Revise Notes Opthal

Question 1

Age Related Macular Degeneration
Pathophysiology

A leading cause of visual loss and blindness in middle-aged/older adults (50s-60s)

It results from a combination of non-vascular and neovascular changes to the retina with resultant visual impairment.

Non-vascular:
Drusen formation - dome-shaped yellow deposits composed of protein/lipids which accumulate beneath the retinal pigment epithelium

Retinal pigment epithelium abnormalities

Hyper and hypopigmentation
Geographic atrophy - well demarcated areas of depigmentation which occurs due to degeneration of the light-sensitive macular cells.

Vascular:
Choroidal neovascularisation (wet ARMD)

AMD can be classified as wet or dry. Wet ARMD is defined by the presence of neovascularisation

Newly formed vessels are fragile and susceptible to rupture and leakage which results in scarring of the retina

Answer 1

Clinical features

Symptoms

Impaired visual acuity - can be insidious or rapidly progressive (normally due to neovascular AMD)
Blurred vision

Distorted near vision, including metamorphopsia (where straight lines appear wobbly)

Identified using amsler grid
Central scotoma - central visual fields are absent, ‘a black patch’

Hallucinations - AMD is a common cause of Charles Bonnet syndrome

Examination/fundoscopy findings

Drusen
Macular changes - pigmentary/atrophic/haemorrhagic

Question 2

Ardm

Investigation and mng

Answer 2

Investigations

Optical coherence tomography - mandatory for diagnosis and monitoring treatment response - high resolution cross sectional imaging of the retina to look for RPE changes/drusen etc.

Fluorescein angiography - to identify the presence of neovascularisation

Management

Non-exudative AMD
Risk factor modification - smoking cessation

Nutritional supplementation - antioxidants (AREDS treatment) - contains beta-carotene (metabolised into vitamin A), vitamins C & E, zinc, copper

Beta-carotene can increase risk of lung cancer in smokers
Exudative AMD

Intravitreal anti-vascular endothelial growth factor (VEGF) injections
Laser treatments

Question 3

Blepharitis
Background

Chronic inflammation of the margin of the eyelids, usually bilateral

Anterior – base of eyelashes are inflamed. Causes include:
Infective blepharitis - staph. aureus most common
Seborrheic blepharitis
Posterior – Meibomian glands (MG) inflammation

Cause: MG dysfunction - The MGs are located on the posterior margin of the eyelid and secrete an oily/ lipid secretion onto the cornea/ conjunctiva, which helps form the tear film -

prevents tear evaporation, maintains smooths eye surface

Answer 3

Clinical features

Symptoms

Itchy, ‘burning’ discomfort of eyelids
Eyelid can be crusty and stick together, especially in the mornings

Bilateral symptoms
Symptoms are often intermittent with periods of exacerbation and remission

Examination Findings

Staphylococcal
Crusting at base of eyelashes, with eyelid erythema/inflammation

May be history of styes
Seborrhoeic
Oily skin, scaly dermatitis, erythema/inflammation of lids

MGD
Foamy discharge can be seen on the eyelid margin, chalazion are often present

Question 4

Mng of blepharitis

Answer 4

Management

1st line: Self-care measures - warm compress and hygiene measures

Also, if co-existent dry eye disease - consider artificial tears/ocular lubricant
2nd line: If self-care measures are ineffective

Anterior blepharitis - consider topical ABx (chloramphenicol) for eyelid margins

Posterior blepharitis - If MGD in the context of rosacea - PO tetracycline (doxy/oxy)

Question 5

Cataracts
Pathophysiology

The cloudy opacification of the crystalline lens of the eye, with resultant visual impairment.

