Red eye is a common clinical sign characterized by hyperemia of the conjunctival, episcleral, or ciliary vessels due to a wide range of conditions including conjunctivitis, uveitis, acute glaucoma, corneal disorders, or subconjunctival hemorrhage.

Red Eye

Red eye refers to hyperaemia (redness) of the eye due to dilation of the conjunctival, episcleral, or scleral blood vessels — or, less commonly, haemorrhage beneath the conjunctiva. It is one of the most common ophthalmic presentations in primary care and emergency departments. The term itself is a clinical sign, not a diagnosis; the critical task is to distinguish benign, self-limiting causes (e.g. subconjunctival haemorrhage, mild allergic conjunctivitis) from sight-threatening or serious causes (e.g. acute angle-closure glaucoma, keratitis, scleritis, anterior uveitis) that require urgent ophthalmological referral ^[1]^[2]^[3].

"Red eye" is an extremely common presenting complaint. The key clinical skill is pattern recognition — distinguishing the 'safe red eye' from the 'dangerous red eye' based on the pattern of redness, presence/absence of pain, vision changes, pupil abnormalities, and corneal clarity. ^[1]^[2]

Core Principle

Not all red eyes are created equal. The approach is to risk-stratify: does this patient have features suggesting a sight-threatening cause? If so, urgent referral is needed. If not, most can be managed in primary care.

Epidemiology and Risk Factors

Red eye accounts for ~6% of all emergency department visits and is the most common ocular complaint in general practice worldwide.
In Hong Kong, the commonest causes seen in primary care are:
1. Conjunctivitis (viral > bacterial > allergic) — overwhelmingly the most frequent
2. Subconjunctival haemorrhage
3. Dry eye / blepharitis
4. Contact lens–related problems (keratitis, giant papillary conjunctivitis) — particularly relevant in Hong Kong where contact lens use is very prevalent (~30–40% of young adults)
5. Allergic conjunctivitis — Hong Kong's subtropical climate with high humidity and air pollution contributes
Serious causes (acute angle-closure glaucoma [AACG], anterior uveitis, scleritis, microbial keratitis) are less common but must not be missed.
Acute angle-closure glaucoma is more common in East Asians (including Chinese/Hong Kong population) due to shallower anterior chambers — this is a high-yield HKU exam point ^[1]^[4].

Condition	Key Risk Factors
Infective conjunctivitis	Close contact (schools, families), poor hand hygiene, swimming pools
Allergic conjunctivitis	Atopy (eczema, asthma, allergic rhinitis), seasonal allergens, air pollution
Microbial keratitis	Contact lens wear (especially overnight/extended wear), corneal trauma, dry eye, immunosuppression ^[1]^[2]
Anterior uveitis	HLA-B27 conditions (ankylosing spondylitis, IBD, psoriatic arthritis, reactive arthritis), sarcoidosis, Behçet's disease, TB, syphilis, herpes viruses
Acute angle-closure glaucoma	East Asian ethnicity, hypermetropia (long-sightedness → shorter axial length → shallow anterior chamber), female sex, older age (> 60), family history, pupil dilation (dim light, mydriatic drugs, anticholinergics)
Scleritis	Systemic autoimmune diseases (especially rheumatoid arthritis, GPA/Wegener's, SLE, relapsing polychondritis) ^[1]^[2]
Episcleritis	Young adults, occasionally associated with autoimmune conditions but often idiopathic
Subconjunctival haemorrhage	Hypertension, anticoagulant/antiplatelet use, Valsalva (coughing, straining, vomiting), trauma, bleeding diathesis
Dry eye	Elderly, female sex, Sjögren's syndrome, medications (antihistamines, antidepressants), screen time, post-LASIK

Anatomy and Function

Understanding the anatomy of the anterior eye is essential to localise the cause of a red eye.

