Ophthamology Flashcards

1
Q

What is normal intraocular pressure?

A

12-20mmHg

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2
Q

Emergency Management of acute angle closure glaucoma Question?

A

Urgent ophthalmology referal.

The initial management includes administering IV Acetazolamide and a topical beta-blocker such as Timolol. Muscarinic agonists such as pilocarpine eye drops may be given.

The definitive management for this condition is a peripheral iridotomy to relief the intraocular pressure.

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3
Q

What angle is affected in acute angle closure glaucoma?

A

Iridio-corneal angle

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4
Q

Presenting features of acute angle closure glaucoma?

A

Red eye, mid dilated pupil.
Sudden headache, nausea, visual disturbance.

“May see haloes when looking at bright lights”.

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5
Q

What separates proliferative vs non-proliferative diabetic retinopathy?

A

Neovascularisation

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5
Q

What separates proliferative vs non-proliferative diabetic retinopathy?

A

Neovascularisation

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6
Q

What is seen on fundoscopy for diabetic retinopathy?

A

Cotton wool spots
Hard exudates
Dot blot haemorrhages
Microaneurysms

Neovascularisation (if proliferative).

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7
Q

Drusen deposits are seen in what condition?

A

Macular degeneration

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8
Q

What is diabetic maculopathy?

A

Macular oedema
Ischaemic maculopathy

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9
Q

Treatment of diabetic maculopathy:

A

*Macular Laser
*Intravitreal anti-VEGF
* Ranibizumab
* Aflibercept
*Intravitreal steroid
* Dexamethasone implant
* Fluocinolone implant

If ischaemic maculopathy - None

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10
Q

What are the consequences of thyroid eye disease?

A

*Sight loss
* Corneal exposure
* Compressive optic neuropathy
*Extraocular muscle malfunction causing double vision

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11
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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12
Q

Anterior uveitis symptoms:

A

Red eye, painful, iregular pupil, hyponon, blurry vision.
PHOTOPHOBIA

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13
Q

Anterior uveitis causes:

A

*Idiopathic (the majority) - first episode not investigated *HLA B27 - ankylosing spondylitis, psoriatic arthritis, inflammatory bowel disease *Sarcoidosis
*Juvenile idiopathic arthritis (JIA) – chronic painless *Infection
* Herpes simplex and zoster (shingles) – unilateral
* Syphilis

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14
Q

Presentation of posterior uveitis:

A
  • Scotoma
  • Floaters
  • Blurred vision
  • Perception of flashes of light
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15
Q

Treatment of posterior uveitis:

A

Steroids
If caused by toxoplasmosis antibiotics.

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16
Q

Distinguishing episcleritis from scleritis:

A

Topical vasoconstrictors such as 10% phenylephrine do not cause blanching of the eye and this can be used to help distinguish episcleritis from scleritis.

Scleritis = more painful and deep

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17
Q

Distinguishing episcleritis from scleritis:

A

Topical vasoconstrictors such as 10% phenylephrine or cotton wool do not cause blanching of the eye and this can be used to help distinguish episcleritis from scleritis.

Scleritis = more painful and deep

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18
Q

Features of scleritis:

A

Severe inflammation of the sclera, patients complain of severe pain in the orbit and pain on eye movement.

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19
Q

Scleritis management:

A

Ophthalmic emergency!!

Requires urgent referral to ophthalmology for systemic immunosuppression.

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20
Q

How does ethambutol affect the eye?

A

Optic neuropathy

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21
Q

Hydroxychloroquine affect on the eye:

A

Bulls eye maculopathy

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22
Q

Oral contraceptive pill and tetracyclines cause what affect the eye?

A

Idiopathic intracranial hypertension - PAPILLOEDEMA

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23
Q

Causes of unilateral optic disc swelling:

A
  • Vascular
    – Diabetes or central retinal vein occlusion
  • Inflammatory
    – Uveitis or sarcoidosis
  • Infective
    – Herpes, toxoplasmosis or viral
  • Multiple sclerosis
  • Lymphoma
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24
Q

Causes of bilateral optic disc swelling:

A
  • Raised intracranial pressure – space occupying lesion, idiopathic intracranial hypertension or hydrocephalus
  • Malignant hypertension
  • Diabetes
  • Toxic
  • Ethambutol
  • Lymphoma
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25
Q

Papilloedema vs optic disc swelling??

A

Papilloedema isa term that is exclusively used when a disc swelling is secondary to increased intracranial pressure (ICP).

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26
Q

How can anticholinergics affect the eye?

