GC125 The Red Eye
The red eye is a clinical presentation characterized by hyperemia of the conjunctival, episcleral, or ciliary vessels resulting from a spectrum of conditions ranging from benign conjunctivitis to sight-threatening emergencies such as acute angle-closure glaucoma, uveitis, or keratitis.
The Red Eye — Comprehensive Exam-Ready Notes
The Big Idea: The red eye is one of the commonest presentations in ophthalmology. Most causes are benign (conjunctivitis, subconjunctival haemorrhage), but a small number are true sight-threatening emergencies (acute angle closure, microbial keratitis, endophthalmitis, scleritis, severe anterior uveitis). The entire lecture is built around a pattern-recognition framework: use the distribution of redness, pain characteristics, visual acuity, and pupil findings to triage the red eye into "safe to manage in primary care" versus "urgent ophthalmology referral." [1]
Learning Objectives (from the lecture): [1]
- Familiarize with a range of common ocular and external eye diseases.
- Describe a framework for diagnosis and treatment.
- Learn the skills to promptly recognize and manage the red eye emergencies.
How this fits into exams: Red eye MCQs appear almost every year—testing your ability to match a clinical vignette to the correct diagnosis, identify the causative organism, and know emergency management (especially for acute angle closure). Past papers have tested viral conjunctivitis organisms, hydroxychloroquine maculopathy (a differential for visual loss in the red eye differential family), and cranial nerve palsies in the context of eye complaints. [3][4]
The lecture references "The Ocular Surface" (Am Fam Physician 2010). [1]
Understanding the layers of the anterior eye is essential:
| Layer | Structure | Clinical relevance |
|---|---|---|
| Conjunctiva | Thin transparent mucous membrane covering the sclera (bulbar) and inner eyelid (tarsal) | Conjunctivitis → diffuse injection |
| Episclera | Thin vascular layer between conjunctiva and sclera; superficial vessels | Episcleritis → sectoral redness, blanches with phenylephrine |
| Sclera | Dense fibrous coat; deep vessels | Scleritis → deep dull redness, does NOT blanch |
| Cornea | Avascular, transparent; epithelium + Bowman's → stroma → Descemet's → endothelium | Keratitis → pain, photophobia, corneal opacity |
| Anterior chamber | Space between cornea and iris, filled with aqueous humour | Uveitis → cells/flare; angle closure → shallow AC |
| Iris/pupil | Controls light entry; pupillary sphincter (parasympathetic CN III) and dilator (sympathetic) | Uveitis → miosis; angle closure → mid-dilated fixed pupil |
Redness, pain, blurred vision; onset, recurring; risk factors: trauma, recent surgery, contact lens use, ophthalmic medications; systemic disease: rheumatological diseases, thyroid. [1]
Why each point matters:
-
Pain character distinguishes diagnoses:
- No pain → SCH, episcleritis, mild conjunctivitis
- Gritty/foreign body sensation → conjunctivitis, dry eye
- Severe deep aching pain → scleritis, acute angle closure
- Sharp pain with photophobia → keratitis, anterior uveitis
-
Visual acuity is the single most important discriminator:
- Preserved VA → likely benign (SCH, conjunctivitis, episcleritis)
- Decreased VA → red flag → keratitis, uveitis, angle closure, endophthalmitis
-
Contact lens use → think Pseudomonas, Acanthamoeba keratitis
-
Recent surgery → endophthalmitis until proven otherwise
-
Rheumatological disease → scleritis, uveitis associations
-
Thyroid disease → proptosis, lid retraction, exposure keratopathy (Graves')
-
Recurrence → herpes simplex keratitis, recurrent anterior uveitis (HLA-B27)
Visual acuity; Pupil: size, reflexes, RAPD; External eye: lid abnormality, proptosis; Inspection; Characteristics of redness: colour (bright/dull, red/pink), distribution (ciliary, sectoral, diffuse); Associated signs: cornea opacity, mass, discharge. [1]
Step-by-step approach:
-
Visual acuity — Always first. Use Snellen chart; with pinhole if < 6/6 (pinhole corrects refractive error). If VA drops with red eye, it's serious until proven otherwise.
-
Pupils — Size symmetry, direct and consensual light reflex, RAPD (swinging flashlight test). A relative afferent pupillary defect (RAPD) indicates optic nerve or extensive retinal disease on that side.
-
External eye — Look at lids (swelling, ptosis, lid malposition), proptosis (thyroid eye disease, orbital cellulitis).