Most are age related, and can occur uni- or bilaterally
Subtypes:
Nuclear - the centre of the lens becomes opacified - agein

Polar - localised opacification - often genetic
Subcapsular - anterior or posterior subcapsular cortex - assoc. w/ steroid

Answer 5

Clinical features

Mostly occur in patients > 60 yrs as a consequence of ageing

Symptoms

Gradual, progressive loss of visual acuity/ blurring of vision
Fading colour vision, especially blues

Glare and ‘halos’ reported around lights
Impaired night vision
Examination Findings

Leukocoria - grey/white discolouration of the pupil
Loss of red reflex

Investigations

Slit lamp examination to examine the lens and visualise cataract

Question 7

Management of cataract

Answer 7

Surgery - Phacoemulsification

Complications:
Posterior capsular thickening is the most common post-op complication, affecting 20% of patients.

Cells remaining post-operatively grow back over the posterior lens capsule.

This results in reduced light transmission to the retina. Patients may report cloudy/blurred vision and difficulty seeing at night.

Glare is another suggestive symptom.

Endophthalmitis: Post-operative infection, presenting with pain, redness and photophobia.

Question 8

Chalazion
Pathophysiology

A chalazion (meibomian cyst) is a sterile, inflammatory granuloma.

It is caused by the obstruction of the sebaceous meibomian glands which enlarges, and then ruptures.

The ruptured gland releases its lipid contents (a component of the tear film) which triggers an inflammatory reaction, and results in the formation of a granuloma.

Answer 8

Clinical features

Symptoms

A firm, localised swelling of one of the eyelids which develops over several weeks
Usually painless/non-tender (although might have been sore initially)

Differential diagnosis: Hordeola - usually develop more acutely, and are more painful

Examination Findings

Unilateral swollen, erythematous eyelid
Firm nodule may be felt, non-tender

Most commonly affect the upper eyelid
A well-defined nodule (the granuloma) can be identified with eversion of the eyelid

Question 9

Chalazion mng

Answer 9

Management

Self-care measures: Warm compress and gentle massage to aid content expression

Chalazions usually self-resolve spontaneously within a few weeks
If no improvement after 1 month,

consider referral to ophthalmologist for consideration of incision/curettage or intralesional steroid injection

Question 10

Conjunctivitis
Background

Inflammation of the thin, transparent, mucous membrane lining the anterior sclera, and palpebral conjunctiva.

Clinical features: Hyperaemia and dilation of conjunctival vessels +/- discharge

Question 11

Allergic conjunctivitis

Ocular IgE hypersensitivity reaction. Allergens bind to mast cells which release histamine and inflammatory mediators.

Common causes include:

Seasonal allergic conjunctivitis (hay fever)
Perennial AC – dust mites/ mould spores/ animal dander
Clinical features:

Bilateral itchy eyes
May be a watery discharge/tearing
Conjunctival inflammation -

hyperaemia, oedema, dilated vessels
May be a history of asthma/eczema/rhinosinusitis

Answer 11

Management:

Initial management - non-pharmacological measures:

Allergen avoidance, cold compress etc.
If non-pharmacological Mx does not provide sufficient symptomatic relief:

Topical antihistamine or mast cell stabilisers - azelastine, sodium cromoglicate etc.

Topical AHs have been found to be more effective than PO/systemic AHs for relief of ocular symptoms

Question 12

Infective conjunctivitis

Causes

Viral
Adenovirus is the most common cause
May be a history of URTI

Herpes simplex virus - unilateral red eye, with vesicular lesions on eyelid

Bacterial
Streptococcus pneumoniae is most common

Others: chlamydia, gonorrhoea
History of STI/unprotected sex

Clinical features

Answer 12

Clinical features

Acute, bilateral conjunctival erythema
Gritty, foreign body sensation
Discharge

Often purulent with crusting in bacterial conjunctivitis, lids may crust and stick together on waking up.

Less discharge in viral conjunctivitis, which is usually watery

Question 13

Mng of conjunctivitis

Answer 13

Management

Refer to ophthalmology if suspected:

Ophthalmia neonatorum - conjunctivitis in first 4 weeks
Suspected gonococcal / chlamydial conjunctivitis
Suspected herpes conjunctivitis

Viral conjunctivitis

Most cases resolve within 2 weeks without treatment

Bacterial conjunctivitis

Most cases self-resolve within 1 week, without treatment
Consider topical antibiotics (chloramphenicol/fusidic acid) if severe symptoms

Question 14

Retinal detachment
Pathophysiology

Retinal detachment occurs when the inner neurosensory retina separates from the outer retinal pigment epithelium (RPE), disrupting retinal function.

