptosis
‘rock hard’ eyelids
relevant afferent pupillary defect

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65
Q

Managment of orbital compartmental syndrome

A

urgent lateral canthotomy (before diagnostic imaging) to decompress the orbit

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66
Q

Subconjunctival haemorrhage

A

result from the bleeding of blood vessels into the subconjunctival space.

Vessels which usually bleed are responsible for supplying conjunctiva or episclera

Cases are typically traumatic or idiopathic (e.g valsalva manoeuvres and several systemic diseases)

Look sinister but rarely are

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67
Q

Epidemiology of subconjuctival haemorrhage

A
  • more common in women than men when no he of trauma
  • newborns and elderly at high risk.
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68
Q

Risk factors for subconjunctival haemorrhage

A
  • trauma
  • control lens
  • idiopathic
  • valsalva manoeuvre
  • hypertension
  • bleeding disorders
  • drugs (aspirin, NSAID, anticoag)
  • diabetes
  • Arterial disease and hyperlipidaemia
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69
Q

Symptoms of subconjunctival haemorrhage

A

Red-eye, usually unilateral
Subconjunctival haemorrhages are mostly asymptomatic,
mild irritation may be present

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70
Q

Signs of subconjunctival haemorrhage

A
  • flat, red patch on conjunctiva
  • well defined edges with normal conjunctiva round it

Traumatic haemorrhages are most common in the temporal region

inferior conjunctiva as the next most commonly affected area

Normal vision and eye movement, normal fundus

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71
Q

Investigations of subconjunctival haemorrhage

A
  • clinical diagnosis
  • check no obvious trauma cause
  • check pt blood pressure
  • if pt takes warfarin, check INR and make appropriate adjustments
  • may need to refer to CT to rule out brain bleed
  • if recurrent, spontaneous or bilateral suboconjunctival haemorrhage, check for bleeding disorder of other pathology
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72
Q

Managment of subconjuctival haemorrhage

A
  • reassure pt it will resolve in 2-3 weeks
  • patch will change colour like a bruise
  • if cause is traumatic consider a referral to the ophthalmologist to ensure no other damage has been caused to the eye
  • advise pt to contact GP if happens again
  • use artificial tears if any mild irritation
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73
Q

Posterior vitreous detachment

A
  • separation of the membrane from the retina.

-This occurs due to natural changes to the vitreous fluid of the eye with ageing

No pain or vision loss but can cause tears to the retina

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74
Q

Epidemiology of PVD

A

Occur in over 75% of people over the age of 65
More common in females

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75
Q

Risk factors for PVD

A
  • ageing
  • highly myopic patients
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76
Q

Symptoms of PVD

A
  • Floaters (ring of floaters temporal to central vision)
  • flashes of light in vision
  • blurred vision
  • cobweb across vision
  • dark curtain descending (can also indicate retinal detachment)
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77
Q

Signs of PVD

A
  • Weiss ring on ophalamscope
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78
Q

Investigation of PVD

A
  • Examined by ophthalmologist within 24hrs
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79
Q

Managment of PVD

A

-no tx needed as usually improves in around 6 months
- may need surgery if retinal detachment

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80
Q

Retinal detachment

A

neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium.

  • it is reversible cause of vision loss
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81
Q

Risk factors for RD

A
  • diabetes mellitus
  • myopia
  • age
  • prev surgery for cataracts
  • eye trauma
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82
Q

Signs and symptoms of RD

A
  • new flashers and floaters
  • painless and progressive visual field loss
    if the macula is involved, central visual acuity and visual outcomes become much worse
    peripheral visual fields may be reduced, and central acuity may be reduced to hand movements if the macula is detached
    the swinging light test may highlight a relative afferent pupillary defect if the optic nerve is involved
    fundoscopy
    the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms
    if the break is small, however, it may appear normal.
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83
Q

Managment of RD

A
  • referr urgently under 24hr to ophthalmologist for assessment
  • slit lamp and indirect ophthalmoscope for pigment cell and haemorrhage
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84
Q

Vitreous haemorrhage

A
  • bleeding into the vitreous humour
  • sudden painless vision loss
  • can range from floaters to complete loss
  • when bleeding stops it starts to clear
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85
Q

Epidemiology of vitreous haemorrhage

A

Spontaneous vitreous haemorrhage has an incidence of around 7 cases per 100000 patient-years1
Incidence by age and sex varies according to the incidence of the underlying causes