-
Distribution of redness — This is the key framework from the lecture:
Distribution of redness: [1]
- Ciliary injection (circumcorneal) → Uveitis, glaucoma
- Sectoral → SCH, scleritis, episcleritis, trauma
- Diffuse → Conjunctivitis, drug toxicity, severe keratitis, endophthalmitis
| Pattern | Appearance | Mechanism | Diagnoses |
|---|---|---|---|
| Ciliary flush | Ring of redness immediately around the cornea (limbus), deeper violaceous colour | Dilation of deep ciliary vessels supplying the iris and ciliary body | Anterior uveitis, acute angle closure |
| Sectoral | Localised patch of redness | Localised vessel dilation or haemorrhage in one area | SCH, episcleritis, scleritis, focal trauma |
| Diffuse | Generalised redness of the entire conjunctiva | Widespread superficial vessel dilation | Conjunctivitis, severe keratitis, endophthalmitis, drug toxicity |
- Associated signs — Corneal opacity (keratitis, angle closure oedema), mass (pterygium, tumour), discharge (type helps differentiate conjunctivitis subtypes).
Case-by-Case Breakdown (Lecture Structure)
60/M, OD redness × 2/7, no pain, BOV or trauma. PMHx: DM, HT, lipids, IHD on aspirin. [1]
Characteristic bright homogenous red, asymptomatic. From ruptured subconjunctival blood vessel → accumulation of blood between conjunctiva and episclera. [1]
Pathophysiology: A small blood vessel under the conjunctiva ruptures → blood pools in the subconjunctival space. The conjunctiva is transparent, so you see a well-demarcated, flat, bright-red area. It does NOT extend past the limbus (the corneal margin) because the conjunctiva is firmly attached there.
Causes: [1]
- Mostly spontaneous and sporadic
- Trauma: minor (e.g. contact lens), post surgery, eye/head injury
- Valsalva (straining, coughing, vomiting)
- Systemic: HT, DM, antiplatelet/anticoagulants, coagulopathy
Self-limiting; consider work-up if recurrence. [1]
Why this case has these PMHx features: The patient is on aspirin (antiplatelet) and has HT/DM — these are risk factors for both vessel fragility and impaired haemostasis. If a patient has recurrent SCH, you should check:
- Blood pressure
- Coagulation profile (PT/aPTT, platelet count)
- Bleeding history
- Medication review (anticoagulants/antiplatelets)
Management: Reassurance — it looks alarming but is benign. Resolves spontaneously in 1–2 weeks (blood is gradually reabsorbed). No treatment needed unless underlying cause identified.
High Yield
SCH is the classic "looks scary but is benign" diagnosis. Key exam point: It is painless, vision is normal, and the redness is bright and homogeneous. If there IS pain or visual loss with what looks like SCH, think deeper pathology (e.g. globe rupture after trauma → need CT orbit/surgical exploration).
Case 2: Conjunctivitis
40/F, OU redness × 1/52, itch and discharge, crusting in the morning, no pain or BOV, recent URTI+, good past health. [1]
This is viral conjunctivitis. The clues: bilateral, watery/mucoid discharge, recent URTI, itch. The bilateral sequential involvement (one eye then the other) is classic for adenovirus.
The lecture shows a classification table of conjunctivitis types. [1]
| Feature | Viral | Bacterial | Allergic |
|---|---|---|---|
| Organism | Adenovirus (most common) | S. aureus, S. pneumoniae, H. influenzae; Gonococcus/Chlamydia (hyperacute) | N/A (IgE-mediated) |
| Discharge | Watery / mucoserous | Purulent / mucopurulent | Ropy, mucoid |
| Itch | Mild | Minimal | Prominent |
| Pain | Mild, gritty | Mild-moderate | Minimal |
| Vision | Normal | Normal (unless corneal involvement) | Normal |
| Laterality | Often starts unilateral → bilateral | Often unilateral | Bilateral |
| Conjunctival signs | Follicles + preauricular lymphadenopathy | Papillae | Papillae (giant papillae in VKC) |
| Associated | URTI | Mucopurulent crusting | Atopy, seasonal |
| Treatment | Supportive (self-limiting 1–2 weeks); hygiene to prevent spread | Topical antibiotics (e.g. chloramphenicol) | Topical antihistamines, mast cell stabilisers |
Papillae: Larger projections with central vascular core. Allergic immune response due to atopy (VKC, AKC) or foreign body (e.g. contact lens, ocular prosthesis). [1]
Follicles: Small, dome-shaped nodules surrounded by conjunctival blood vessels (red base). Inflammation by pathogens, e.g. virus, atypical bacteria or toxins (including eyedrops). [1]
| Feature | Papillae | Follicles |
|---|---|---|
| Histology | Vascular core surrounded by inflammatory cells | Lymphoid follicle (germinal centre) surrounded by conjunctival vessels |
| Appearance | Cobblestone, red surface (vessels on top) | Dome-shaped, pale/yellowish with vessels around base |
| Associations | Allergic conjunctivitis, GPC (contact lens), VKC, AKC | Viral conjunctivitis, chlamydial infection, drug toxicity (e.g. eyedrops) |
Why this matters: Seeing follicles → think viral or chlamydial. Seeing papillae → think allergic or mechanical (foreign body/CL). This is a classic exam discriminator.
