Ophthalmology Flashcards

1
Q

External Anatomy of the Eye

A

• Average length 24mm; Discrepancies in length lead to Refractory Errors
• Cornea – 78% refractive power; Highly Innervated, Avascular
o Layers of the Cornea – Epithelium, Bowman’s Membrane, Stroma, Descemet’s
Membrane, Endothelium (Responsible for maintaining clarity by continuously
pumping fluid out of tissue; Disruption leads to Corneal Oedema and Blurred vision)
• Sclera – White opaque structure, covers 4/5ths of globe, continuous with Cornea at Limbus;
Attachment of six extraocular muscles and perforation of Optic nerve
• Conjunctiva – Anterior surface of the Sclera; Richly vascularised, innervated mucous
membrane; Stretched from Limbus, over Anterior Sclera (= Bulbar Conjunctiva) and reflected onto undersurface of eyelids (Tarsal Conjunctiva)

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2
Q

Internal Anatomy of the Eye

A

• Anterior Segment comprises Anterior (In front of Iris) and Posterior Chambers (Behind Iris)
• The Uveal Tract comprises Iris anteriorly, Ciliary Body and Choroid
o Aqueous Humour is produced by Ciliary Body at 2Ul/min; ULN pressure 21mmHg
o Aqueous Humour provides nutrients and oxygen for the avascular Cornea
• The Lens – Immediately posterior to pupil; 22% of refractive power; Anterior to Vitreous
humour; Transparent, Biconvex structure; Shape starts to decline by fourth decade, becomes
less transparent and develop cataracts
• Contraction of Ciliary muscles relaxes Suspensory Ligaments, Increasing the Refractive Power
of the Lens (for Accommodation)
• Three Layers – Retinal (Neural), Choroid (Vascular) and Sclera (Fibrous)
• Macula and Fovea Centralis – Recession of Choroid layer and lack of overlying vessels; Point
of highest Visual Acuity and concentration of Cone cells for Colour vision
• Optic Disc – CN II; Accounts for visual blind spot

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3
Q

Neurovascular Supply

A

• Ophthalmic Artery – Divides into Central Retinal Artery to supply inner retinal layers; Venous
return through Central Retinal/Ophthalmic Veins; LN Drainage to Preauricular and Submental
• Sensory innervation through Trigeminal (CN V1) Ophthalmic br

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4
Q

Refractive Error

A

Abnormalities of focusing mechanism of the eye;

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5
Q

Myopic or Hyper-metropic

A

o Myopia is usually inherited, discovered in
childhood; Progresses throughout teenage
years when body is growing
o Hypermetropia also inherited

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6
Q

Astigmatism

A

Refractory error which there is a different degree of refraction in different meridians of curvature (i.e. Defect in another plane)

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7
Q

Presbyopia

A

Normal ageing of the lens resulting in
change in refractory state; Lens less able to alter
curvature, resulting in difficulties in near-vision

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8
Q

Keratoconus

A

Non-inflammatory Degenerative disorder resulting in Cornea thinning and
change into Conical shape; Unknown Aetiology

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9
Q

Treatment of Refractory Errors

A

• Spectacles (Negative Lenses for Myopia, Positive Lenses for Hypermetropia) or Contact lenses
(better quality vision but risk of infection)
• Surgical Techniques – Excimer laser to reprofile Corneal Curvature (e.g. PRK. LASIK, LASEK);
Either removal of Central Corneal tissue to flatten in Myopia, or steepen in Hypermetropia

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10
Q

Eyelids

A

Eyelids protect the eyes and help distribute tear over front surface of globe; Excess tears
drained by Punctae and Lacrimal System

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11
Q

Entropion

A

Lid margin rolls inwards, causing lashes to be against globe, causing irritation
o Can mimic conjunctivitis; Occasionally constant rubbing leads to Corneal Abrasion
o Commonly due to ageing; Surgery is usually required

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12
Q

Ectropion

A

Lid margin rolls outwards, no apposition to globe; Puncta are in poor position to
drain tears, patient complains of watery eye; RF: Age, CN VII Palsy, Skin conditions; Surgery usually required for repair