A

Acute angle closure glaucoma

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27
Q

Tamulosin can cause what eye abnormality?

A

Tamsulosin and “floppy iris” abnormality in cataract surgery.

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28
Q

Red eye that is painless with normal vision, differentials:

A

Subconjunctival haemorrhage
Conjunctivitis

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29
Q

Red eye that is painful with normal vision, differentials:

A

Episcleritis
Stye
Blepharitis

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30
Q

Red eye that is painful with loss of vision, differentials:

A

Slceritis
Keratitis
Iritis
Acute angle closure glaucoma

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31
Q

What is allergic conjunctivitis treated with?

A

Sodium cromoglycate

Systemic and topical antihistamines.

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32
Q

Signs of viral conjunctivitis?

A

Often occurs during URTI
Watery rather than purulent discharge
Conjunctival redness and haemorrhages
Conjunctival folicles / papillae visible.

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33
Q

What condition is scleritis commonly associated with?

A

Rheumatoid arthritis!

also granulomatosis with polyangiitis so look for systemic symptoms.

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34
Q

What is an external hordeolum?

A

Commonly called a stye, is an abscess at an eyelash follicle often caused by staphylococcus.

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35
Q

Classic description of a stye:

A

Red hot lump!

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36
Q

What is an internal hordeolum?

A

Internal hordeolumis an abscess of the Meibomian gland, it is initially painful, and if the blockage of the gland occurs it can leave behind a non-tender swelling called a chalazion.

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37
Q

Define blepharitis:

A

Inflammation of the eye lid.

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38
Q

Causes of blepharitis:

A

Common causes are Staphyloccus, Seborrheic dermatitis and Rosacea.

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39
Q

How do patients with blepharitis present?

A

Patients often present with sore, itchy eyelid margins with a crusty appearance at the base of the eyelashes.

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40
Q

Blepharitis management:

A

Good eyelid hygeine and a warm compress.

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41
Q

Definitive test of acute angle closure glaucoma:

A

Gonioscopy describes the use of a goniolens in conjunction with a slit lamp in order to gain a view of the angle between the eye’s cornea and iris. It is the definitive test for diagnosing acute angle closure glaucoma.

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42
Q

How does latanoprost affect AACG?

A

Latanoprost is a prostaglandin analogue, it increases uveoscleral outflow by increasing the sclera’s permeability to aqueous humour.

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43
Q

Initial treatment of AACG:

A

Initial treatment involves admission to hospital for ophthalmology review, reduction of the intraocular pressure (IOP) and providing analgesia to the patient.

Pilocarpine / Acetazolamide to reduce IOP.

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44
Q

Categories of things that may cause keratitis:

A

Bacteria
Viruses
Fungi
Amoeba
Auto-immune

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45
Q

Common bacterial causes of keratitis:

A
  • typicallyStaphylococcus aureus
  • Pseudomonas aeruginosais seen in contact lens wearers very bad.
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46
Q

Viral cause of keratitis:

A

Herpes simplex virus
Adenovirus

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47
Q

Auto-immune causes of keratitis:

A
  • Sjogren’s syndrome - RA, SLE, Granulomatosis with polyangitis.
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48
Q

Presentation of keratitis:

A
  • red eye: pain and erythema
  • photophobia
  • foreign body, gritty sensation
  • hypopyon may be seen
49
Q

Investigation for keratitis:

A

Slit lamp examination with fluorescein eye drops may help diagnosis and visualising abrasions/ulcerations.

50
Q

Management of keratitis:

A
  • Refer!!
  • Swab!
  • stop using contact lenses until the symptoms have fully resolved
  • topical antibiotics
    • typically quinolones are used as first-line
  • cycloplegic for pain relief
    • e.g. cyclopentolate

Keratitis caused by viral infection may be treated with topical antiviral drops. Traumatic keratitis requires referral to ophthalmology for consideration of corticosteroid treatment.

51
Q

Complications of keratitis:

A
  • corneal scarring
  • perforation
  • endophthalmitis
  • visual loss
52
Q

What is preseptal cellulitis?

A

Preseptal cellulitis refers to infection of tissue not spreading past the orbital septum.

53
Q

Causes of preseptal cellulitis:

A

Commonly caused by sinusitis or damage to the overlying skin.

54
Q

Presentation of preseptal cellulitis:

A

The typical patient is a child with an erythematous swollen eyelid, mild fever and erythema surrounding the orbit.

55
Q

Treatment for preseptal cellulitis:

A

Treat with intravenous empirical antibiotics. If there is doubt over the diagnosis, treat it as orbital cellulitis.