Conjunctiva — A thin, transparent mucous membrane lining the inner eyelids (palpebral conjunctiva) and covering the anterior sclera (bulbar conjunctiva) up to the limbus. Rich in goblet cells (mucin production for tear film). Supplied by the posterior conjunctival arteries (branches of the ophthalmic artery).
- Inflammation here = conjunctivitis → diffuse redness, often with discharge
Episclera — A thin layer of loose connective tissue between the conjunctiva and sclera, containing the episcleral vascular plexus.
- Inflammation here = episcleritis → sectoral (localised) redness, mild discomfort, no vision threat
Sclera — The tough, white, outer fibrous coat of the eye (composed of type I collagen). Relatively avascular. Supplied by the deep episcleral plexus and anterior ciliary arteries.
- Inflammation here = scleritis → deep, boring pain; violaceous (blue-purple) hue; may be sight-threatening; associated with systemic autoimmune disease
Cornea — The transparent, avascular anterior structure that provides ~2/3 of the eye's refractive power. Five layers: epithelium → Bowman's membrane → stroma → Descemet's membrane → endothelium. Richly innervated by CN V₁ (ophthalmic branch of trigeminal) — hence corneal pathology is extremely painful and causes photophobia and tearing.
- Damage/infection here = keratitis / corneal ulcer / corneal abrasion / foreign body → pain, photophobia, ciliary injection
Anterior Chamber — Space between cornea and iris filled with aqueous humour. The trabecular meshwork at the iridocorneal angle drains aqueous.
- Blockage of drainage = acute angle-closure glaucoma → raised IOP → pain, red eye, blurred vision, haloes, fixed mid-dilated pupil
Uveal tract — Iris + ciliary body + choroid. The iris and ciliary body are the anterior uvea.
- Inflammation here = anterior uveitis (iritis/iridocyclitis) → ciliary flush, photophobia, pain, small pupil (miosis), cells/flare in anterior chamber

This is the single most important anatomical concept for red eye assessment:

Feature	Conjunctival injection	Ciliary (circumcorneal) injection
Vessels	Posterior conjunctival aa.	Anterior ciliary aa. (deep)
Location	Diffuse, worst in fornices, sparing limbus	Perilimbal (circumcorneal) — a ring of deep redness around the cornea
Colour	Bright red	Deep red / violaceous
Vessel movement	Vessels move with conjunctiva when you press on them	Vessels do NOT move (they are deep)
Blanching with phenylephrine 2.5%	Yes (superficial vessels constrict)	No (deep vessels do not respond)
Implies	Conjunctivitis, episcleritis, subconjunctival haemorrhage	Keratitis, anterior uveitis, acute angle-closure glaucoma, scleritis

The presence of ciliary (circumcorneal/perilimbal) injection is a RED FLAG — it suggests a deeper, more serious inflammatory process involving the cornea, uvea, or raised intraocular pressure. ^[1]^[2]^[3]

High Yield Anatomy Concept

Why does ciliary injection occur in uveitis/keratitis/AACG? The anterior ciliary arteries supply the iris, ciliary body, and deep cornea. When these structures are inflamed, their blood supply dilates → deep, circumcorneal flush that does not blanch with topical phenylephrine.

Three layers: lipid (meibomian glands) → aqueous (lacrimal gland) → mucin (goblet cells in conjunctiva)
Disruption → dry eye → chronic irritation → redness, foreign body sensation

Aetiology and Pathophysiology

The causes of red eye can be systematically organised by anatomical structure (outside → inside). Below, each aetiology is paired with its pathophysiological mechanism.

A. Eyelid and Adnexal Causes

Definition: Chronic inflammation of the eyelid margins
Types: Anterior (staphylococcal, seborrhoeic) vs posterior (meibomian gland dysfunction/MGD)
Pathophysiology: Bacterial colonisation (Staph. aureus) of lid margin → chronic low-grade inflammation → unstable tear film (lipid layer deficiency in MGD) → secondary ocular surface irritation → redness, burning, crusting
Why red eye? Chronic conjunctival inflammation secondary to lid margin disease and tear film instability

External hordeolum: Acute infection of the glands of Zeis or Moll (sebaceous/sweat glands at lash follicle) — essentially a lid margin abscess
Internal hordeolum: Acute infection of a meibomian gland — points internally
Pathophysiology: Usually Staph. aureus → localised abscess → tender, red swelling at lid margin