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13
Q

Dacryocystitis

A

Inflammation of Lacrimal Sac; Tender lump on medial side (Nasal) adjacent to
lower eyelid; Oral Broad-spectrum Abx and watched carefully for signs of Cellulitis
o Referred to Ophthalmology – Mucocoele or dilated sac requiring surgical repair

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14
Q

Blepharitis

A

Inflammation of Lid Margins ± Lashes and Follicles;
Results in Stye (= Hordeolum, Inflammation/Blockage of Meibomian
gland); Itchy, burning eyes (Tear Film instability)
o Commonly due to Meibomian gland dysfunction,
Seborrhoea, S aureus (Frequently responsible for Chronic
Blepharo-conjunctivitis
o Lid Hygiene, Short course Topical Chloramphenicol or
Fusidic acid; If Acne Rosacea suspected, Oral Doxycycline required
o Chalazion – Residual cystic lump; Requires Incision/Curettage for cosmesis

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15
Q

Conjunctivitis

A

• Commonest cause for Red Eye (=Pink Eye); Can arise from Viral, Bacterial and Allergic causes
commonly; Soreness, Redness, Discharge without disruption to Visual Acuity
• Hx – Speed of onset, Colour and Consistency of discharge, Recent Hx Cold or Sore Throat; In
Neonate important to exclude Gonococcal or Chlamydial conjunctivitis

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16
Q

Conjunctivitis Red Flags

A

Severe pain, Photophobia, Sudden Visual Acuity loss, Coloured Halos, Proptosis,
Smaller Pupil in affected eye, High IOP, Keratitis, Shallow Anterior Chamber depth

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17
Q

Bacterial Conjunctivitis

A

• 5% of cases; Sore and Gritty eye in presence of good vision; Invariably bilateral, suspected
with purulent discharge
o Gonococcal – Rapid onset, copious discharge, ocular inflammation includes
Conjunctival Oedema (Chemosis) and Lid Oedema; Palpable preauricular LN
▪ Gram Stain of Conjunctival Swab – Presence of Gram -ve Diplococci
o Less acute Purulent Conjunctivitis with moderate discharge – HiB, S pneumo
• Chronic Conjunctivitis – Mild injection with scanty discharge; S aureus and Moraxella
• Oral and Topical Penicillin for Gonococcal to reduce rate of Corneal Perforation
• Topic Broad-Spectrum (E.g. Chloramphenicol) for other causes

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18
Q

Chlamydial Conjunctivitis

A

• C trachomatis; Direct or indirect contact with genital secretions; Shared eye cosmetics
o Trachoma – Same organism but usually not sexually transmitted; Tropics and Middle
East; Common cause of blindness in the world; Chronic inflammation leads to
Progressive Scarring, Trichiasis, Entropion and Corneal Scarring; Blindness from
Opacification or Ulceration

• Slow onset; Scanty mucopurulent discharge in some; Preauricular LN
o In Neonates – 2/52 onset (C/f Gonococcal, which occurs within days); Swabs taken
and NAAT performed to confirm before starting treatment

• Topical Erythromycin BD; Referral to GUM; Neonates referred to Paediatrician; Assoc with
Otitis Media or Pneumonitis

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19
Q

Viral Conjunctivitis: Adenovirus

A

Highly Contagious, Epidemics; Direct or Indirect contact; May have prodromal
symptoms; Inflammation associated with Chemosis, Lid Oedema and Palpable Preauricular LN
o Some develop membrane on Tarsal conjunctiva, and Haemorrhage on Bulbar
o Can cause deterioration in visual acuity due to focal Corneal Inflammation
o Self-limiting, Eye Lubricants, Cold Compress, Strict Hygiene; Topical steroids for
Inflammation or Corneal Involvement

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20
Q

Viral Conjunctivitis: HSV

A

Typically unilateral; Palpable Preauricular LN, Cutaneous Eyelid Vesicles; 50% develop
Dendritic Corneal Ulcers; Typically, self-limiting; Topical Aciclovir to reduce risk of Corneal
Epithelial involvement

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21
Q

Phthiriasis Palpebrarum

A

Infestation with Phthirus pubis (crab lice); Leads to Blepharitis with marked Conjunctival
Inflammation, Preauricular LN, and rarely secondary infections
• Mechanical removal with fine forceps, Physostigmine 1.25%, and Pilocarpine 4% gel

