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.
Safety rule
Do not let the redness pattern overrule the red flags. Measure IOP only when it is safe and within your competence; avoid tonometry if an open globe is possible. A contact-lens wearer with pain, photophobia or reduced vision is not routine conjunctivitis.
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 | Transparent mucous membrane reflected from the inner lids (palpebral) onto the globe (bulbar); it ends at the limbus | Conjunctivitis → superficial diffuse injection; SCH remains outside the cornea |
| 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 |
How to read the lecture's surface diagram: the palpebral and bulbar conjunctiva are one continuous sheet folded at the fornix. The cornea interrupts that sheet at the limbus. Aqueous made behind the iris normally passes through the pupil, then leaves the anterior chamber through the trabecular meshwork and Schlemm canal at the iridocorneal angle. These two boundaries explain why subconjunctival blood respects the limbus and why forward bowing of peripheral iris can obstruct aqueous drainage.
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, one eye at a time and with the patient's usual distance correction. Use pinhole if reduced (improvement suggests a refractive component). Reduced VA in a red eye is serious until proved otherwise.
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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).
-
Cornea and anterior chamber — Use a bright light/slit lamp if available. Look for loss of corneal clarity, a focal white infiltrate, an epithelial defect after fluorescein, cells/flare or hypopyon. Evert the upper lid when a retained foreign body is plausible.
-
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 |
-
IOP and angle assessment — Tonometry and gonioscopy refine suspected glaucoma, but only after open globe has been excluded; gonioscopy is a trained examination. A hard globe by digital palpation is neither a safe nor reliable substitute for tonometry.
-
Associated signs — Corneal opacity (keratitis, angle-closure oedema), mass (pterygium, tumour), discharge (type helps differentiate conjunctivitis subtypes), lid vesicles and preauricular lymph nodes.
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.
Reading the case photograph: identify a flat, homogeneous red sheet rather than branching dilated vessels. Its sharp edge and respect for the limbus distinguish extravasated blood from injection. The cornea remains clear and the pupil looks normal. In a spontaneous SCH, visual acuity should also be normal.
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 usually benign. It commonly changes colour like a bruise and clears over roughly 1–3 weeks. Review blood pressure and relevant medication/bleeding history; do not stop prescribed antiplatelet or anticoagulant therapy solely because of an uncomplicated SCH without discussing the indication. Recurrent, bilateral or otherwise unexplained haemorrhage warrants targeted assessment.
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. Pain, reduced vision, significant trauma, a peaked/irregular pupil, a bullous or 360° haemorrhage, or inability to see the posterior limit should trigger urgent assessment for deeper injury rather than routine reassurance.
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.
Reading the second case photograph: the pale sheet on the intensely inflamed tarsal conjunctiva is a pseudomembrane, not ordinary discharge. It can occur in severe adenoviral keratoconjunctivitis; marked pain, photophobia, reduced vision, corneal involvement or membrane formation warrants ophthalmic assessment. A true adherent membrane may bleed when disturbed, so removal and any anti-inflammatory treatment belong under specialist direction.
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; meticulous hand/towel hygiene and no shared eye products | Often self-limiting; topical antibiotic only when clinically indicated/local protocol supports it | Allergen avoidance, cool compresses, topical dual-action antihistamine/mast-cell stabiliser |
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) |
How to read the two lecture images:
- Papillae give the everted tarsal conjunctiva a red, polygonal/cobblestone surface. Each projection has a vessel rising through its centre; the histology diagram therefore shows a central vascular core separated by septa.
- Follicles are paler, round, dome-shaped elevations. Vessels skirt their base rather than entering the centre; the histology diagram shows a subepithelial lymphoid aggregate/germinal centre.
Why this matters: Follicles favour viral, chlamydial or toxic conjunctivitis; papillae favour allergic, bacterial or mechanical disease. Neither sign is diagnostic in isolation—interpret it with discharge, chronicity, contact-lens use and corneal findings.
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.
Do not label every sticky red eye as conjunctivitis
Hyperacute copious purulence, corneal involvement, contact-lens use, pain, photophobia or reduced vision needs urgent ophthalmic assessment. Stop contact lenses immediately. Gonococcal disease is a systemic-treatment emergency; a painful contact-lens red eye is microbial keratitis until excluded.
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 — relative pupil block: [1]
The ciliary body produces aqueous behind the iris. It normally crosses the pupil into the anterior chamber and drains through the trabecular meshwork at the iridocorneal angle. In a crowded anterior segment, resistance between the posterior iris and anterior lens creates a posterior-to-anterior pressure gradient: the iris bows forward (iris bombé) → its periphery covers the trabecular meshwork → aqueous outflow collapses → IOP rises rapidly.