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86
Q

Common cause of vitreous haemorrhage

A

proliferative diabetic retinopathy (over 50%)
posterior vitreous detachment
ocular trauma: the most common cause in children and young adults

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87
Q

Patient acute presentation of vitreous haemorrhage

A

painless visual loss or haze (commonest)
red hue in the vision
floaters or shadows/dark spots in the vision

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88
Q

Signs of vitreous haemorrhage

A

decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
visual field defect if severe haemorrhage

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89
Q

Investigation of vitreous haemorrhage

A

dilated fundoscopy: may show haemorrhage in the vitreous cavity
slit-lamp examination: red blood cells in the anterior vitreous
ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
fluorescein angiography: to identify neovascularization
orbital CT: used if open globe injury

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90
Q

Corneal foreign body features

A

eye pain
foreign body sensation
photophobia
watering eye
red eye

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91
Q

When to refer to ophthalmology for corneal foreign body

A

Suspected penetrating eye injury due to high-velocity injuries (e.g. drilling, lawn moving or hammering) or sharp objects (e.g. as glass, knives, pencils or thorns)
Significant orbital or peri-ocular trauma has occurred.
A chemical injury has occurred (irrigate for 20-30 mins before referring)
Foreign bodies composed of organic material (such as seeds, soil) should be referred to ophthalmology as these are associated with a higher risk of infection and complications
Foreign bodies in or near the centre of the cornea
Any red flags e.g. severe pain; irregular, dilated or non-reactive pupils; significant reduction in visual acuity.

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92
Q

Keratitis

A

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

93
Q

Causes of keratitis

A

bacterial
typically Staphylococcus aureus
Pseudomonas aeruginosa is seen in contact lens wearers
fungal
amoebic
acanthamoebic keratitis
accounts for around 5% of cases
increased incidence if eye exposure to soil or contaminated water
pain is classically out of proportion to the findings
parasitic: onchocercal keratitis (‘river blindness’)

Viral: herpes simplex keratitis

Environmental
- photokeratitis e.g. welder’s arc eye
exposure keratitis
contact lens acute red eye (CLARE)

94
Q

Features of keratitis

A

red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen

95
Q

When to refer cases of keratitis

A

contact lens wearers
assessing contact lens wearers who present with a painful red eye is difficult
an accurate diagnosis can only usually be made with a slit-lamp, meaning same-day referral to an eye specialist is usually required to rule out microbial keratitis

96
Q

Managment of keratitis

A

stop using contact lens until the symptoms have fully resolved
topical antibiotics
typically quinolones are used first-line
cycloplegic for pain relief
e.g. cyclopentolate

97
Q

Complications of keratitis

A

corneal scarring
perforation
endophthalmitis
visual loss

98
Q

Cataracts

A

common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy.

This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision.

Cataracts are the leading cause of curable blindness worldwide.

99
Q

Epidemiology of cataracts

A

Cataracts are more common in women than in men
The incidence of cataracts increases with age. One study found that 30% of individuals aged 65 and over had a visually-impairing cataract in either one or both eyes

100
Q

Causes of cataracts

A
  • normal ageing process
    -smoking
    -increased alcohol consumption
  • trauma
  • DM
  • Long-term corticosteroids
    -Radiation exposure
    -Myotonic dystrophy
    -Metabolic disorders: hypocalcaemia
101
Q

Patients with cataracts gradual onset of…

A

Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights

102
Q

Signs of cataracts

A
  • reduced red reflex
103
Q

Investigations for cataracts

A

Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract

104
Q

Classification of cataracts

A

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

105
Q

Managment of cataracts

A
  • provide pt with stronger glasses and encourage brighter light use
  • surgical tx

the cloudy lens and replacing this with an artificial one. NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice.

106
Q

Complications following cataract surgery

A

Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour

107
Q

Optic atrophy

A

Pale, well demarcated disc on fundoscopy
- causes gradual loss of vision
- can be congenital or acquired

108
Q

Acquired causes of optic atrophy

A

multiple sclerosis
papilloedema (longstanding)
raised intraocular pressure (e.g. glaucoma, tumour)
retinal damage (e.g. choroiditis, retinitis pigmentosa)
ischaemia
toxins: tobacco amblyopia, quinine, methanol, arsenic, lead
nutritional: vitamin B1, B2, B6 and B12 deficiency

109
Q

Congenital causes of optic atrophy

A

Friedreich’s ataxia
mitochondrial disorders e.g. Leber’s optic atrophy
DIDMOAD - the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)

110
Q

Bitemporal Hemianopia

A

optic chiasm

111
Q

Optic lesions

A
112
Q

Orbital cellulitis

A
  • Infection affecting the fat and muscles posterior to the orbital septum, within the orbit
  • Not involving the globe
113
Q

How serious is orbital cellulitis?