Exam Trap
Don't confuse papillae and follicles. The mnemonic: Follicles = vessels around Foundation (base); Papillae = vessels Penetrate the Peak (central core). Follicles = viral/toxic; Papillae = allergic/mechanical.
Case 3: Acute Primary Angle Closure (APAC) — EMERGENCY
60/F, OS redness since this evening, pain+++, vomiting+, BOV+. Past health: Hyperope +4D, common cold meds+. [1]
This is the quintessential ophthalmic emergency in the red eye lecture.
Mechanism — Pupil Block: [1]
The aqueous humour is produced by the ciliary body behind the iris, flows through the pupil into the anterior chamber, and drains via the trabecular meshwork at the iridocorneal angle. In susceptible individuals, the iris can bow forward and block the pupil → aqueous accumulates behind the iris → pushes the peripheral iris forward → blocks the drainage angle → IOP rises rapidly (can reach 50–80 mmHg; normal is 10–21 mmHg).
Predisposing factors: Short axial length, thick lens, pupil mid-dilatation (e.g. dim light, dilating eyedrops, systemic antihistamine or sinus decongestants). [1]
Why this patient is at risk:
- Hyperope +4D → short eyeball → shallow anterior chamber → narrow angle
- Common cold meds → likely contain antihistamines or sympathomimetics → pupil mid-dilation → triggers pupil block
Why mid-dilatation specifically? At mid-dilatation (~4 mm), the contact between the iris and the lens is maximal, creating the greatest resistance to aqueous flow through the pupil. Full dilation actually stretches the iris away from the lens and may paradoxically relieve block in some cases.
Severe ocular pain; frontal headache; blurring of vision; halos around lights; nausea ± vomiting. [1]
- Halos → corneal oedema from high IOP scatters light prismatically
- Nausea/vomiting → vagal response to severe pain + very high IOP (can mimic acute abdomen or migraine — classic exam trap!)
- Frontal headache → shared innervation (V1)
Fixed mid-dilated pupil; corneal haze; shallow anterior chamber; conjunctival injection; very high intraocular pressure. [1]
| Sign | Explanation |
|---|---|
| Fixed mid-dilated pupil | Iris sphincter ischaemia from very high IOP → cannot constrict; pupil caught in the triggering mid-dilated position |
| Corneal haze | Corneal endothelial pump failure from high IOP → corneal oedema |
| Shallow AC | Anatomical predisposition; iris bowed forward |
| Conjunctival injection | Ciliary flush pattern — congestion of deep ciliary vessels |
| Very high IOP | Measured by Goldmann tonometry; often > 40 mmHg |
To miose and medically abort pupil block: [1]
- Pilocarpine 4% (cholinergic agonist)
To decrease intraocular pressure: [1]
- Timolol 0.5% (beta-blocker)
- Apraclonidine 0.5% (alpha-2-adrenergic agonist)
- IV acetazolamide 500mg (carbonic anhydrase inhibitor)
- IV mannitol 20% 200ml (hyperosmotic agent)
| Drug | Class | Mechanism in APAC |
|---|---|---|
| Pilocarpine 4% | Cholinergic (muscarinic) agonist | Constricts pupil (miosis) → pulls iris away from trabecular meshwork → breaks pupil block |
| Timolol 0.5% | Beta-blocker (topical) | Reduces aqueous production by ciliary body |
| Apraclonidine 0.5% | Alpha-2 agonist (topical) | Reduces aqueous production + increases uveoscleral outflow |
| IV Acetazolamide 500mg | Carbonic anhydrase inhibitor | Reduces aqueous production systemically (most powerful medical IOP-lowering) |
| IV Mannitol 20% 200ml | Hyperosmotic agent | Creates osmotic gradient → draws water out of vitreous → rapidly lowers IOP |
Exam Trap
Pilocarpine may not work initially when IOP is very high because the iris sphincter is ischaemic. You must lower IOP first (with timolol, acetazolamide, mannitol), then pilocarpine becomes effective once IOP drops enough to restore iris sphincter blood supply. Examiners may ask "why doesn't pilocarpine alone suffice?"
