Ophthalmology Flashcards
External Anatomy of the Eye
• 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)
Internal Anatomy of the Eye
• 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
Neurovascular Supply
• 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
Refractive Error
Abnormalities of focusing mechanism of the eye;
Myopic or Hyper-metropic
o Myopia is usually inherited, discovered in
childhood; Progresses throughout teenage
years when body is growing
o Hypermetropia also inherited
Astigmatism
Refractory error which there is a different degree of refraction in different meridians of curvature (i.e. Defect in another plane)
Presbyopia
Normal ageing of the lens resulting in
change in refractory state; Lens less able to alter
curvature, resulting in difficulties in near-vision
Keratoconus
Non-inflammatory Degenerative disorder resulting in Cornea thinning and
change into Conical shape; Unknown Aetiology
Treatment of Refractory Errors
• 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
Eyelids
Eyelids protect the eyes and help distribute tear over front surface of globe; Excess tears
drained by Punctae and Lacrimal System
Entropion
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
Ectropion
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
Dacryocystitis
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
Blepharitis
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
Conjunctivitis
• 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
Conjunctivitis Red Flags
Severe pain, Photophobia, Sudden Visual Acuity loss, Coloured Halos, Proptosis,
Smaller Pupil in affected eye, High IOP, Keratitis, Shallow Anterior Chamber depth
Bacterial Conjunctivitis
• 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
Chlamydial Conjunctivitis
• 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
Viral Conjunctivitis: Adenovirus
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
Viral Conjunctivitis: HSV
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
Phthiriasis Palpebrarum
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
Allergic Conjunctivitis
• 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
Traumatic Injury to the Cornea: Corneal Abrasion
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
Traumatic Injury to the Cornea: Corneal Foreign Body
Associated with Lacrimation and Photophobia; EUA, should include
eversion of Eye Lid
o Removal of foreign body and Topical Abx
KERATITIS
=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
Keratitis: HSV
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
Keratitis: Bacterial Causes
S aureus, or P aeruginosa in contact lens wearers
o Potentially sight threatening in Contact-lens wearers; Referral to Ophthalmology
Fuch’s Corneal Dystrophy
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
Glaucoma
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
Primary Open-Angle Glaucoma (POAG)
• 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)
Primary Open-Angle Glaucoma (POAG) Treatment
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
Acute Angle-Closure Glaucoma
• 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)
Acute Angle-Closure Glaucoma Presentation
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
Acute Angle-Closure Glaucoma Treatment
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
Uveitis
• 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
Anterior Uveitis
• 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
Cataracts
• 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
Age Related Macular Degeneration
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
Non-exudative (Dry) Macular Degeneration
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)
Exudative Macular Degeneration
10%
Development of abnormal
Subfoveal Choroidal
Neovascularisation in Macula;
Causes severe central visual loss
Management of Macular Degeneration
• 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
Acute Visual Loss
• 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
Central Retinal Vein Occlusion
• 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
Central Retinal Artery Occlusion
• 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
Vitreous Haemorrhage
• 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)
Retinal Detachment
• 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
Diabetic Eye Disease
• 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
Diabetic Retinopathy
• 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)
Maculopathy
• 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
Assessment of Diabetic Retinopathy
- 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
Management of Diabetic Eye Disease
• 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
Thyroid Eye Disease
• 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
Treatment of Thyroid Eye Disease
• 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