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22
Q

Allergic Conjunctivitis

A

• Itching, Pink-to-reddish Eyes; Seasonal and Perennial Conjunctivitis mediated by Mast cells;
easily treated with cold compress, eye-wash and allergen avoidance
• Affects 20% of UK populace; Reaction to grass, pollen, fungal spores or HDM
• Reduce allergen load, Antihistamine Eye Drops and Topical Mast-cell Stabilising agents; Oral
Antihistamines reduce itching; Avoid Corticosteroids

23
Q

Traumatic Injury to the Cornea: Corneal Abrasion

A

Removal of focal area of Corneal Epithelium; Usually occurs due to finger
poking, brushing or foreign body
o Severe pain (Cornea is richly innervated), Lacrimation, Inability to open eye (Blepharospasm); Visual acuity usually reduced
o Topical Anaesthetics (e.g. Oxybuprocaine, Tetracaine) for examination
o Cornea inspected under blue light after instillation of Fluorescein drops
o Broad-spectrum Topical Abx QDS for 5/7; Common practice of padding

24
Q

Traumatic Injury to the Cornea: Corneal Foreign Body

A

Associated with Lacrimation and Photophobia; EUA, should include
eversion of Eye Lid
o Removal of foreign body and Topical Abx

25
Q

KERATITIS

A

=Corneal Inflammation; Commonly due to HSV, Contact lens
infection and Blepharitis; Sensation of foreign body or pain
(depending on size and ulcer depth), Photophobia and Lacrimation; Vision might be reduced

26
Q

Keratitis: HSV

A

Causes Epithelial Lysis and forming Dendritic Ulcer (50%); Stains Green under
Blue light with Fluorescein dye
▪ Topical Steroids or Systemic Immunosuppression can lead to centrifugal
spread =Geographic Ulcer
▪ HSV dormant infection can be triggered by UV light, stress or menstruation
▪ Ointment Aciclovir five times daily for 2/52

27
Q

Keratitis: Bacterial Causes

A

S aureus, or P aeruginosa in contact lens wearers

o Potentially sight threatening in Contact-lens wearers; Referral to Ophthalmology

28
Q

Fuch’s Corneal Dystrophy

A

Genetically associated Degeneration leading to Corneal Oedema
and Vision Loss; Bilateral, more common in females, Gradual onset to blindness in 40-60s
o Accumulation of corneal deposits; Thickening of Descemet’s membrane
o Treatment with Corneal Transplantation

29
Q

Glaucoma

A

Raised IOP causing Optic Nerve damage resulting in Visual Field Defects Normal 10-21mmHg;
Second commonest cause of blindness worldwide, third most common in UK

30
Q

Primary Open-Angle Glaucoma (POAG)

A

• Commonest form of Glaucoma; High IOP due to reduced Aqueous
Humour outflow through trabecular meshwork; RF: Age, Race (Black),
Positive FMHx, Myopia
• Gradual, Insidious, Painless loss of peripheral visual field; Initially
asymptomatic, central vision remains good till end-stage; Typically,
identified on routine Ophthalmic examination (Enlarged cup with thin
Neuro-retinal Rim)
• Diagnosis only made if IOP measured (by e.g. Tonometry)

31
Q

Primary Open-Angle Glaucoma (POAG) Treatment

A

Treatment reduces IOP either through reducing Aqueous Humour
production, or Increasing Aqueous Drainage
o Topical Beta-blockers (Timolol, Carteolol, Levobunolol) reduce
Aqueous production; CI in COPD, Asthma, and Heart Block
o Prostaglandin Analogues (Latanoprost, Travoprost) increased
Outflow; Reduces IOP up to 30%
o Carbonic Anhydrase Inhibitors (Acetazolamide) reduce
production; Oral or Topical; CI in Sulfonamide Allergy

32
Q

Acute Angle-Closure Glaucoma

A

• Ophthalmic Emergency; Sudden rise in IOP
>50mmHg due to reduced Aqueous drainage due
to Lens pushing Iris forward against Trabecular
Meshwork; More likely to occur in reduced light
conditions in pupil dilation
o RF: Shallow Anterior Chamber
(Hypermetropia, Women)