56
Q

Orbital cellulitis presents similarly to preseptal cellulitis, but there are 3 important features that set it apart:

A
  1. Painful eye movements
  2. Diplopia
  3. Visual impairment

If any of these features are present, the patient should be treated for orbital cellulitis.

57
Q

Causes of orbital cellulitis:

A

Common causes of orbital cellulitis are the spread of infection from sinusitis or upper respiratory tract infection.

58
Q

Read summary of orbital cellulitis features aloud:

A

The typical patient is a feverish child with a swollen eyelid, reduced eye mobility, painful eye movements, and diplopia in some. Visual impairment may manifest as reduced visual acuity, ‘red desaturation’ and a relative afferent pupillary defect. Proptosis may also be present. Visual loss may occur due to compression of the optic nerve or optic neuritis. Death may occur due to cavernous sinus thrombosis or intracranial spread of infection.

59
Q

Orbital cellulitis treatment:

A

Patients should be admitted for immediate CT scan, ENT review and urgent intravenous antibiotics.

60
Q

Main causes of acute loss of vision:

A

*Retinal detachment
*Retinal vascular occlusions
*Amaurosis fugax
*Ischaemic optic neuropathy

60
Q

Main causes of acute loss of vision:

A

*Retinal detachment
*Retinal vascular occlusions
*Amaurosis fugax
*Ischaemic optic neuropathy

61
Q

Common features of retinal detachment:

A

New onset floaters / flashes

Sudden onset, painless and progressive visual field loss, described as a curtain or shadow progressing to the centre of the visual field from the periphery should also raise suspicion of detachment.

62
Q

What do new onset flashes and floaters indicate in retinal detachment?

A

Indicate pigment cells entering the vitreous space or traction on the retina respectively

63
Q

Management of suspected retinal detachment:

A

Any patients with new onset flashes and floaters should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage.

63
Q

What is meant by Amaurosis Fugax?

A

‘Amaurosis fugax’ - Ischaemic / vascular sudden vision loss.

wide differential including large artery disease (atherothrombosis, embolus, dissection), small artery occlusive disease (anterior ischemic optic neuropathy, vasculitis e.g. temporal arteritis), venous disease and hypoperfusion
may represent a form of transient ischaemic attack (TIA). It should therefore be treated in a similar fashion, with aspirin 300mg being given
altitudinal field defects are often seen: ‘curtain coming down’
ischaemic optic neuropathy is due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve

64
Q

Features of central retinal vein occlusion:

A

Sudden, painless reduction or loss of visual acuity, usually unilaterally

65
Q

What is seen on fundoscopy for central retinal vein occlusion?

A

Stormy sunset appearance!

Widespread hyperaemia.`

66
Q

What is seen on funduscopy for central retinal artery occlusion:

A

Pale retina, cherry red macula.

67
Q

Management of central retinal vein occlusion:

A
  • Emergency same-day referral.
  • indications for treatment in patients with CRVO include:
    • macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents
    • retinal neovascularization - laser photocoagulation.
68
Q

Say out loud how you would explain what central retinal artery occlusion is:

A

Central retinal artery occlusion is a relatively rare cause of sudden unilateral visual loss. It is due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis).

69
Q

Features of central retinal artery occlusion:

A
  • sudden, painless unilateral visual loss
  • relative afferent pupillary defect
  • ‘cherry red’ spot on a pale retina
70
Q

Treatment for central retinal artery occlusion:

A
  • Emergency referral
  • Any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)
  • If a patient presents acutely then intraarterial thrombolysis may be attempted but currently, trials show mixed results.
71
Q

Two key investigations for optic neuritis:

A
  • for MS look at oligoclonal bands
  • MRI to investigate
72
Q

Features of optic neuritis:

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 - an area of depressed vision that corresponds with the point of fixation and interferes with central vision. It suggests a lesion between the optic nerve head and the chiasm.

Possible causes include: multiple sclerosis - which may cause unilateral or asymmetrical bilateral scotoma.

73
Q

Optic neuritis management:

A
  • high-dose steroids
  • recovery usually takes 4-6 weeks
74
Q

What is the tetrad often seen in optic neuritis:

A
  1. Monocular visual field defect (usually a central scotoma)
  2. Reduced colour vision
  3. Relative afferent pupillary defect (unless the damage to each optic nerve is symmetrical - remember the pathological pupil only seems to dilate because it is failing to constrict as well as the healthy pupil. So if both pupils can’t constrict well, then a relative afferent pupillary defect (RAPD) will not be seen)
  4. Acutely: optic disc swelling; chronically, with the death of optic nerve fibres: atrophy (seen as a pale disc).
75
Q

What protozoal infection can cause keratitis?