A

Medical emergency

114
Q
A
115
Q

Risk factors of orbital cellulitis

A
  • Childhood
  • Mean age of hospitalisation 7-12 years
  • Previous sinus infection
  • Lack of Haemophilus influenzae type b (Hib) vaccination
  • Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
  • Ear or facial infection
116
Q

Oribital celulitis presentation

A

Redness and swelling around the eye
Severe ocular pain
Visual disturbance
Proptosis
Ophthalmoplegia/pain with eye movements
Eyelid oedema and ptosis
Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)

117
Q

Orbital cellulitis investigation

A

Full blood count - WBC elevated, raised inflammatory markers.
Clinical examination involving complete ophthalmological assessment - Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema.
CT with contrast - Inflammation of the orbital tissues deep to the septum, sinusitis.
Blood culture and microbiological swab to determine the organism. Most common bacterial causes - Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.

118
Q

Managment of oribital cellulitis

A

IV antibiotic

119
Q
A
120
Q

What is strabismus commonly known as?

A

Squint

Strabismus is characterized by misalignment of the visual axes.

121
Q

What are the two main types of squints?

A
  • Concomitant
  • Paralytic

Concomitant is more common, while paralytic is rare.

122
Q

What can uncorrected squint lead to?

A

Amblyopia

Amblyopia occurs when the brain fails to fully process inputs from one eye.

123
Q

What is the primary cause of concomitant squint?

A

Imbalance in extraocular muscles

Convergent squint is more common than divergent squint.

124
Q

What causes paralytic squint?

A

Paralysis of extraocular muscles

125
Q

What test is used to detect squint?

A

Corneal light reflection test

This test involves holding a light source 30cm from the child’s face.

126
Q

What does the cover test help identify?

A

The nature of the squint

127
Q

Describe the steps of the cover test.

A
  • Ask the child to focus on an object
  • Cover one eye
  • Observe movement of uncovered eye
  • Cover other eye and repeat test
128
Q

What is one management strategy for squints?

A
  • Referral to secondary care
  • Eye patches may help prevent amblyopia
129
Q

What is strabismus commonly known as?

A

Squint

Strabismus is characterized by misalignment of the visual axes.

130
Q

What are the two main types of squints?

A
  • Concomitant
  • Paralytic

Concomitant is more common, while paralytic is rare.

131
Q

What can uncorrected squint lead to?

A

Amblyopia

Amblyopia occurs when the brain fails to fully process inputs from one eye.

132
Q

What is the primary cause of concomitant squint?

A

Imbalance in extraocular muscles

Convergent squint is more common than divergent squint.

133
Q

What causes paralytic squint?

A

Paralysis of extraocular muscles

134
Q

What test is used to detect squint?

A

Corneal light reflection test

This test involves holding a light source 30cm from the child’s face.

135
Q

What does the cover test help identify?

A

The nature of the squint

136
Q

Describe the steps of the cover test.

A
  • Ask the child to focus on an object
  • Cover one eye
  • Observe movement of uncovered eye
  • Cover other eye and repeat test
137
Q

What is one management strategy for squints?

A
  • Referral to secondary care
  • Eye patches may help prevent amblyopia
138
Q

What is central retinal artery occlusion?

A

A relatively rare cause of sudden unilateral visual loss

139
Q

What are the primary causes of central retinal artery occlusion?

A

Thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)

140
Q

List three features of central retinal artery occlusion.

A
  • Sudden, painless unilateral visual loss
  • Relative afferent pupillary defect
  • ‘Cherry red’ spot on a pale retina
141
Q

What is the prognosis for central retinal artery occlusion?

A

Poor

142
Q

What should be done regarding underlying conditions in cases of central retinal artery occlusion?

A

They should be identified and treated

143
Q

What treatment may be attempted if a patient presents acutely with central retinal artery occlusion?