33
Q

Acute Angle-Closure Glaucoma Presentation

A

Presents with sudden onset, painful red eye and blurred vision; Unwell with N+V, complains
of Headache and Severe Ocular Pain
o Hazy Cornea, Semi-dilated Pupil, Conjunctival injections and Tenderness

34
Q

Acute Angle-Closure Glaucoma Treatment

A

Prompt treatment to preserve sight
o IV Acetazolamide 500mg to reduce IOP, Pilocarpine 4% (Pupil Constrictor) to improve
Aqueous Outflow and reduce Iris adhesion to Trabecular meshwork
o Topical Beta blockers, Prostaglandin analogues, Analgesia, Antiemetics
o Oral Glycerol and IV Mannitol for non-responding patients under Ophthalmologist
care; Definitive management through laser or surgical incision of Peripheral Iris

35
Q

Uveitis

A

• Inflammation of Iris, Ciliary Body and Choroid; If confined to Anterior Segment = Anterior
Uveitis (=Iritis); If Ciliary Body involved = Intermediate, and if Choroid Involved = Posterior
o If all three regions involved = Pan-uveitis; Posterior involvement – Ophthalmology r/v
• Most commonly Blurred vision, Pain, Redness, Photophobia and Floaters
• Associated with Ank Spond (HLA-B27 pos), Arthritis, IBD, Sarcoidosis, TB, Syphilis,
Toxoplasmosis, Behçet’s syndrome, Lymphoma and Viral Infections

36
Q

Anterior Uveitis

A

• Triad of Redness (General or Limbus Injection), Pain and
Photophobia; Keratic precipitates, Pus and cellular
debris within Anterior Chamber; Pupil might have
adhered to lens (Posterior Synechiae)
• IOP may be raised due to either debris clogging, or
Posterior Synechiae, with the aqueous build-up forcing
the Iris against the trabecular meshwork
• Reduction of Inflammation with Topic Steroids (Dexamethasone), Pupil Dilation to prevent
Posterior Synechiae (Cyclopentolate); Examination of Posterior Segment
o If IOP raised – Topic Beta Blockage, Prostaglandin Analogues or Acetazolamide

37
Q

Cataracts

A

• By far, commonest cause of Preventable
Blindness in the world with effective surgical
treatment; 250,000 Cataract operations per
year in the UK = Commonest Surgery
• Age-related Opacification; 30% over 65yrs
having Snellen <6/12 (Below safe for driving)
o Other Aetiologies include Congenital
(Maternal Infection, Familial),
Metabolic (Diabetes,
Hypocalcaemia, Wilson’s Disease),
Drug Induced, Traumatic,
Inflammatory (Uveitis), or Disease
Associated (E.g. Down Syndrome)
o Cataract in Infants demand urgent
referral to Ophthalmology to minimise subsequent development of Amblyopia
• Gradual, Painless deterioration of vision; Early changes correctable by spectacles, but
eventually opacification requires surgery
• Investigations – Glucose for DM, Ca, LFTs to diagnose metabolic disorders
• Surgical Management – Small incision extracapsular, or Phacoemulsification with insertion of
Intraocular lens

38
Q

Age Related Macular Degeneration

A

Commonest cause of Visual Impairment >50yrs in
developed nations, and blind registration; 10% of
>65yrs, 30% of >80yrs; Unknown cause but RF
include Age, Smoking, HTN,
Hypercholesterolaemia and UV Exposure

39
Q

Non-exudative (Dry) Macular Degeneration

A
Painless, Progressive loss of Central Vision
o Lipofuscin (=Drusen) deposits between
Retinal Pigment Epithelium and Bruch’s
Membrane; Might cause focal RPE
detachment
o Not all affected visually; Some might
develop distortion and blurring of central
vision
o Extensive Atrophy can
occur (Geographic Atrophy)
40
Q

Exudative Macular Degeneration

10%

A

Development of abnormal
Subfoveal Choroidal
Neovascularisation in Macula;
Causes severe central visual loss

41
Q

Management of Macular Degeneration

A
• Patients with Central Distortion or
Frank Macular Pathology for urgent
Ophthalmology R/v
• Anti-VEGF (E.g. Ranibizumab,
Bevacizumab) by Intravitreal
injections; Vision maintained in 95%, improves in about 1/3 of patients
• Monthly OCT monitoring recommended
• Severe visual loss if possible; Low vision aids, such as Magnifiers, may help
42
Q