A

Acanthamoeba (especially in contact lens wearers) (from tap water)

76
Q

When should you give steroid eye drops for keratitis:

A

After you have confirmed the causative organism!

The use of topical corticosteroids along with empirical antibiotic therapy make it difficult to distinguish the causative agent of the infection in suspected keratitis, either by culture or by the corneal findings and clinical course, and as a result, may delay the appropriate treatment and cause unfortunate outcomes.

77
Q

What is Hutchinson’s sign?

A

Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement (this is due to innervation with the trigeminal nerve).

78
Q

How does varicella zoster affect the eye?

A

*Very hard to manage
* Corneal involvement
* Iritis
* Elevated eye pressure
* Neuropathic cornea (no sensation)
* Post herpetic neuralgia

79
Q

How does varicella zoster affect the eye?

A

*Very hard to manage
* Corneal involvement
* Iritis
* Elevated eye pressure
* Neuropathic cornea (no sensation)
* Post herpetic neuralgia

80
Q

4 medications given to treat emergency AACG:

A
  • Pilocarpine drops to constrict the pupil
  • Intravenous acetazolamide
  • Timolol eye drops
  • Steroid eye drops
81
Q

Definitive treatment for AACG:

A

Laser iridotomy

82
Q

Risk factors for retinal detachment:

A
  • Myopia: the higher the greater
  • Direct trauma (not head injury)
  • Acute posterior vitreous detachment
83
Q

Summary of posterior vitreous detachment:

A

*The vitreous gel is attached to the retina in places
*When it detaches (an ageing phenomenon?) it can tear the retina
*Fluid passes through the tear and the retina detaches
*Vitreous degeneration and detachment cause floaters
* Net curtain, spider’s web
* Flashing lights due to traction on the retina

84
Q

Interventional management of retinal detachment:

A

Tear (laser or cryotherapy) vs detachment (surgery)

85
Q

There are no emergency treatments for retinal vascular occlusion what are the two treatable problems that arise?

A

Macular oedema
Neovascular glaucoma

86
Q

How is macular oedema treated?

A

Anti-vegf
Macular laser

87
Q

How is neovascular glaucoma treated?

A
  • The ischaemic retina produces vascular endothelial growth factor
  • Laser to destroy the retina
  • Anti-VEGF into the vitreous

Note: This is very painful.

87
Q

How to approach ischaemic optic neuropathy:

A

*Is it arteritic?
*TAKE A GOOD HISTORY!
* Jaw pain, unilateral headache, scalp tenderness, symptoms of polymyalgia
(shoulder stiffness and weakness)
*Examine the scalp, the temporal arteries
*ESR and CRP
*REFER!

88
Q

How is arteritic ischaemic optic neuropathy diagnosed and managed?

A

*A clinical diagnosis
* ESR and CRP help
* Doppler ultrasound of the temporal arteries may help
* Temporal artery biopsy cannot give a quick enough result, may be a false
negative.
Most helpful if positive
* Response to treatment may help
*Intravenous methyl prednisolone
*Oral prednisolone

89
Q

When should you reduce and stop oral prednisolone in arteritic ischaemic optic neuropathy?

A

See lecture 2

90
Q

How does amaurosis fugax present?

A

Transient vision loss

He has had a TIA affecting his right eye. The clues are in his multiple risk factors for vascular disease, and his largely normal examination findings (excluding the diabetic changes in his retina). His comorbidities put him at higher risk of future TIA and stroke.

91
Q

Risk factors for AACG?

A

Farsighted (hypermetropia)
Asian

92
Q

Treatment for infective conjunctivitis:

A

Topical chloramphenicol

93
Q

A patient with signs of an oculomotor nerve palsy (cranial nerve 3) with pupillary signs (dilated pupil - mydriasis) should be assumed to have what until proven otherwise?

A

An aneurysm of their IPSILATERAL posterior communicating artery until proven otherwise.

94
Q

How does CNVI palsy present?

A
  • Double vision
  • Crossing of the eyes
  • Unable to move the eye out to the side.
95
Q

Rheumatoid arthritis is a risk factor for what painful red eye?

A

Scleritis

96
Q

Hutchinson’s signs causes what ocular involvement in Herpes zoster ophthalmicus?