Peripheral iridotomy: provide alternative pathway for aqueous flow. Lens extraction: to open up angle. Fellow eye: prophylaxis. [1]
- Peripheral iridotomy (PI): Nd:YAG laser creates a small hole in the peripheral iris → allows aqueous to bypass the pupil → equalises pressure between posterior and anterior chambers → prevents iris from bowing forward. This is curative for pupil-block mechanism.
- Lens extraction: Removing the thickened lens (phacoemulsification + IOL) deepens the AC and permanently opens the angle. Increasingly preferred as definitive treatment.
- Fellow eye prophylaxis: The fellow eye has the same anatomical risk → prophylactic PI to prevent attack.
Case 4: Microbial Keratitis (Contact Lens-Related)
20/F, OS redness × 1/7, pain+++, BOV+, long-term contact lens user: one-month disposable, overnight wear, swim with CL. [1]
This patient has multiple risk factors: overnight wear (hypoxia), swimming with CL (water exposure → Acanthamoeba), extended use disposable lenses.
1. Identify the causative micro-organism: [1]
- Corneal scraping of infiltrate for culture and sensitivity testing
- Contact lens, contact lens case, solution
2. Start empirical antibiotics: [1]
- Intensive: up to q1h round the clock
- Requires both Gram+ and Gram− coverage
- Monotherapy (e.g. moxifloxacin, levofloxacin 1.5%)
- Combination (e.g. fortified vancomycin + gentamicin/ceftazidime)
Why corneal scraping? Unlike conjunctivitis where empirical treatment is fine, microbial keratitis can be caused by bacteria, fungi, or Acanthamoeba — each requiring different treatment. You need to know the organism.
Why "fortified"? Standard ophthalmic antibiotic drops are not concentrated enough for severe keratitis. Fortified drops are pharmacy-compounded at higher concentrations (e.g. fortified cefazolin 5%, fortified gentamicin 1.4%).
CL-related: Pseudomonas, Acanthamoeba [1] Vegetative matters: fungus [1] Common: normal skin flora (Staphylococcus, coagulase-negative Streptococcus) [1]
| Risk Factor | Likely Organism | Key Feature |
|---|---|---|
| Contact lens | Pseudomonas aeruginosa | Rapidly progressive, melting ulcer, green discharge |
| Contact lens + water | Acanthamoeba | Ring infiltrate, severe pain out of proportion, perineural infiltrates |
| Trauma with plant/soil | Fungus (Fusarium, Aspergillus) | Satellite lesions, feathery edges, slow progression |
| General/elderly | Staph, Strep | Common bacterial ulcer |
High Yield
Acanthamoeba keratitis classically presents with pain disproportionate to clinical signs and ring-shaped corneal infiltrate. Treatment is prolonged (months) with polyhexamethylene biguanide (PHMB) or chlorhexidine + propamidine (Brolene). It is NOT responsive to standard antibiotics.
Mostly herpes simplex virus (HSV). A clinical diagnosis – laboratory testing rarely needed. Antiviral agents: Topical (acyclovir ointment, ganciclovir gel); Oral (acyclovir, valacyclovir). [1]
HSV ulcers: dendritic vs geographic. [1]
| Type | Description | Mechanism |
|---|---|---|
| Dendritic ulcer | Branching, tree-like ulcer with terminal bulbs; stains with fluorescein | Active viral replication in corneal epithelium; terminal bulbs are pathognomonic |
| Geographic ulcer | Larger, map-shaped amoeboid ulcer | Progression/coalescence of dendritic ulcer, often from inappropriate steroid use |
Key points:
- Clinical diagnosis — the dendritic pattern is pathognomonic for HSV. No need for culture in most cases.
- NEVER give steroids to an active epithelial HSV ulcer → steroids suppress immune response → virus replicates unchecked → geographic ulcer → corneal perforation.
- HSV can also cause stromal keratitis (immune-mediated, deeper) and endotheliitis — these DO require steroids (under antiviral cover), but this is specialist management.