Definition: Chronic, sterile lipogranulomatous inflammation of an obstructed meibomian gland
Pathophysiology: Meibomian gland duct obstruction → retained lipid secretions → granulomatous foreign body reaction → painless, firm nodule
Not typically 'red eye' per se, but worth distinguishing from hordeolum

B. Conjunctival Causes

4. Conjunctivitis (Most Common Cause of Red Eye)

Conjunctivitis is the most common cause of red eye in primary care. ^[1]^[2]

General pathophysiology: Inflammation of the conjunctiva → vasodilation of posterior conjunctival vessels → diffuse injection (worst in fornices, sparing limbus) ± discharge ± chemosis (oedema of conjunctiva)

Most common cause of infective conjunctivitis ^[1]^[2]
Causative organisms: Adenovirus (most common; serotypes 3, 4, 7, 8, 19, 37), enterovirus, HSV, VZV
Pathophysiology: Direct viral invasion of conjunctival epithelium → immune response → lymphoid follicle formation on palpebral conjunctiva (follicular conjunctivitis) → watery discharge (serous exudate, not pus)
Key features: Watery discharge, follicular reaction (small, round, pale elevations on palpebral conjunctiva), pre-auricular lymphadenopathy (lymphatic drainage of conjunctiva → pre-auricular and submandibular nodes) ^[1]^[2]
Epidemic keratoconjunctivitis (EKC): Adenovirus 8, 19, 37 → severe form with corneal subepithelial infiltrates → can cause prolonged visual blur
Highly contagious — hand hygiene is critical ^[1]

Causative organisms: Staph. aureus (most common in adults), Strep. pneumoniae, H. influenzae (common in children), Moraxella
Hyperacute: Neisseria gonorrhoeae — extremely purulent, rapid progression, can perforate cornea within 24–48 hours → ophthalmological emergency ^[1]^[2]
Pathophysiology: Bacterial infection → neutrophilic infiltration → purulent (mucopurulent) discharge — this is what distinguishes it from viral (which is watery)
Key features: Mucopurulent discharge (lids stuck together in morning), papillary reaction on palpebral conjunctiva (papillae = red, polygonal elevations with central vessels — represent hyperplastic conjunctival epithelium with inflammatory infiltrate) ^[1]^[2]
Why papillae in bacterial but follicles in viral? Papillae form when inflammation is driven by a non-specific immune response (neutrophils, mast cells) — the conjunctival epithelium hyperplasia and the central fibrovascular core forms over existing conjunctival septae. Follicles form when there is a lymphocyte-predominant response — aggregates of lymphoid tissue form new germinal centres on the conjunctiva.

Common in Hong Kong due to subtropical climate, dust mites, air pollution ^[1]
Types: Seasonal allergic conjunctivitis (SAC), perennial allergic conjunctivitis (PAC), vernal keratoconjunctivitis (VKC — children, giant papillae), atopic keratoconjunctivitis (AKC — adults with atopic dermatitis)
Pathophysiology: Type I (IgE-mediated) hypersensitivity → allergen cross-links IgE on mast cells in conjunctival substantia propria → mast cell degranulation → histamine, tryptase, prostaglandins, leukotrienes → vasodilation, oedema (chemosis), itching (histamine on H₁ receptors on nerve endings)
Key features: Itching is the hallmark symptom, bilateral, watery/mucoid discharge, chemosis, papillary reaction ^[1]^[2]
Vernal keratoconjunctivitis: giant cobblestone papillae on upper tarsal conjunctiva, Horner-Trantas dots (limbal eosinophilic infiltrates) ^[1]

Chlamydia trachomatis:
- Serotypes A–C → trachoma (leading infectious cause of blindness worldwide; not common in Hong Kong but exam-relevant)
- Serotypes D–K → inclusion conjunctivitis (sexually transmitted, associated with genital chlamydia)
Pathophysiology (trachoma): Repeated infection → chronic follicular conjunctivitis → scarring of tarsal conjunctiva → entropion (lid turns inward) → trichiasis (lashes rub cornea) → corneal scarring → blindness
Trachoma SAFE strategy (WHO): Surgery, Antibiotics, Facial cleanliness, Environmental improvement ^[1]