Acute Visual Loss

A

• Crucial Hx includes Onset, Progression,
Redness, Unilateral or Bilateral, Field Visual
Defect, Relative Afferent Pupillary Defects
• Acute causes include Uveitis, Acute Glaucoma,
Keratitis (Corneal Ulcer), Retinal Detachment,
Vascular Occlusion (CRA, CRV, etc), Acute
Optic Neuropathy and other Macular or
Retinal Diseases

43
Q

Central Retinal Vein Occlusion

A

• Profound, sudden, painless loss of vision with
Thrombosis of CRV at or posterior to where optic
nerve exits globe; Obstruction leads to raised
intravascular pressure, causing vein dilation,
Retinal Haemorrhage, Cotton-Wool spots and
Retinal Oedema
o In severe cases, RAPD might be present,
especially in Ischaemia

• RF: Age, HTN, CVS disease, DM, Glaucoma; Blood
dyscrasias and Vasculitides in the young
• Ophthalmology R/v – Neovascularisation as a

result from retinal ischaemia; Intravitreal Anti-
VEGF therapy or steroids

44
Q

Central Retinal Artery Occlusion

A

• Painless severe loss of vision; Infarction of inner
2/3rds of Retina; Arterial stenosis and Retina
becomes Opaque and Oedematous
o Cherry red spot on Fovea –
Neovascularisation appears on thinnest
part of retina
o RAPD is usually present
• Arteriosclerosis-related Thrombosis is the most
common cause of CRAO; Emboli from Atheroma and Vulvar disease possible
• Need to rule out Giant Cell Arteritis (Temporal Arteritis)
• Ophthalmic Emergency; Irreversible Retinal damage occurs after 90 mins; Ocular Massage, IV
Acetazolamide to reduce IOP, which might dislodge emboli
o Breathing into paper bag – CO2 retention can act as a vasodilator
o Thorough medical review for aetiology of emboli/thrombus
o Should start on Aspirin as secondary prevention

45
Q

Vitreous Haemorrhage

A

• Extravasation of blood into or around Vitreous
Humour; Most commonly due to Diabetic
Retinopathy (Neovascularisation leads to weaker
blood vessels), Trauma, Retinal Detachment
• Blurry vision, Floaters, Reddish tint to vision and
Photopsia (Flashes)
• Management involves Head Elevation and limiting
eye movement to allow blood to settle and
discontinuing Antiplatelets/anticoagulants; Repair of Retinal Tear
o Vitrectomy may be necessary to remove for longstanding haemorrhage, or evidence
of rubeosis (Neovascularisation of the Iris)

46
Q

Retinal Detachment

A

• Painless, Progressive Visual Field Loss; Shadow
corresponds to area of detachment; If macular
affected, central vision lost
• Following tear, Fluid collects in space between
Sensory Retina and RPE
o Tear can occur from Posterior Vitreous
Detachment, Injury or Inflammation;
• RF includes Myopia and Previous Cataract Surgery
• Patients report sudden onset of floaters, often
associated with Photopsia (Flashes)
• For urgent Ophthalmology referral; Management
involves isolating the defect and preventing the detachment from spreading; Either
Cryotherapy, Laser Photocoagulation; Pneumatic Retinopexy or Vitrectomy

47
Q

Diabetic Eye Disease

A

• 90% of young patients T1DM develop retinal changes, but only few progress to sight-
threatening retinopathy; 30-50% require Laser Photocoagulation to limit Proliferative

Retinopathy; Diabetes is the most common cause of blindness <65yrs
• Cataracts – Develop earlier in people with DM; Very poor diabetic control plus ketosis can
lead to rapid, acute Snowflake Cataracts
o Fluctuations in Blood Glucose can lead to osmotic changes in the lens, leading to
refractive variability (Temporary Hypermetropia)

• Extraocular Palsies – VI and III most commonly; III not associated with pain; May recover
spontaneously in 3 – 6/12