Exam Trap
Topical steroids are contraindicated in epithelial HSV keratitis (dendritic/geographic ulcer). However, steroids ARE used in HSV stromal keratitis (disciform keratitis) — always with antiviral cover. The exam may try to trick you by offering "topical steroids" as a management option for a dendritic ulcer.
Case 5: Scleritis
40/M, OS redness × 3/7, dull aching pain+, no BOV. PMHx: unremarkable. Non-blanchable with 2.5% phenylephrine. [1]
Phenylephrine test: blanching of blood vessels in episcleritis (phenylephrine constricts superficial vessels only). [1]
| Episcleritis | Scleritis | |
|---|---|---|
| Pain | Mild, tender | Dull, deep, boring ache (may wake from sleep) |
| Redness | Bright red/salmon pink, sectoral | Deep violaceous/blue-red |
| Phenylephrine 2.5% | Blanches (superficial vessels constrict) | Does NOT blanch (deep scleral vessels) |
| Vision | Normal | May be affected (posterior scleritis) |
| Systemic association | Rare (< 30%) | Up to 50% |
| Treatment | Observation, topical lubricants, oral NSAIDs if needed | Oral NSAIDs → systemic steroids → immunosuppressants |
Why phenylephrine works as a test: Phenylephrine is an alpha-1 adrenergic agonist that constricts superficial (episcleral) vessels. In episcleritis, the superficial vessels are inflamed and dilated — they constrict with phenylephrine → redness fades. In scleritis, the deep scleral vessels are inflamed — these are not reached by topical phenylephrine → redness persists.
Systemic associations in up to 50% (e.g. rheumatoid arthritis, relapsing polychondritis, Wegener's, Polyarteritis nodosa). No known HLA association. Other causes: Infective (e.g. TB, syphilis); Post surgery (e.g. pterygium surgery with beta-irradiation). [1]
Systemic work-up: [1]
- Blood pressure, body weight (systemic immunosuppressants)
- Baseline CBC, L/RFT
- Inflammatory markers: ESR, rheumatoid factor (RA), ANA (lupus), c-ANCA (Wegener's), p-ANCA (vasculitis, PAN)
- Hepatitis serology (steroid workup)
- VDRL (syphilis)
- Chest x-ray (steroid workup, TB)
Why this workup? Scleritis is frequently a manifestation of systemic autoimmune or vasculitic disease. Finding the underlying cause changes management dramatically (you may need long-term immunosuppression rather than just treating the eye).
Oral NSAIDs: first line. Corticosteroids (1mg/kg/day). Immunosuppressants. Biologics (e.g. infliximab). [1]
This follows a stepwise escalation:
- Oral NSAIDs (e.g. indomethacin, flurbiprofen) — works for mild/moderate
- Systemic corticosteroids (prednisolone 1 mg/kg/day) — for non-responsive or severe
- Steroid-sparing immunosuppressants (methotrexate, azathioprine, mycophenolate) — for chronic/recurrent or to facilitate steroid taper
- Biologics (infliximab, rituximab) — refractory cases
Note: Topical steroids alone are insufficient for scleritis (unlike episcleritis) because the inflammation is deep.
Case 6: Anterior Uveitis
25/M, OD redness × 3/7, no pain, mild BOV+. PMHx: Ankylosing spondylitis. [1]
Ciliary flush; AC cells; keratic precipitates (KPs). [1]
| Sign | What it is | Why |
|---|---|---|
| Ciliary flush | Circumcorneal injection | Deep ciliary vessel dilation from intraocular inflammation |
| AC cells | White cells floating in the anterior chamber (seen on slit lamp) | Inflammatory cells entering the aqueous from iris/ciliary body vessels (breakdown of blood-aqueous barrier) |
| Keratic precipitates (KPs) | Deposits on the corneal endothelium | Inflammatory cells (WBCs) settle on the inner corneal surface by gravity; small KPs → non-granulomatous; large mutton-fat KPs → granulomatous (TB, sarcoid) |
| Flare | Hazy aqueous (like a beam of light through smoke) | Protein leak from inflamed iris vessels |
| Posterior synechiae | Iris adhesions to the lens | Inflammatory exudate causes iris to stick to lens → irregular pupil |
Steroids: topical, local injection, systemic. Cycloplegics. [1]
- Topical steroids (e.g. prednisolone acetate 1% or dexamethasone 0.1%) — first-line to suppress inflammation
- Cycloplegics (e.g. cyclopentolate 1%, atropine 1%) — two purposes:
- Pain relief: the inflamed ciliary body is in spasm → cycloplegic relaxes it
- Prevent posterior synechiae: keeps the pupil dilated so iris doesn't stick to the lens
- Periocular/intravitreal injection — for refractory or posterior segment involvement
- Systemic steroids/immunosuppressants — for severe, bilateral, or recurrent cases
No routine or standard work-up for anterior uveitis. Many are isolated disease without systemic association. Some commonly suggested tests: VDRL (syphilis); TB (in endemic areas); Lumbo-sacral spine x-ray, HLA-B27 (if suspect AS). [1]
High Yield
HLA-B27-associated anterior uveitis is the most common identifiable cause of acute anterior uveitis. It is classically unilateral, acute, recurrent, non-granulomatous and associated with ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and IBD. The case specifically uses a young male with AS — classic exam presentation.