Neonatal Conjunctivitis (Ophthalmia Neonatorum)

Conjunctivitis in the first 28 days of life — must consider:

Chemical: Day 1 (from silver nitrate prophylaxis — now rarely used)
N. gonorrhoeae: Days 2–5 — hyperacute, purulent, can perforate cornea → emergency
Chlamydia trachomatis: Days 5–14 — mucopurulent; treat with systemic erythromycin (topical alone insufficient as it can cause chlamydial pneumonia)
Other bacteria / HSV: variable timing ^[1]^[2]

Definition: Bleeding beneath the conjunctiva, appearing as a well-demarcated, bright red patch
Pathophysiology: Rupture of small conjunctival or episcleral blood vessels → blood trapped between conjunctiva and sclera → flat, bright red patch with sharp borders
Causes: spontaneous (most common), Valsalva (coughing, sneezing, straining, vomiting), trauma, hypertension, anticoagulants/antiplatelets, bleeding diathesis ^[1]^[2]
Key features: painless, no vision loss, no discharge. Vision is completely normal. Resolves spontaneously in 1–2 weeks ^[1]^[2]
When to worry: Recurrent SCH → check BP, bleeding profile. Post-traumatic SCH without visible posterior border → suspect globe rupture or orbital fracture (blood tracking from orbit).
If the subconjunctival haemorrhage has no posterior visible border ("360-degree SCH" or haemorrhage extending posteriorly), suspect a ruptured globe or base of skull fracture ^[1]^[5]

Pterygium ("pteron" = wing): Wing-shaped fibrovascular growth of conjunctiva that encroaches onto the cornea, usually from nasal side
Pinguecula ("pinguis" = fat): Yellowish, slightly raised conjunctival degeneration near the limbus that does NOT cross onto the cornea
Pathophysiology: UV light exposure and chronic irritation → elastotic degeneration of subconjunctival collagen (actinic damage) → abnormal fibrovascular proliferation
Red eye: Secondary inflammation of the pterygium/pinguecula → localised redness
Common in Hong Kong (subtropical, outdoor workers) ^[1]

C. Episcleral and Scleral Causes

Definition: Inflammation of the episclera (superficial to sclera)
Pathophysiology: Usually idiopathic; occasionally associated with autoimmune disease. Self-limiting inflammatory process of episcleral tissue.
Key features: Sectoral (localised) redness, mild discomfort (not severe pain), NO vision loss, blanches with phenylephrine 2.5% ^[1]^[2]
Types: Simple (diffuse or sectoral) vs nodular (localised tender nodule)
Usually self-limiting; treat with lubricants ± topical NSAIDs ^[1]
Distinguishing from scleritis: episcleritis is superficial, bright red, mild discomfort, blanches with phenylephrine. Scleritis is deep, violaceous, severe boring pain, does NOT blanch. ^[1]^[2]

Definition: Inflammation of the sclera — a serious, sight-threatening condition
Pathophysiology: Immune complex–mediated vasculitis of the scleral vessels → necrotising inflammation of scleral collagen → tissue destruction. Often associated with systemic autoimmune disease (50% of cases) — especially rheumatoid arthritis (most common), GPA (Wegener's), SLE, relapsing polychondritis, IBD ^[1]^[2]
Types (Watson & Hayreh classification):
- Anterior scleritis: Diffuse, nodular, or necrotising (with or without inflammation)
  - Necrotising scleritis with inflammation = most severe form; scleral thinning → risk of perforation
  - Necrotising scleritis without inflammation = "scleromalacia perforans" — seen in long-standing RA; painless scleral thinning ^[1]
- Posterior scleritis: Rare; can cause exudative retinal detachment, disc oedema, proptosis
Key features: Severe, deep, boring pain (may wake patient from sleep), radiates to forehead/jaw; violaceous (blue-purple) hue; pain on eye movement; tender globe; does NOT blanch with phenylephrine 2.5% ^[1]^[2]
Vision may be affected. Requires systemic treatment (oral NSAIDs, systemic steroids, immunosuppressants). Always screen for underlying systemic disease. ^[1]^[2]