Types include rhegmatogenous (due to retinal tears or holes), tractional (from fibrous tissue pulling the retina), and exudative (from fluid accumulation under the retina).

Answer 14

Clinical Features

Painless
Visual impairment - feeling of dots, cobwebs or a curtain passing over the eye

New onset photopsias, flashes of light or persistent new floaters suggest a retinal tear, which can be followed by retinal detachment

Detachment is suggested by a progressive loss of vision - often described as a dense shadow, which starts peripherally and moves centrally.

Fundoscopy - pale, opaque retina often with wrinkling and loss of the normal choroidal pattern

Management

Ophthalmological emergency - requiring immediate referral.

Slit lamp examination should be performed.

Question 16

Retinitis pigmentosa
Pathophysiology

Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies characterised by progressive photoreceptor degeneration, primarily affecting rods and later cones.

Genetic mutations lead to the gradual loss of retinal cells, resulting in vision impairment.
Clinical Features

Night blindness (nyctalopia) is often the initial symptom.
Progressive peripheral visual field loss, leading to tunnel vision.

Photopsias (flashes of light) and difficulty with dark adaptation.

Central vision loss occurs in advanced stages.

Fundoscopy: Bone-spicule black pigmentation predominantly affecting the peripheral retina, attenuated retinal vessels, and optic disc pallor.

Answer 16

Management

There is no cure for RP. Management focuses on maximising remaining vision and improving quality of life.

Supportive Care: Low vision aids, mobility training, and psychological support.

Monitoring: Regular ophthalmic evaluations to monitor disease progression.

Emerging Therapies: Participation in clinical trials for gene therapy and retinal implants.

Question 18

Central retinal vein occlusion

CRVO results from thrombosis in the central retinal vein, causing retinal congestion and haemorrhage.

Risk factors include hypertension, diabetes, glaucoma, and hypercoagulable states.

Answer 18

Clinical features

Sudden, painless unilateral loss of vision, may be partial or complete.

Fundoscopy: Retinal haemorrhages, dilated tortuous veins, and cotton-wool spots
Central retinal vein occlusion

Figure 165: Central retinal vein occlusion. Werner JU, Böhm F, Lang GE, Dreyhaupt J, Lang GK, Enders C, Fondo de ojo Ostrucción Vena central, CC BY 4.0

Question 19

Central retinal artery occlusion (thromboembolism, arteritis)

CRAO occurs due to embolic or thrombotic obstruction of the central retinal artery,

leading to retinal ischaemia.

Common causes include atherosclerosis and emboli from carotid artery disease or cardiac sources

Answer 19

.

Clinical features

Sudden, painless unilateral loss of vision
O/E: RAPD may be present.
Fundoscopy: Cherry red spot on pale retina

Figure 166: Central retinal artery occlusion- Cherry red spot and retinal swelling.

Dr. Gopal Bisht, Cherry red spot in patient with central retinal artery occlusion (CRAO), CC BY-SA 4.0

Question 23

Hyertensive retinopathy vs DM retinopathy

Hypertensive retinopathy is characterised by the following

Answer 23

:

Arteriolar narrowing
Arteriovenous nipping
Cotton wool spots/haemorrhages
Papilloedema

Question 24

Diabetic Eye Disease
Diabetic eye disease is the most common cause of blindness in patients aged 30-65 yrs.

Screening for eye disease

Patients with type 1 and type 2 diabetes should have annual screening for diabetic eye disease (except T2DM with very low risk - no retinopathy on last 2 x screening tests, where screening may be biannual).