When to investigate:
- First episode, mild, unilateral → often no workup needed
- Recurrent, bilateral, granulomatous KPs, or systemic symptoms → full workup:
- HLA-B27, sacroiliac XR
- Chest XR + ACE level (sarcoidosis)
- VDRL/RPR (syphilis)
- Quantiferon/tuberculin test (TB)
- ANA (juvenile idiopathic arthritis in children)
The lecture shows a slide on acute post-operative endophthalmitis. [1]
This is an ophthalmic emergency — intraocular infection after surgery (most commonly after cataract surgery).
| Feature | Details |
|---|---|
| Timing | Usually 2–7 days post-op |
| Symptoms | Severe pain, rapid vision loss, red eye |
| Signs | Lid swelling, hypopyon (pus in AC), vitritis (hazy vitreous), reduced/absent red reflex |
| Common organisms | Coagulase-negative Staphylococci (most common), S. aureus, Streptococci, Gram-negatives |
| Management | Vitreous tap/biopsy + intravitreal antibiotics (vancomycin + ceftazidime); may need vitrectomy |
RED FLAGS: Ocular pain; Decreased vision; Photophobia; Ciliary injection; Corneal clouding/opacities; Abnormal pupil; High IOP. [1]
RED FLAGS for Urgent Ophthalmology Referral
Any of the following in a red eye mandates urgent specialist assessment:
- Ocular pain — suggests intraocular or corneal pathology
- Decreased vision — the eye is threatened
- Photophobia — suggests anterior segment inflammation (uveitis, keratitis)
- Ciliary injection — indicates deep anterior segment inflammation
- Corneal clouding/opacities — keratitis, corneal oedema from high IOP
- Abnormal pupil — fixed mid-dilated (angle closure), irregular (posterior synechiae/uveitis)
- High IOP — acute angle closure or secondary glaucoma
If ANY red flag is present, the patient should NOT be managed in primary care and needs same-day ophthalmology referral.
| Condition | Pain | Vision | Redness Pattern | Pupil | Discharge | Key Feature | Urgency |
|---|---|---|---|---|---|---|---|
| SCH | None | Normal | Sectoral, bright red | Normal | None | Painless, homogeneous red patch | Benign |
| Viral conjunctivitis | Mild/gritty | Normal | Diffuse | Normal | Watery | Follicles, preauricular LN, recent URTI | Benign |
| Bacterial conjunctivitis | Mild | Normal | Diffuse | Normal | Purulent | Papillae, crusting | Non-urgent |
| Allergic conjunctivitis | Itch > > pain | Normal | Diffuse | Normal | Ropy/mucoid | Papillae, bilateral, atopy | Non-urgent |
| Episcleritis | Mild tender | Normal | Sectoral | Normal | None | Blanches with phenylephrine | Non-urgent |
| Scleritis | Deep, severe | May ↓ | Sectoral, deep violaceous | Normal | None | Non-blanchable, systemic associations | Urgent |
| Anterior uveitis | Ache, photophobia | Mildly ↓ | Ciliary flush | Small (miosis) or irregular | None | AC cells, KPs, HLA-B27 | Urgent |
| Acute angle closure | Severe | Markedly ↓ | Ciliary + diffuse | Fixed mid-dilated | None | Corneal haze, shallow AC, very high IOP | EMERGENCY |
| Microbial keratitis | Severe | ↓ | Diffuse (severe) | Normal or small | Variable | Corneal infiltrate/ulcer, CL history | EMERGENCY |
| Endophthalmitis | Severe | Markedly ↓ | Diffuse | Variable | Hypopyon | Post-surgical, loss of red reflex | EMERGENCY |
Integration with Related Lectures
The 2022 MCQ asked about mucin production in tears:
Tear fluid layer: mucin, aqueous, lipid. Mucin is produced by conjunctival goblet cells. Aqueous by the lacrimal gland. Lipid by Meibomian (tarsal) glands. [4]
Q13 from 2021 MCQ: Patient on hydroxychloroquine for 8 years → bilateral progressive blurring → Bull's eye maculopathy (answer C). [3]
This is not a "red eye" per se but tests knowledge of drug-related eye toxicity in the ophthalmology module. Hydroxychloroquine accumulates in the retinal pigment epithelium → photoreceptor damage → characteristic bull's eye pattern on fundoscopy. Screening: baseline eye exam, then annually after 5 years.