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 an intermediate pupil diameter, iris–lens contact and peripheral iris crowding can be greatest. Dim light and anticholinergic or sympathomimetic medicines can therefore precipitate an attack in an anatomically susceptible eye. Do not try to reproduce this diagnostically by dilating a suspected narrow-angle eye.
| Slide image | What to identify | What it means |
|---|---|---|
| Open-versus-closed cross-section | In the open eye, the peripheral iris leaves the red trabecular meshwork exposed. In the closed eye, the iris bows forward and lies against it | The problem is outflow obstruction at the angle, not overproduction of aqueous |
| Oblique slit-beam photographs | A broad dark gap between corneal and iris reflections indicates a deep chamber; a very narrow gap indicates a shallow chamber | A shallow chamber supports angle crowding, but gonioscopy confirms angle status |
| Acute case photograph | Diffuse/ciliary injection, steamy corneal haze and a larger poorly reactive pupil in the symptomatic eye | Corneal oedema explains blur/haloes; the abnormal pupil plus pain/vomiting is an emergency pattern |
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 | Confirmed with tonometry after open globe has been excluded; gonioscopy later establishes the mechanism |
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 from the lecture | Class | Role and safety qualification |
|---|---|---|
| Pilocarpine 4% (lecture-era/local slide dose) | Cholinergic (muscarinic) agonist | Miosis helps relieve primary pupil-block closure, but defer it while IOP is > 40 mmHg because the ischaemic iris may not respond. The current RCOphth pathway specifies 2%, once appropriate; pilocarpine is unsuitable in lens/retrolenticular and topiramate-related closure [10] |
| Timolol 0.5% | Topical beta-blocker | Suppresses aqueous production; avoid or seek an alternative in asthma/bronchospasm, marked bradycardia or heart block |
| Apraclonidine 0.5% | Topical alpha-2 agonist | Suppresses aqueous production and augments outflow; check cardiovascular and medication contraindications |
| Systemic acetazolamide (slide: 500 mg IV) | Carbonic anhydrase inhibitor | Rapid aqueous suppression; route and repeat dosing depend on the patient, renal function and local emergency protocol |
| Mannitol 20% (slide: 200 mL IV) | Hyperosmotic agent | An escalation option when pressure remains very high; actual dosing is weight/clinical-status based and it may be unsafe in cardiac or renal failure |
Practical sequence: call ophthalmology immediately; give analgesia and an antiemetic, confirm that this is a primary pupillary-block/plateau-iris mechanism and check contraindications. Start combined pressure-lowering treatment without delaying definitive care, then recheck IOP and systemic observations after 30-60 minutes. The current RCOphth pathway uses topical aqueous suppressants and systemic acetazolamide when IOP is > 40 mmHg, deferring pilocarpine until IOP has fallen to 40 mmHg or below; proceed to laser iridotomy in both eyes as soon as the cornea and patient permit [10].
Exam Trap
Pilocarpine is not a stand-alone rescue drug. At IOP > 40 mmHg, defer it while the ischaemic iris sphincter is unlikely to respond; lower pressure first with appropriate aqueous suppressants/systemic therapy. More importantly, confirm the mechanism: secondary angle closure from lens/retrolenticular causes or topiramate-related uveal effusion is managed differently and can be worsened by pilocarpine [10].
Peripheral iridotomy: provide alternative pathway for aqueous flow. Lens extraction: to open up angle. Fellow eye: prophylaxis. [1]
- Laser peripheral iridotomy (LPI): creates a small peripheral opening, bypassing the pupil and equalising pressure across the iris. On the post-treatment photograph, the small dark opening is placed superiorly/peripherally rather than in the visual axis.
- Lens extraction: deepens the chamber and opens the angle. In an acute presentation it is generally considered after the IOP is controlled and the cornea is clear; timing depends on cataract, residual angle closure and specialist assessment. [10]
- Fellow eye: shares the anatomical risk and requires prompt gonioscopic assessment; bilateral LPI is generally performed after the acute attack is controlled when pupil block is the mechanism. [10]
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.
Reading the case photograph: the yellow-green focal spot is on the cornea, not conjunctival discharge. It represents a stromal infiltrate with an overlying fluorescein-staining epithelial defect; surrounding ciliary/conjunctival injection marks inflammation. A focal corneal white spot plus pain and reduced vision in a contact-lens wearer is microbial keratitis until proved otherwise.