Answer 24

Staging of diabetic eye disease

Stage 1: Mild Non-Proliferative Diabetic Retinopathy (NPDR)

Microaneurysms present

Stage 2: Moderate NPDR

Blot haemorrhages
Exudates
Cotton wool spots
Venous looping

Stage 3: Severe NPDR

Dots and blots in all 4 quadrants with venous beading in 2 or more quadrants and intraretinal microvascular abnormality (IRMA) in 1 or more quadrants

Question 25

Proliferative Diabetic Retinopathy (PDR)

Answer 25

PDR is defined by the presence of retinal neovascularisation New vessels may cause vitreous haemorrhage (presenting with sudden loss of vision) 50% of patients with PDR are registered blind within 5 years

Question 26

Glaucoma Glaucoma describes the group of eye diseases associated with increased intraocular pressure (>21mmHg) which results in damage to the optic nerve.

Answer 26

Risk factors Increasing age Family history Black people are 3 x more affected than white people Myopia - risk of POAG Hyperopia - risk of PACG Diabetes Steroid usage

Question 27

Primary Open Angle Glaucoma (POAG)

Answer 27

Pathology Glaucoma in which the angle between the cornea and the iris is normal Clinical features Often asymptomatic Symptoms usually present in late disease - narrowed peripheral visual fields Fundoscopy findings Optic disc cupping (C:D ratio > 0.7) Optic disc pallor Bayonetting of vessels Cup notching, haemorrhages Diagnosis Applanation tonometry - IOP > 21mmHg Gonioscopy - checks drainage angle

Question 28

Mng of open angle glaucoma

Answer 28

Management 1st line: 360 degree selective laser trabeculoplasty (SLT) 1st Line topical Tx (if SLT refused/fails) - Prostaglandin analogue drops (latanoprost) Improve uveoscleral outflow SEs: long eyelashes, brown discolouration of iris 2nd line topical - add, or switch to: Dorzolamide - CAH - reduced AH production Timolol - BB - reduced AH production Brimonidine - sympathomimetic - inc. outflow, reduced AH production

Question 29

Primary Acute Angle Closure Glaucoma (PAACG) Pathophysiology The angle between the cornea and the iris is reduced or closed, which results in impaired aqueous outflow, and increased intraocular pressure. Clinical Features Acutely painful red eye Severe ocular pain and headache Impaired visual acuity with halos surrounding lights May complain of abdominal pain, nausea and vomiting

Answer 29

Examination Findings A red eye which feels ‘hard’ on palpation, reflecting v. high IOP. Semi-dilated pupil which does not react to light Pupil becomes fixed in an oval shape A hazy cornea may be seen due to oedema Management In the acute setting, management of PCAG comprises a combination of pilocarpine, timolol, apraclonidine and IV acetazolamide to reduce IOP. Pilocarpine - a parasympathomimetic - constricts pupil, opening angle and improving aqueous outflow Timolol - a beta blocker - reduced production of aqueous humour Apraclonidine - alpha-2 agonist - dual mech: Reduced AH production, inc. outflow. IV Acetazolamide - carbonic anhydrase inhibitor - reduced AH production Definitive management - laser peripheral iridotomy

Question 31

Hordeola Background A hordeolum, or stye, is an acute, localised area of inflammation affecting the eyelid margin, most commonly caused by infection (staph. aureus) of either a meibomian gland (internal) or eyelash follicle and associated sebaceous gland (external). Clinical features A unilateral, acute swelling adjacent to the eyelid margin. Hordeola usually develop over a matter of days and are painful (which differentiates them from chalazion - usually develop over 1-2 weeks and are less sore) There are two types of stye - internal, and external

Answer 31

External Caused: infection of an eyelash follicle and associated glands A papule/furuncle can be seen on the eyelid margin, localised around the affected eyelash Management Mainstay of management: Self-care advice - warm compress QDS If external stye - consider plucking the eyelash to allow drainage Consider topical chloramphenicol if there is evidence of spreading conjunctivitis (e.g. mucopurulent discharge).