A

Intraarterial thrombolysis

144
Q

True or False: Current trials show consistent positive results for intraarterial thrombolysis in central retinal artery occlusion.

A

False

145
Q

Fill in the blank: Central retinal artery occlusion is due to _______ or arteritis.

A

[thromboembolism]

146
Q

What type of steroids may be administered for temporal arteritis associated with central retinal artery occlusion?

A

Intravenous steroids

147
Q

What does left homonymous hemianopia indicate?

A

Visual field defect to the left due to lesion of right optic tract

Left homonymous hemianopia affects the same side of both eyes’ visual fields.

148
Q

What are homonymous quadrantanopias associated with?

A

PITS (Parietal-Inferior, Temporal-Superior)

This mnemonic helps remember which lesions cause specific quadrantanopias.

149
Q

What is the difference between incongruous and congruous defects?

A

Incongruous defects = optic tract lesion; congruous defects = optic radiation lesion or occipital cortex

Congruous defects are symmetrical visual field losses, while incongruous defects are asymmetrical.

150
Q

What does a congruous defect mean?

A

Complete or symmetrical visual field loss

This indicates a lesion in the optic radiation or occipital cortex.

151
Q

What does an incongruous defect indicate?

A

Incomplete or asymmetric visual field loss

This typically results from a lesion of the optic tract.

152
Q

What is macula sparing associated with?

A

Lesion of the occipital cortex

Macula sparing refers to preservation of central vision despite other visual field losses.

153
Q

What causes superior homonymous quadrantanopia?

A

Lesion of the inferior optic radiations in the temporal lobe (Meyer’s loop)

This type of quadrantanopia affects the upper half of the visual field.

154
Q

What causes inferior homonymous quadrantanopia?

A

Lesion of the superior optic radiations in the parietal lobe

This type of quadrantanopia affects the lower half of the visual field.

155
Q

What is bitemporal hemianopia associated with?

A

Lesion of the optic chiasm

This condition typically results in loss of vision in the outer (temporal) fields of both eyes.

156
Q

What does upper quadrant defect > lower quadrant defect indicate?

A

Inferior chiasmal compression, commonly a pituitary tumour

This pattern of visual field loss can suggest specific types of lesions.

157
Q

What does lower quadrant defect > upper quadrant defect indicate?

A

Superior chiasmal compression, commonly a craniopharyngioma

This pattern of visual field loss can also suggest specific types of lesions.

158
Q

True or False: Most quadrantanopias are caused by occipital lobe lesions.

A

True

While the exam suggests PITS, actual studies indicate a higher occurrence from occipital lobe issues.

159
Q

What is orbital cellulitis?

A

An infection affecting the fat and muscles posterior to the orbital septum, within the orbit but not involving the globe.

160
Q

What usually causes orbital cellulitis?

A

A spreading upper respiratory tract infection from the sinuses.

161
Q

Is orbital cellulitis a medical emergency?

A

Yes, it requires hospital admission and urgent senior review.

162
Q

What is periorbital (preseptal) cellulitis?

A

A less serious superficial infection anterior to the orbital septum, resulting from a superficial tissue injury.

163
Q

What can periorbital cellulitis progress to?

A

Orbital cellulitis.

164
Q

What are common risk factors for orbital cellulitis?

A
  • Childhood
  • Mean age of hospitalisation 7-12 years
  • Previous sinus infection
  • Lack of Haemophilus influenzae type b (Hib) vaccination
  • Recent eyelid infection/insect bite on eyelid
  • Ear or facial infection
165
Q

What are the typical presentations of orbital cellulitis?

A
  • Redness and swelling around the eye
  • Severe ocular pain
  • Visual disturbance
  • Proptosis
  • Ophthalmoplegia/pain with eye movements
  • Eyelid oedema and ptosis
  • Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
166
Q

Which symptoms indicate orbital cellulitis rather than preseptal cellulitis?

A
  • Reduced visual acuity
  • Proptosis
  • Ophthalmoplegia/pain with eye movements
167
Q

What investigations are used to diagnose orbital cellulitis?

A
  • Full blood count - WBC elevated, raised inflammatory markers
  • Clinical examination - Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema
  • CT with contrast - Inflammation of the orbital tissues, sinusitis
  • Blood culture and microbiological swab
168
Q

What are the most common bacterial causes of orbital cellulitis?

A
  • Streptococcus
  • Staphylococcus aureus
  • Haemophilus influenzae B
169
Q

What is the management for orbital cellulitis?