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)
Modern qualification: this is a same-day ophthalmic emergency. Stop and retain the contact lenses, case and solution for possible culture. Scraping is especially indicated for a large, central, deep, atypical, chronic, sight-threatening or treatment-unresponsive ulcer; a small peripheral low-risk infiltrate may be treated empirically after specialist assessment. Do not delay initial intensive topical antimicrobial therapy in a severe ulcer while awaiting results. [11]
Why scrape selected ulcers? Microbial keratitis can be bacterial, fungal or amoebic, and organism identification changes treatment. The specimen should come from the active edge/base before antibiotics where feasible, but treatment urgency takes priority.
Why "fortified"? Pharmacy-compounded high-concentration drops are used for severe or vision-threatening bacterial ulcers. Fluoroquinolone monotherapy may be suitable for selected less severe disease; choice depends on ulcer severity, local resistance and culture results. Therapy is reassessed closely—often daily at first. [11]
Immediate safeguards
Remove contact lenses, do not patch the eye, and do not start topical steroid independently. Steroid may occasionally be added by a corneal specialist only after effective antimicrobial therapy and a demonstrated response; avoid it when fungal, Acanthamoeba or Nocardia infection is possible. [11]
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 | Rapid stromal necrosis/melt; do not rely on discharge colour |
| 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 |
| Compromised surface/older patient | Staphylococcus spp. (including coagulase-negative staphylococci), Streptococcus spp. | Common bacterial pathogens; the slide's phrase “coagulase-negative streptococci” should read staphylococci |
High Yield
Acanthamoeba keratitis classically raises suspicion when pain is disproportionate, water exposure occurred in a contact-lens wearer, or perineural/ring infiltrates develop. Early appearances can be nonspecific and the ring is often late. Treatment requires prolonged specialist anti-amoebic therapy; routine antibacterial drops alone are inadequate.
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 | Fine branching epithelial defect with dichotomous branches and terminal bulbs | The ulcer bed stains green with fluorescein; swollen virus-infected edge cells stain with rose bengal/lissamine green |
| Geographic ulcer | Broad map-like epithelial defect with scalloped/amoeboid borders | Enlarged or coalescent epithelial HSV ulcer; risk is increased by topical steroid exposure, immunocompromise or atopy |
Reading the fluorescein slide: image A is dendritic—trace the narrow branching lines and look for bulbous endpoints. Image B is geographic—a single broad irregular green defect. Fluorescein marks absent epithelium, so the bright area is the ulcer bed, not the virus itself. Terminal bulbs help distinguish HSV from a herpes-zoster pseudodendrite. [12]
Key points:
- Clinical diagnosis — a true dendrite with terminal bulbs is highly characteristic of HSV; testing is reserved for atypical, severe or uncertain cases.
- Do not give topical steroid for active epithelial HSV. It promotes enlargement to a geographic ulcer and delays epithelial healing.
- 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 active epithelial HSV keratitis (dendritic/geographic ulcer). A specialist may use steroid for stromal/endothelial disease with antiviral cover; that does not make steroid appropriate for an undifferentiated red eye. [12]
Case 5: Scleritis
40/M, OS redness × 3/7, dull aching pain+, no BOV. PMHx: unremarkable. Non-blanchable with 2.5% phenylephrine. [1]
Reading the case photograph: look beyond “sectoral redness.” The vessels are deep, tortuous and cross one another; the background has a dusky red/violaceous quality rather than the salmon-pink superficial network of episcleritis. Severe boring pain, globe tenderness and pain waking the patient or radiating to the face are more dependable triage clues than colour alone.
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 | Less frequent | Common enough to require directed review; the lecture quotes up to 50% |
| Treatment | Observation/lubricants; oral NSAID if required after diagnosis | Urgent ophthalmology; systemic anti-inflammatory or immunosuppressive therapy according to subtype/cause |
Why phenylephrine works as a test: phenylephrine constricts superficial vessels, so the lecture's paired photographs show marked blanching in episcleritis while the deep congestion of scleritis persists. Treat this as an ophthalmic examination aid, not a self-test or a substitute for assessing pain, vessel depth and the sclera at the slit lamp. Do not use blanching alone to reassure a patient with red flags.
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]
Current terminology: “Wegener's” is now granulomatosis with polyangiitis (GPA). The lecture's “p-ANCA (PAN)” linkage is misleading: classic polyarteritis nodosa is usually ANCA-negative; p-ANCA/MPO-ANCA more strongly supports microscopic polyangiitis and related small-vessel vasculitides.
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)
How to use this list: it is a menu, not a mandatory shotgun panel. History and examination should look for inflammatory arthritis, ENT/renal/pulmonary vasculitis, relapsing cartilage inflammation, infection, prior ocular surgery and immunosuppression; investigations are then targeted with ophthalmology/rheumatology or infectious-disease input. Always consider infectious scleritis before escalating immunosuppression.