Question 32

Oculomotor (CN3) Palsy Pathophysiology Oculomotor nerve palsy involves the disruption of the third cranial nerve, which innervates most of the extraocular muscles, levator palpebrae superioris, and the pupillary sphincter. This disruption can be caused by aneurysms, tumours, infections, or microvascular disease (commonly in diabetes). The parasympathetic fibres, which control pupil constriction, are located peripherally on the nerve and are thus more susceptible to compressive lesions.

Answer 32

Clinical Features Eye positioned down and out due to unopposed action of the lateral rectus and superior oblique muscles Ptosis from loss of function in the levator palpebrae superioris Diplopia (double vision) Pupil involvement helps differentiate the cause: Surgical third nerve palsy: Pupil is dilated due to loss of parasympathetic function Suggests a compressive lesion such as a posterior communicating artery aneurysm. Medical third nerve palsy: Pupil sparing suggests a medical (non-compressive) lesion such as microvascular pathology caused by diabetes or hypertension.

Question 33

Horner's Syndrome Pathophysiology Horner's syndrome results from disruption of the sympathetic nerves supplying the eye and face. This can occur due to lesions at various levels: Central - e.g. stroke, tumour Preganglionic - e.g. lung apex tumour, cervical rib Postganglionic - e.g. carotid artery dissection, cluster headaches

Answer 33

Clinical Features Classic triad of: Ptosis: Mild drooping of the upper eyelid due to loss of sympathetic innervation to the Muller muscle. Miosis: Constricted pupil from unopposed parasympathetic activity. Anhidrosis: Decreased sweating on the affected side of the face.

Question 34

Internuclear Ophthalmoplegia (INO) Pathophysiology INO results from a lesion in the medial longitudinal fasciculus (MLF) The MLF coordinates horizontal eye movements by connecting the abducens nucleus of one side with the oculomotor nucleus of the other. Common causes include multiple sclerosis in young patients and stroke in older individuals. Alongside optic neuritis, INO is often a buzzword/key phrase suggesting MS in question vignettes

Answer 34

Clinical Features Impaired adduction of the ipsilateral eye. Nystagmus of the contralateral eye when it abducts, i.e. while attempting horizontal gaze. Diplopia during horizontal eye movements. Bilateral INO can occur, especially in multiple sclerosis.

Question 35

Argyll-Robertson Pupil Pathophysiology Argyll-Robertson pupil is associated with lesions in the pretectal region of the midbrain. It is classically linked to neurosyphilis, a manifestation of tertiary syphilis. Other causes include diabetes mellitus and multiple sclerosis.

Answer 35

Clinical Features Small, irregular pupils. Pupils react to accommodation but not to light. Mnemonic: Argyll-Robertson Pupil: ARP LRA Accommodation Reflex Present, Light Reflex Absent Usually bilateral but can be asymmetric. Often associated with other neurological signs of syphilis, such as tabes dorsalis and general paresis (dementia and motor weakness).

Question 36

Holmes-Adie Pupil Pathophysiology Holmes-Adie pupil is due to postganglionic parasympathetic denervation of the pupil, often idiopathic. It is a benign condition. Clinical Features

Answer 36

It classically affects young women (often a clue in questions). Unilateral dilated pupil that reacts sluggishly to light but better to accommodation. Hence, a common differential diagnoses in questions vs Argyll-Robertson pupil May be associated with diminished or absent deep tendon reflexes, particularly the Achilles reflex. H-A pupil is part of the Holmes-Adie syndrome, which includes absent deep tendon reflexes.