Q14 from 2021 MCQ: Bilateral red eyes, itchy, watery discharge, recent cold, enlarged preauricular LN → Most common organism = Adenovirus species (answer B). [3]
From the lecture history: thyroid disease as a systemic cause. Graves' ophthalmopathy causes proptosis, lid retraction, exposure keratopathy, and restrictive strabismus — can present as red eye from corneal exposure.
Exam Intelligence
| Trap | Correct Thinking |
|---|---|
| Mistaking APAC for migraine/acute abdomen | APAC causes nausea/vomiting and frontal headache — always check pupils and IOP in elderly patients with "headache + vomiting" |
| Giving steroids for dendritic HSV ulcer | Contraindicated — worsens epithelial disease. Steroids only for stromal/disciform keratitis |
| Treating scleritis with topical steroids alone | Scleritis needs systemic NSAIDs/steroids; topical alone is insufficient for deep inflammation |
| Assuming all red eyes need antibiotics | Most are viral or benign — only bacterial conjunctivitis/keratitis needs antibiotics |
| Confusing episcleritis and scleritis | Use phenylephrine test: blanching = episcleritis (benign); non-blanching = scleritis (serious) |
| Missing APAC in hyperopes on cold medications | Antihistamines/decongestants cause pupil dilation → trigger angle closure in anatomically predisposed eyes |
| Forgetting to check the fellow eye in APAC | Prophylactic PI to fellow eye is standard of care |
| CL-related keratitis: only thinking of bacteria | Must also consider Acanthamoeba (especially if water exposure) and Pseudomonas |
- Distribution of redness → diagnosis mapping (ciliary = uveitis/glaucoma; sectoral = SCH/scleritis; diffuse = conjunctivitis)
- Papillae vs follicles → allergic vs viral
- APAC management — the drug names, classes, and their mechanisms
- Risk factors for APAC — hypermetropia, thick lens, medications
- Red flags requiring urgent referral
- Organisms by risk factor — CL = Pseudomonas/Acanthamoeba; plant = fungus
- Scleritis workup — the autoimmune panel
- HLA-B27 and anterior uveitis
Past Paper Questions
Stem: "A 54-year-old lady with systemic lupus erythematosus on hydroxychloroquine for 8 years complains of bilateral progressive blurring of vision over the past 9 months. Which of the following conditions is the MOST LIKELY cause of her visual loss? A. Acute angle closure. B. Anterior uveitis. C. Bull's eye maculopathy. D. Central retinal vein occlusion."
Answer: C. Bull's eye maculopathy.
- Rationale: Hydroxychloroquine is toxic to the retinal pigment epithelium. After prolonged use ( > 5 years), it causes a characteristic "bull's eye" pattern of macular damage → bilateral progressive visual loss.
- Discriminators: Acute angle closure → sudden onset, painful (not progressive over months). Anterior uveitis → would cause pain/photophobia. CRVO → sudden unilateral loss.
Stem: "Mr. Chan, a 30-year-old gentleman, visits your clinic for bilateral redness of his eyes for 3 days. The redness started in the left eye and in 2 days the right eye was also involved. His eyes were itchy with watery discharge. He had an episode of common cold a week ago. On clinical examination, you noted enlarged preauricular lymph nodes. What is the MOST COMMON organism causing his eye problem? A. Acanthamoeba. B. Adenovirus species. C. Chlamydia trachomatis. D. Staphylococcus aureus."
Answer: B. Adenovirus species.
- Rationale: Classic viral conjunctivitis: bilateral sequential involvement, watery discharge, recent URTI, preauricular lymphadenopathy → adenovirus.
- Discriminators: Acanthamoeba → keratitis in CL wearers, not conjunctivitis. Chlamydia → chronic, follicles, no URTI link. S. aureus → purulent discharge, not watery.