Oral NSAIDs: first line. Corticosteroids (1mg/kg/day). Immunosuppressants. Biologics (e.g. infliximab). [1]
The slide summarises an escalation ladder, but treatment is subtype- and cause-dependent:
- Non-necrotising, non-infectious anterior scleritis: an oral NSAID may be appropriate after ophthalmic assessment.
- Severe, necrotising, posterior or NSAID-unresponsive disease: systemic glucocorticoid and early steroid-sparing therapy may be needed; the slide's 1 mg/kg/day is a specialist dose, not a universal prescription.
- Associated vasculitis or refractory disease: immunomodulator/biologic choice is coordinated with rheumatology.
- Infectious scleritis: antimicrobial and sometimes surgical treatment; immunosuppression without antimicrobial control can be disastrous.
Note: topical steroid alone is insufficient for scleritis because the inflammation is deep. Necrotising disease threatens globe integrity and requires emergency specialist care.
Case 6: Anterior Uveitis
25/M, OD redness × 3/7, no pain, mild BOV+. PMHx: Ankylosing spondylitis. [1]
The painless wording is deliberate: pain and photophobia are common in acute anterior uveitis, but their absence does not exclude it. The lecture image is a slit-lamp view—tiny white deposits on the posterior corneal surface are keratic precipitates, while inflammatory cells are seen as moving particles in the illuminated anterior-chamber beam.
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) | Inflammatory-cell deposits on corneal endothelium, often inferiorly distributed | Fine KPs favour a non-granulomatous pattern; large greasy “mutton-fat” KPs favour granulomatous inflammation but are not disease-specific |
| 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 — first-line after slit-lamp confirmation by ophthalmology; epithelial HSV and microbial keratitis must be excluded first
- 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
Before prescribing a steroid drop
An undifferentiated painful red eye with a corneal epithelial defect is not presumed uveitis. Fluorescein examination and ophthalmic assessment are essential because topical steroid can accelerate epithelial HSV, fungal or amoebic keratitis. Treatment intensity and taper are guided by anterior-chamber activity and IOP.
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:
- A first, mild, unilateral, clearly non-granulomatous episode in a systemically well adult often needs no broad laboratory panel.
- Recurrent, bilateral, granulomatous, treatment-resistant or atypical disease, posterior involvement, or systemic clues merits a targeted work-up. Depending on phenotype this can include syphilis serology, TB testing, HLA-B27 assessment, chest imaging for sarcoidosis/TB, or paediatric ANA assessment; a normal ACE level neither confirms nor excludes ocular sarcoidosis.
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 | Often during the first postoperative week, but any recent intraocular surgery or injection remains relevant; severe pain or visual loss within 2 weeks is an emergency presentation [14] |
| Symptoms | Rapid visual deterioration and redness; pain is common but can be mild or absent, so its absence does not reassure |
| 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 | Immediate ophthalmic sampling and intravitreal antimicrobial treatment; vitrectomy is considered according to vision, severity and specialist protocol |
Reading the image-heavy slide: the left photograph shows a horizontal white hypopyon—inflammatory material layering inferiorly in the anterior chamber—plus a markedly inflamed eye. The right B-scan ultrasound shows mobile/dense echoes within the normally dark vitreous, supporting vitritis when the fundus view is obscured.
Endophthalmitis is time-critical
Pain and reduced vision after intraocular surgery or injection—especially with hypopyon or loss of the red reflex—requires immediate same-day ophthalmic treatment. Do not discharge with topical antibiotics alone and do not delay intravitreal therapy while waiting for culture results.
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:
- Moderate/severe ocular pain or marked tenderness — suggests intraocular, corneal or scleral pathology
- Decreased vision — the eye is threatened
- True/consensual 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
Also escalate major trauma/chemical exposure, possible open globe, a painful contact-lens red eye, proptosis or restricted eye movements, and pain/vision loss after ocular surgery or injection. The urgency ranges from same-day review to immediate emergency transfer; begin time-critical first aid (for example copious irrigation for chemical injury) while arranging help.