48
Q

Diabetic Retinopathy

A

• Most commonly diagnosed DM
complication; Increasing prevalence with
duration of DM; Intramural Pericyte death
with Thickening of Basement Membrane;
Incompetence and increased Vascular
Permeability, leading to occlusion
• Damage to small vessels leads to
Microaneurysms in retina; when breached,
Blot Haemorrhages occur, with leakages
into Retina; Deposition of protein and
lipids known as hard exudates
• Microinfarctions of occluded vessels leads to cotton wool spots (Accumulation of axoplasmic
debris; White spot can occur after clearance by macrophages)
• Venous damage leads to variance in diameter (Beading) and Elongation (Loops); Blockage
leads to capillary non-perfusion, leading to release of neovascularisation factors causing new
intraretinal vessel growth (Intraretinal Microvascular Abnormalities)
• Bleeding of new, weak vessels results in Pre-Retinal Haemorrhages (Boat-shaped) and
Vitreous Haemorrhage, which threatens vision; Collagen growth leads to fibrotic band
formation, which may contract and cause Retinal Detachment
• Neovascularisation of Pupil Margin (Rubeosis) can lead to rapid rise in IOP (Rubeotic
Glaucoma)

49
Q

Maculopathy

A

• Fluid leaking is cleared poorly; Macular Oedema forms; Distortion and Thickening of the
Macula can lead to loss of central vision; Not visible on Ophthalmoscopy; Capillary occlusion
can lead to loss of central vision as well

50
Q

Assessment of Diabetic Retinopathy

A
  • Visual Acuity (Pinhole and Spectacles), Ocular Movements; Iris examined for Rubeosis
  • Dilation with 1% Tropicamide; Examination for Cataract and Retinal Quadrants
  • Screening – All diabetics >12yrs Annual Acuity measurement and Retinal Photography
51
Q

Management of Diabetic Eye Disease

A

• Cataracts – Extraction and IOL implantation if causing Visual Disability; Pre-existing
Retinopathy might worsen after extraction
• Reduce Risk of Eye Disease through good metabolic control of DM and HTN
• Fluorescein Angiography to define extent of potentially sight-threatening Retinopathy, OCT to
image content of layers of Retina at the Macula; Detect Oedema
• Neovascularisation is an indication for Laser Photocoagulation; New vessels on disc have poor
prognosis requiring urgent therapy
o Laser ablation of new vessels and area of Ischaemia
• Pan-Retinal Photocoagulation – Proliferative Retinopathy progressing to new vessels on disc;
Also used in Rubeosis
• Vitreoretinal Surgery for Recurrent bleeds; Also used to reduce Vitreous Haemorrhage; Also,
to treat Fibrotic Traction Retinal Detachment
• Treatment for Maculopathy – Laser Photocoagulation for encroaching Foveal Exudates; If
centre of Macula affected, Grid Photocoagulation is used; Also, Anti-VEGF Drugs

52
Q

Thyroid Eye Disease

A

• Due to Immune Response that causes Retro-Orbital Inflammation; Swelling and Oedema of
Extraocular Muscles, Proptosis, Increased pressure on Optic nerve leading to Atrophy
o Likely due to Antigen in Retro-Orbital tissue with similar immunoreactivity to TSH
o Can occur regardless to Thyroid status of patients in Grave Disease; Typically occurs
within 2yrs of each other; TSHR Auto Antibodies invariably

• Soreness, Painful Watering and Eye Prominence, Lid Retraction; Severe Proptosis in minority
of cases; Limitation in Eye Movement and Visual Impairment (CN II compression)
o Corneal Damage, Periorbital Oedema, Conjunctival Oedema and Inflammation
• Few investigations required if appearance characteristic and bilateral; Serum TSH, T3 and T4
• Hx – Eye Movements, Degree of Oedema and Inflammation; MRI and CT Orbit to exclude
Retro-orbital SOL, Reveal Oedema and Muscle damage

53
Q

Treatment of Thyroid Eye Disease

A

• Lubricant Eyedrops – Methylcellulose, Hypromellose
• Eyelids can be taped shut to ensure closure at night
• Systemic Steroids (Prednisolone 30 -120mg OD) reduces inflammation if more severe
symptoms present; Pulse IV Methylpred may be more effective in severe cases
• Surgical Decompression – If pressure threatens vision; Also for Cosmesis
• Lid Surgery – Protect cornea if lids are unable to close; Also for Cosmesis
• Corrective Eye Muscle Surgery – Deferred until stable for 6/12
• Currently under investigation – Irradiation of the Orbits, Immunomodulatory agents