Stem: "Tear fluid layer is composed of the mucin, aqueous, and lipid. Dry eye disease can be the result of abnormality in the production of anyone or combination of the tear composition. Which of the following structures is responsible for the production of mucin in the tear fluid layer? A. Conjunctival goblet cells. B. Lacrimal gland. C. Meibomian gland. D. Tarsal gland."
Answer: A. Conjunctival goblet cells.
- Rationale: The three-layer tear film: inner mucin (conjunctival goblet cells) → middle aqueous (lacrimal gland) → outer lipid (Meibomian/tarsal glands). Note Meibomian gland = tarsal gland (same structure, two names — both are distractors for the lipid layer).
Stem (excerpt): "A 69-year-old gentleman... drooping of left eyelid, double vision and unsteady gait... left partial ptosis with reactive and equal pupils, impairment of left eye adduction, upward and downward gaze... (a) What are the cranial nerves responsible for extraocular eye movements?"
Answer: CN III (oculomotor), CN IV (trochlear), CN VI (abducens).
- This tests fundamental neuro-ophthalmology knowledge relevant to the red eye exam because CN III palsy (with pupil involvement) can present with a red eye and must be distinguished from other causes.
Stem: "A 30-year-old woman presented with a feeling of sand in her eyes and xerostomia for several months. You ordered a panel of tests, and anti-Ro and anti-La antibodies both came back positive..."
Relevance: This is Sjögren's syndrome → dry eye (keratoconjunctivitis sicca). While the question focuses on RTA, the "sand in eyes" presentation connects to dry eye differential in the red eye workup. Anti-Ro/Anti-La → Sjögren's → dry eye.
High Yield Summary
Red Eye Key Takeaways for the Exam:
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Distribution of redness is your primary triage tool: ciliary → uveitis/APAC; sectoral → SCH/scleritis/episcleritis; diffuse → conjunctivitis/keratitis/endophthalmitis.
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Red flags = urgent referral: pain, ↓vision, photophobia, ciliary injection, corneal opacity, abnormal pupil, high IOP.
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APAC emergency management: Pilocarpine (miosis), Timolol (↓aqueous), Apraclonidine (↓aqueous), IV Acetazolamide (↓aqueous), IV Mannitol (osmotic). Definitive = peripheral iridotomy. Always treat fellow eye prophylactically.
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Papillae (central vascular core) = allergic/mechanical. Follicles (lymphoid, vessels at base) = viral/toxic/chlamydial.
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Phenylephrine blanching test: blanches = episcleritis (benign); doesn't blanch = scleritis (serious, workup needed).
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Scleritis has systemic associations in up to 50% — needs autoimmune workup (RF, ANA, ANCA, VDRL, CXR).
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CL-related keratitis: Pseudomonas and Acanthamoeba. Management = corneal scraping + intensive empirical broad-spectrum antibiotics q1h.
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HSV keratitis is a clinical diagnosis (dendritic ulcer is pathognomonic). Treat with antivirals. NEVER steroids for epithelial disease.
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Anterior uveitis associated with HLA-B27/AS. Treat with topical steroids + cycloplegics. No routine workup unless recurrent/atypical.
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Adenovirus is the most common cause of viral conjunctivitis.
Active Recall - The Red Eye
[1] Lecture slides: GC 125. The Red Eye.pdf (all pages) [2] Senior notes: Ryan Ho Opthalmology.pdf (p16 - Approach to the Red Eye; p74 - Pupillary disorders; p117 - Refractive error) [3] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (Q13, Q14) [4] Past papers: 2022 Fourth Summative MCQ.pdf (Q15) [5] Past papers: 2021 Fourth Summative SAQ.pdf (Q6) [6] Past papers: 2017 Fourth Summative SAQ.pdf (Q3) [7] Senior notes: Ryan Ho Fundamentals.pdf (p182-188 - Examination of the Eye) [8] AOS material: AOS - Ophthalmology.pdf (p17) [9] Senior notes: Block A - Deterioration of eyesight in a diabetic patient_ diabetic complications.pdf (p1)
GC124 Neuro Ophthalmology
Neuro-ophthalmology is the subspecialty concerned with visual disturbances arising from disorders of the central and peripheral nervous system, including optic nerve diseases, cranial nerve palsies, pupillary abnormalities, and disorders of ocular motility.
GC126 Trauma And Ocular Emergency
Acute ophthalmic conditions resulting from mechanical, chemical, or thermal injury to the eye and adnexa, or non-traumatic emergencies such as acute glaucoma, retinal detachment, or central retinal artery occlusion, requiring urgent evaluation and management to preserve vision.