Question 37

Ocular Herpes Simplex Pathophysiology Cause: HSV-1 most commonly HSV infection causes inflammation in different parts of the eye, commonly the cornea resulting in HSV keratitis. Epithelial inflammation can result in the formation of dendritic ulcers. Clinical features 90% of cases are unilateral, and usually occur in the context of previous HSV infection Symptoms Non-resolving blepharoconjunctivitis Eye pain Watering/tearing Blurred vision Photophobia

Answer 37

Examination findings Acute red eye with a fixed, irregular pupil - suggests iritis/uveitis Eyelid erythema with crops of vesicles or pustules +/- crusting Cloudy cornea - suggests keratitis Investigations Fluorescein staining may show evidence of dendritic ulcer (branching, fine lined lesions) Slit lamp examination - vesicular corneal lesions Corneal scrapings/viral swaps with PCR/cultures - HSV DNA Management Refer all suspected ocular HSV for same day specialist assessment Specialist management involves: Topical/ oral antivirals Steroids can be used for stromal keratitis

Question 41

Optic Neuritis Key learning Inflammatory optic neuropathy Typically presents in females aged 20-40 Associated with MS (50% chance of developing MS following episode)as well as infective and other autoimmune causes Usually results in unilateral acute visual loss over hours to days Other signs include retrobulbar pain worse on eye movement, disturbed colour vision and RAPD Clinical diagnosis, investigate underlying cause i.e. MRI/LP for MS Can be managed acutely with high dose systemic corticosteroids (IV methylprednisolone)

Answer 41

Pathophysiology Inflammation of the optic nerve Often autoimmune-mediated Leads to demyelination and impaired transmission of visual signals. Epidemiology Most commonly affects young adults aged 20-40 years Female predominance Causes MS (70% of MS will have one episode of optic neuritis) Other autoimmune: SLE Neurosarcoidosis Infectious: Lyme disease HZV Syphilis Antibody-mediated: Neuromyelitis optica spectrum disorders Myeline ooligdendrocyte glycoprotein antibosy disease Post-infection: EBV

Question 44

Optic neuritis findings History?

Answer 44

History Acute/subacute (hours to days) unilateral vision loss Often preceded by retro/peri-ocular pain with eye movement May have history of recent viral illness Examination Findings Relative afferent pupillary defect Reduced visual acuity Optic disc swelling (papilloedema)- 1/3 of patients Internuclear opthalmoplegia (common in MS) Impaired colour vision Reduced vision field loss

Question 45

Optic neuritis Investigation Mng Complication

Answer 45

Investigations MRI brain and orbit with gadolinium contrast to assess for demyelinating lesions Lumbar puncture Oligoclonal bands (MS) Management High-dose intravenous corticosteroids (e.g., methylprednisolone) followed by oral steroids Complications Vision usually starts to recover with or without treatment within 2 weeks (90% recover) Colour vision /contrast sensitivity abnormalities Loss of visual fields (multitude of patterns possible) Risk of recurrence 30%

Question 46

Orbital cellulitis Orbital cellulitis is a bacterial infection involving the tissues posterior to the orbital septum. Pathophysiology Most commonly due to spread of infection from the paranasal sinuses (ethmoidal or frontal 90%). It often results from sinusitis, trauma, or spread from adjacent infections.Infection posterior to the orbital septum. Common pathogens include Staphylococcus aureus, Streptococcus species, and Haemophilus influenzae.

Answer 46

Clinical features History of recent URTI or sinusitis is common Acute onset severe ocular pain and reduced visual acuity Pain is worse on eye movements Ophthalmoplegia with diplopia Lid oedema, erythema

Question 47

Optic neuritis Investigation Mng

Answer 47

Investigations & Management Investigation of choice: CT with contrast Management: Admission, urgent ophthalmology involvement, IV antibiotics.

Question 48

Pre-septal Cellulitis Caused by infection anterior to the orbital septum. Causes include local infection -e.g. following a stye, impetigo etc.

Answer 48

Difficult to distinguish from the more serious orbital cellulitis. Distinguishing factors include: Pre-septal cellulitis does NOT cause visual impairment, limitation of or pain on eye movement, or proptosis.