A

Admission to hospital for IV antibiotics.

170
Q

What is preseptal cellulitis also known as?

A

Periorbital cellulitis

171
Q

What does preseptal cellulitis infect?

A

Soft tissues anterior to the orbital septum, including eyelids, skin, and subcutaneous tissue of the face

172
Q

What is the difference between preseptal cellulitis and orbital cellulitis?

A

Preseptal cellulitis infects anterior to the orbital septum; orbital cellulitis infects behind the orbital septum and is more serious

173
Q

How does infection typically spread to preseptal cellulitis?

A

From nearby sites, commonly from skin breaks or local infections like sinusitis

174
Q

What are the most frequently causative organisms of preseptal cellulitis?

A
  • Staph. aureus
  • Staph. epidermidis
  • Streptococci
  • Anaerobic bacteria
175
Q

In which demographic does preseptal cellulitis commonly occur?

A

Children, with 80% of patients under 10 years

176
Q

What is the median age of presentation for preseptal cellulitis?

A

21 months

177
Q

During which season is preseptal cellulitis more common?

A

Winter

178
Q

What are the common symptoms of preseptal cellulitis?

A

Red, swollen, painful eye of acute onset, likely with fever

179
Q

What signs are associated with preseptal cellulitis?

A
  • Erythema and oedema of the eyelids
  • Partial or complete ptosis
  • Absence of orbital signs
180
Q

What must be absent in preseptal cellulitis to differentiate it from orbital cellulitis?

A

Orbital signs (e.g., pain on movement, restriction of eye movements)

181
Q

What are significant differentials for preseptal cellulitis?

A
  • Orbital cellulitis
  • Allergic reaction
182
Q

What investigations are typically conducted for preseptal cellulitis?

A
  • Blood tests for raised inflammatory markers
  • Swab of any discharge
  • Contrast CT of the orbit
183
Q

What is the management protocol for preseptal cellulitis?

A

Referral to secondary care, often treated with oral antibiotics like co-amoxiclav

184
Q

In what situation may children with preseptal cellulitis require admission?

A

For observation

185
Q

What is a potential complication of preseptal cellulitis?

A

Bacterial infection may spread into the orbit and evolve into orbital cellulitis

186
Q

What is the most common cause of blindness in adults aged 35-65 years-old?

A

Diabetic retinopathy

187
Q

What condition is thought to cause increased retinal blood flow and abnormal metabolism in retinal vessel walls?

A

Hyperglycaemia

188
Q

What leads to increased vascular permeability in diabetic retinopathy?

A

Endothelial dysfunction

189
Q

What are the characteristic exudates seen on fundoscopy caused by?

A

Increased vascular permeability

190
Q

What predisposes to the formation of microaneurysms in diabetic retinopathy?

A

Pericyte dysfunction

191
Q

What is thought to cause neovascularization in diabetic retinopathy?

A

Production of growth factors in response to retinal ischaemia

192
Q

What are the three classifications of diabetic retinopathy?

A

Non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR), and maculopathy

193
Q

What characterizes Mild Non-Proliferative Diabetic Retinopathy (NPDR)?

A

1 or more microaneurysms

194
Q

List the features of Moderate NPDR.

A
  • Microaneurysms
  • Blot haemorrhages
  • Hard exudates
  • Cotton wool spots
  • Venous beading/looping
  • Intraretinal microvascular abnormalities (IRMA)
195
Q

What characterizes Severe NPDR?

A
  • Blot haemorrhages and microaneurysms in 4 quadrants
  • Venous beading in at least 2 quadrants
  • IRMA in at least 1 quadrant
196
Q

What are key features of Proliferative Diabetic Retinopathy (PDR)?

A
  • Retinal neovascularisation
  • Fibrous tissue forming anterior to retinal disc
  • More common in Type I DM
197
Q

What is the rate of blindness within 5 years for those with Proliferative Diabetic Retinopathy?

A

50%

198
Q

What characterizes Maculopathy?

A

Based on location rather than severity; hard exudates and other ‘background’ changes on macula

199
Q

What should be optimized in the management of diabetic retinopathy for all patients?

A
  • Glycaemic control
  • Blood pressure
  • Hyperlipidemia
200
Q

What should be done if there is a change in visual acuity in Maculopathy?