| 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/gritty | Normal | Diffuse | Normal | Purulent | Mattering/crusting; hyperacute copious discharge is different | Usually non-urgent; urgent if hyperacute, CL wearer or corneal signs |
| Allergic conjunctivitis | Itch > > pain | Normal | Diffuse | Normal | Ropy/mucoid | Papillae, bilateral, atopy | Non-urgent |
| Episcleritis | Mild discomfort/tenderness | Normal | Sectoral, superficial salmon-pink vessels | Normal | None | Superficial vessels may blanch on specialist examination | Usually non-urgent after diagnosis |
| Scleritis | Deep, severe, boring | May ↓ | Deep violaceous vessels, sectoral or diffuse | Usually normal | None | Globe tenderness; deep vessels do not blanch | 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 | Often severe; may be disproportionate in Acanthamoeba | ↓ | Ciliary/diffuse | Normal or small | Variable | Focal corneal infiltrate + epithelial defect; 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 drug-related retinal toxicity. A visible bull's-eye maculopathy is a late manifestation; modern screening aims to detect parafoveal or pericentral outer-retinal damage before fundus changes or symptoms. The 2025 AAO revision advises a baseline examination soon after starting hydroxychloroquine, including fundus examination, OCT and wide-pattern fundus autofluorescence, with annual OCT/FAF thereafter; annual testing may be deferred during the first 5 years only when dose is appropriate and no major risk factor is present. Screening should cover both parafoveal and pericentral patterns, particularly in East Asian patients. Follow the local monitoring programme and coordinate any treatment change with the prescriber rather than stopping hydroxychloroquine on one equivocal result [13].
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 | Prioritise pain, tenderness, deep violaceous vessels and specialist slit-lamp assessment; phenylephrine blanching is an adjunct, not a sole triage test |
| 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 — immediate combined pressure lowering, mechanism-specific pilocarpine, prompt ophthalmology and definitive LPI
- Risk factors for APAC — hypermetropia, thick lens, medications
- Red flags requiring urgent referral
- Organisms by risk factor — CL = Pseudomonas/Acanthamoeba; plant = fungus
- Scleritis workup — directed systemic and infectious assessment rather than an indiscriminate autoimmune panel
- HLA-B27 and anterior uveitis
High Yield Summary
- Red Eye Key Takeaways for the Exam
- Triage before diagnosis: visual acuity, pain/photophobia, pupil and corneal clarity outrank redness pattern. Avoid tonometry if open globe is possible.
- Redness pattern: ciliary → uveitis/APAC/keratitis; sectoral → SCH/episcleritis/scleritis/trauma; diffuse → conjunctivitis or severe intraocular/corneal disease.
- Red flags: reduced vision, significant pain, true photophobia, ciliary injection, corneal opacity/defect, abnormal pupil, high IOP, trauma, contact-lens risk or recent ocular procedure.
- APAC: hazy cornea + fixed mid-dilated pupil + shallow chamber + high IOP. Begin combined IOP lowering with immediate ophthalmic input; LPI treats pupil block and the fellow eye also needs assessment/prophylaxis.
- Papillae have a central vascular core; follicles are pale lymphoid domes with vessels at the base.
- Scleritis: deep boring pain/tenderness and violaceous deep vessels; urgent review and directed systemic/infectious assessment. Phenylephrine blanching is only an examination adjunct.
- Contact-lens keratitis: think Pseudomonas and Acanthamoeba. Stop lenses, arrange same-day scraping when indicated and intensive specialist-directed topical therapy.
- HSV epithelial keratitis: dendrite with terminal bulbs or geographic ulcer. Antiviral treatment; no topical steroid in active epithelial disease.
- Anterior uveitis: ciliary flush, AC cells and KPs. Ophthalmic steroid + cycloplegic treatment after corneal infection has been excluded; work-up is phenotype-directed.
- Endophthalmitis: postoperative pain/vision loss, hypopyon and vitritis → immediate sampling plus intravitreal therapy.
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) [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) [10] Royal College of Ophthalmologists. The Management of Angle-Closure Glaucoma: Clinical Guidelines. 2022. https://www.rcophth.ac.uk/wp-content/uploads/2021/10/The-Management-of-Angle-Closure-Glaucoma-Clinical-Guidelines.pdf [11] Lin A, Rhee MK, Akpek EK, et al. Bacterial Keratitis Preferred Practice Pattern®. Ophthalmology. 2019;126(1):P1–P55. doi:10.1016/j.ophtha.2018.10.018. [12] American Academy of Ophthalmology EyeWiki. Herpes Simplex Virus Keratitis. https://eyewiki.aao.org/Herpes_Simplex_Virus_Keratitis [13] Marmor MF, Ahn SJ, Ehlers JP, et al; American Academy of Ophthalmology. Special AAO Report: Recommendations on Screening for Hydroxychloroquine Retinopathy (2025 Revision). Ophthalmology. 2026;133(4):439-450. doi:10.1016/j.ophtha.2025.11.001. [14] Royal College of Ophthalmologists. Emergency Eye Care Commissioning Guidance. 2020.
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.