Question 49

Red eye - Differential diagnosis

Answer 49

❤️Acute Anterior Uveitis (Iritis): Painful, red eye, photophobia, tearing. O/E: Irregular pupil, ciliary injection, and hypopyon. May be systemic features - joint pain and inflammatory bowel disease. ❤️Keratitis: Eye pain, redness. May be a history of contact lens wear. O/E: cloudy corneal opacity (yellow or white) or ulceration. Conjunctivitis Eye redness and discharge ❤️Acute Angle-Closure Glaucoma Severe eye pain, redness, blurred vision. O/E: Mid-dilated, non-reactive pupil with increased intraocular pressure. ❤️Scleritis: Deep, boring eye pain and redness. Pain worsens with eye movement O/E: diffuse scleral redness with a possible blue or violet hue, and normal cornea and pupil.

Question 50

Keratitis Bacterial Keratitis: Pathogens: Pseudomonas spp., Staphylococcus spp., Streptococcus spp. Clinical Features: Mucopurulent discharge, yellow-white infiltrate with clearly defined margins, hypopyon present. Treatment: Topical antibiotics, steroids, and occasionally oral antibiotics.

Answer 50

Viral Keratitis: Viruses: Herpes Simplex Virus (HSV), Varicella Zoster Virus (VZV). Clinical Features: Clear discharge or epiphora, dendritic ulcers with linear branching and terminal bulbs, reduced corneal sensation, no hypopyon. Treatment: Topical antivirals and cycloplegics Ocular Herpes Simplex

Question 51

Subconjunctival haemorrhage Pathophysiology Bleeding from subconjunctival vessels Causes: Trauma. Coughing, sneezing or straining (e.g. lifting) due to transient hypertension. Other: hypertension, DM, anticoagulation.

Answer 51

Clinical features A red patch of discolouration Painless, does not affect vision

Question 52

Endophthalmitis Pathophysiology Purulent inflammation of the vitreous and aqueous intraocular fluid Post-operative complication

Answer 52

Clinical features Usually presents within 3-7 days of surgery with rapidly worsening painful red eye, discharge, visual impairment O/E: Impaired visual acuity, red eye with hazy cornea, hypopyon may be present

Question 53

Episcleritis Pathophysiology Inflammation of the episclera (between the conjunctive and sclera), unknown aetiology Clinical features

Answer 53

Painless (differentiates from scleritis) Red eye with lacrimation and photophobia O/E: segmental redness, normal pupillary reflexes, vision is unaffected

Question 54

Scleritis Pathophysiology Inflammation of the sclera Commonly occurs on a background of autoimmune disease (rheumatoid arthritis, SLE)

Answer 54

Clinical features Severe pain, which is worse on eye movements Reduced visual acuity

Question 55

Anterior Uveitis Pathophysiology Inflammation of the anterior uvea (involving the iris & ciliary body) Causes

Answer 55

Idiopathic Autoimmune disease Seronegative spondyloarthropathies (HLA-B27 assoc.) - ankylosing spondylitis, reactive arthritis, psoriatic arthropathy Inflammatory bowel disease - Crohn’s/ UC Bechet’s disease Sarcoidosis Infective - herpes simplex, herpes zoster, CMV Symptoms Most commonly unilateral (can be bilateral if assoc. with autoimmune disease), and develop over hours or days (though can be chronic uveitis with more insidious onset) Pain or aching Red eye Blurred vision Tearing Photophobia

Question 56

Management of anterior uveitis Refer for same day ophthalmology review Non-infective - corticosteroids (eye drops/oral/IV) Cycloplegics - paralyse ciliary body and relieve pain (atropine/cyclopentolate)

Answer 56

Examination findings A small, irregular, oval-shaped pupil Fixed, unreactive pupil Ciliary flush - red ring around cornea Hypopyon - a white fluid level (accumulation of WBCs) Investigations Slit lamp examination with pupil dilatation

Question 57

Red eye The differential diagnosis of the red eye is broad and includes:

Answer 57

Acute angle closure glaucoma Keratitis (e.g. herpes simplex) Conjunctivitis Anterior uveitis Scleritis Episcleritis Endophthalmitis Subconjunctival haemorrhage