A

Intravitreal vascular endothelial growth factor (VEGF) inhibitors

201
Q

What is the management approach for Severe/Very Severe Non-Proliferative Retinopathy?

A

Consider panretinal laser photocoagulation

202
Q

What is the primary treatment for Proliferative Retinopathy?

A

Panretinal laser photocoagulation

203
Q

What are potential complications following treatment for Proliferative Retinopathy?

A
  • Decrease in night vision
  • Generalised decrease in visual acuity
  • Macular oedema
204
Q

What are examples of intravitreal VEGF inhibitors used in treatment?

A

Ranibizumab

205
Q

True or False: A generalised decrease in visual acuity is a potential complication of Proliferative Retinopathy treatment.

A

True

206
Q

Fill in the blank: Intravitreal VEGF inhibitors are often used in combination with _______.

A

panretinal laser photocoagulation

207
Q

What is the recommended action if severe or vitreous haemorrhage occurs in diabetic retinopathy?

A

Vitreoretinal surgery

208
Q

What is glaucoma?

A

A group of disorders characterised by optic neuropathy due to raised intraocular pressure (IOP) in most patients.

209
Q

True or False: All patients with raised IOP have glaucoma.

A

False

210
Q

What are the predisposing factors for acute angle-closure glaucoma (AACG)?

A
  • Hypermetropia (long-sightedness)
  • Pupillary dilatation
  • Lens growth associated with age
211
Q

List the key features of acute angle-closure glaucoma (AACG).

A
  • Severe pain
  • Decreased visual acuity
  • Symptoms worsen with mydriasis
  • Hard, red-eye
  • Halos around lights
  • Semi-dilated non-reacting pupil
  • Corneal oedema
  • Systemic upset (nausea, vomiting, abdominal pain)
212
Q

What is the purpose of tonometry in glaucoma assessment?

A

To assess for elevated intraocular pressure (IOP).

213
Q

What is gonioscopy?

A

A special lens for the slit lamp that allows visualisation of the angle of the eye.

214
Q

What is the initial management for acute angle-closure glaucoma?

A

Emergency medical treatment to lower IOP and urgent referral to an ophthalmologist.

215
Q

Fill in the blank: A direct parasympathomimetic used in the treatment of AACG is _______.

A

[pilocarpine]

216
Q

What role does acetazolamide play in the management of AACG?

A

It reduces aqueous secretions.

217
Q

What is the definitive management for acute angle-closure glaucoma?

A

Laser peripheral iridotomy.

218
Q

What condition is also referred to as iritis?

A

Anterior uveitis.

219
Q

List the associated conditions with anterior uveitis.

A
  • Ankylosing spondylitis
  • Reactive arthritis
  • Ulcerative colitis
  • Crohn’s disease
  • Behcet’s disease
  • Sarcoidosis
220
Q

What are the key features of anterior uveitis?

A
  • Acute onset
  • Ocular discomfort & pain
  • Small or irregular pupil
  • Intense photophobia
  • Blurred vision
  • Red eye
  • Lacrimation
  • Ciliary flush
  • Hypopyon
221
Q

What is the first-line management for anterior uveitis?

A
  • Urgent review by ophthalmology
  • Cycloplegics (e.g., Atropine)
  • Steroid eye drops
222
Q

What are the distinguishing features of acute angle closure glaucoma?

A
  • Severe pain
  • Decreased visual acuity
  • Patient sees haloes
  • Semi-dilated pupil
  • Hazy cornea
223
Q

What is scleritis?

A

Full-thickness inflammation of the sclera, generally non-infective, causing a red, painful eye.

224
Q

List the risk factors associated with scleritis.

A
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Sarcoidosis
  • Granulomatosis with polyangiitis
225
Q

What are the key features of scleritis?

A
  • Red eye
  • Classically painful
  • Watering and photophobia are common
  • Gradual decrease in vision
226
Q

What is the management approach for scleritis?

A
  • Same-day assessment by an ophthalmologist
  • Oral NSAIDs first-line
  • Oral glucocorticoids for severe cases
  • Immunosuppressive drugs for resistant cases
227
Q

What type of discharge is associated with bacterial conjunctivitis?

A

Purulent discharge.

228
Q

What is a possible cause of subconjunctival haemorrhage?

A

History of trauma or coughing bouts.

229
Q

What are the typical symptoms of endophthalmitis?

A

Red eye, pain, and visual loss following intraocular surgery.