A

Anterior uveitis

97
Q

Differentials for new onset floaters:

  • How should all of these patients be managed?
A

Retinal detachment
Vitreous haemorrhage
Posterior uveitis

Any patient who presents with new-onset flashes or floaters should be referred urgently for assessment by an ophthalmologist within 24 hours.
The ophthalmology team may need to urgently perform an operation to prevent loss of sight if a retinal detachment is detected.

98
Q

Diagnosis of AACG:

A

Gonioscopyand Tonometry: Tonometry identifies an increased intraocular pressure and gonioscopy confirms that closure of the angle is its cause, diagnosing acute angle-closure glaucoma. Both are mandatory for the diagnosis of acute angle-closure glaucoma.

99
Q

What type of vision loss is seen in primary open angle closure glaucoma?

A

Peripheral field loss

100
Q

Keratitis pathogen associated with contact lens use.

A

Pseudomonas infection should be suspected in contact lens associated keratitis.

101
Q

What are cotton wool spots in DR?

A

In diabetic retinopathy, cotton wool spots represent areas of retinal infarction

102
Q

Tests for AMD

A

AMSLER GRID testing - distorted line of perception
Funduscopy - drusen spots

103
Q

What classification is used for hypertensive retinopathy?

A

Keith-Wagener classification

104
Q

Causes of vitreous haemorrhage:

A
  • Proliferativediabetic retinopathy (over 50%)
  • Posterior vitreous detachment
  • Ocular trauma: the most common cause in children and young adults
105
Q

Vitreous haemorrhage presentation:

A
  • Painless visual loss or haze (commonest)
  • Red hue in the vision
  • Floaters or shadows/dark spots in the vision
106
Q

Vitreous haemorrhage tx

A

The treatment of vitreous haemorrhage depends on the underlying cause.

  • Proliferative diabetic retinopathy: Anti-VEGF, panretinal photocoagulation (PRP), vitrectomy.
  • Posterior vitreous detachment: Observation.
  • Ocular trauma: Observation, vitrectomy.

If the vitreous haemorrhage is severe enough to cause significant visual impairment, surgical intervention may be required. Vitrectomy may be necessary to remove the blood from the eye and repair any underlying damage.

107
Q

Management of new onset flashes and floaters?

A

Any patients with new onset flashes and floaters should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage.

108
Q

How are retinal tears managed?

A

Management ofretinal tearsaims to create adhesions between the retina and the choroid to prevent detachment. This can be done using:

  • Laser therapy
  • Cryotherapy
109
Q

Management of retinal detachment (answer)

A

Reattaching the retina can be done using one of three options:

  • Vitrectomy
  • Scleral buckling
  • Pneumatic retinopexy
110
Q

Management of retinal detachment (to read).

A

Management ofretinal detachmentaims to reattach the retina and reduce any traction or pressure that may cause it to detach again. This needs to be followed by treating retinal tears as above. Reattaching the retina can be done using one of three options:

  • Vitrectomyinvolves removing the relevant parts of the vitreous body and replacing it with oil or gas.
  • Scleral bucklinginvolves using a silicone “buckle” to put pressure on the outside of the eye (the sclera) so that the outer eye indents to bring the choroid inwards and into contact with the detached retina.
  • Pneumatic retinopexyinvolves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble creates pressure that flattens the retina against the choroid and close the detachment.
111
Q

Vitrectomy

A

Vitrectomy involves removing the relevant parts of the vitreous body and replacing it with oil or gas.

112
Q

Scleral bulking

A

Involves using a silicone “buckle” to put pressure on the outside of the eye (the sclera) so that the outer eye indents to bring the choroid inwards and into contact with the detached retina.

113
Q

Pneumatic retinopexy

A

Involves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble creates pressure that flattens the retina against the choroid and close the detachment.

114
Q

What visual field impairment is seen in retinal detachment?

A

Visual field impairment is a typical feature of retinal detachment. In this case, the field loss is likely to affect the inferior part of the visual field as the superior retina is detached

115
Q

PAINLESS blurred vision, floaters and photopsia (perception of flashes of light) - likely diagnosis?

A

Posterior uveitis

116
Q

Management of posterior uveitis

A
  • Steroids e.g prednisolone
  • Antibiotics for toxoplasmosis (if that’s the cause)
117
Q

Causes of posterior uveitis

A

Non-infectious causes:

Associated with systemic autoimmune conditions

  • Sarcoidosis
  • Behcet’s Disease
  • Wegener’s granulmatosis
  • Ankylosing spondylitis
  • Psoriasis
  • Arthropathies

Infectious Causes:

  • Toxoplasmosis
  • Viral retinitis - Herpes simplex, Varicella zoster, CMV, HIV.