"If a patient with RA presents with a painful, violaceous red eye — think scleritis. If you see scleral thinning without pain — think scleromalacia perforans." ^[1]^[2]

D. Corneal Causes

Definition: Disruption of the corneal epithelium (outermost layer) due to trauma (fingernail, paper edge, foreign body)
Pathophysiology: Loss of epithelial barrier → exposed corneal nerve endings (CN V₁) → intense pain, tearing, photophobia. Fluorescein stains the denuded area bright green under cobalt blue light.
Key features: Acute onset pain after trauma, foreign body sensation, tearing, photophobia, ciliary injection. Positive fluorescein staining. ^[1]^[2]^[5]

Pathophysiology: Embedded foreign body (metal, dust) → ongoing corneal epithelial/stromal damage → pain, tearing, reflex blepharospasm. Metal FBs → rust ring within hours (iron oxidation).
Always evert the upper lid to look for a subtarsal foreign body — a retained FB under the upper lid will cause linear corneal abrasions (vertical scratches seen on fluorescein) ^[1]^[5]
Metallic FBs require removal of the rust ring (with a needle or burr under slit lamp) to prevent ongoing inflammation ^[5]

11. Keratitis (Corneal Infection/Inflammation)

Definition: Inflammation of the cornea; when infectious, often called a corneal ulcer

The single most important risk factor is contact lens wear — especially extended/overnight wear, poor lens hygiene, swimming with lenses ^[1]^[2]
Causative organisms:
- Bacteria: Pseudomonas aeruginosa (most common in contact lens wearers — aggressive, rapidly progressive), Staph. aureus, Strep. pneumoniae
- Fungi: Fusarium, Aspergillus — think of agricultural injury, organic matter trauma
- Acanthamoeba: Protozoan; associated with contact lens wear + tap water/swimming pool exposure; severe pain disproportionate to signs; ring infiltrate
Pathophysiology: Breach in corneal epithelium (from CL wear, trauma) → microbial invasion of stroma → inflammatory infiltrate (white opacity = infiltrate/ulcer) → stromal necrosis → risk of corneal perforation
Key features: Painful red eye, photophobia, decreased vision, ciliary injection. White corneal infiltrate/opacity visible (may see hypopyon = layering of WBCs in anterior chamber) ^[1]^[2]
Hypopyon: layered white cells in the inferior anterior chamber — indicates severe keratitis or endophthalmitis ^[1]^[2]

Any contact lens wearer presenting with a painful red eye must have keratitis excluded. They should STOP wearing lenses immediately and be referred urgently. ^[1]^[2]

HSV-1 is the most common infectious cause of corneal blindness in developed countries ^[1]
Pathophysiology: Primary HSV-1 infection (often in childhood, may be subclinical) → virus establishes latency in trigeminal ganglion → reactivation → viral shedding along CN V₁ → dendritic ulcer on cornea (branching pattern with terminal bulbs)
Key features: Dendritic ulcer (pathognomonic) — branching epithelial defect with terminal bulbs, stains with fluorescein (ulcer base) and rose bengal (devitalised cells at edges) ^[1]^[2]
Reduced corneal sensation (virus damages corneal nerves)
Recurrent episodes → stromal keratitis (immune-mediated) → corneal scarring → visual loss ^[1]
CRITICAL: Do NOT give topical steroids in epithelial HSV keratitis — steroids suppress immune clearance of virus → worsening, amoeboid ulcer, stromal melting ^[1]^[2]

Steroids in Herpetic Eye Disease

Topical steroids are CONTRAINDICATED in active epithelial herpes simplex keratitis. They enhance viral replication and cause the dendritic ulcer to enlarge into a geographic (amoeboid) ulcer. Steroids may be used cautiously ONLY for stromal/disciform keratitis or uveitis secondary to HSV — but always with antiviral cover and under ophthalmologist supervision. ^[1]^[2]

VZV reactivation in CN V₁ (ophthalmic division) distribution
Hutchinson's sign: vesicles on the tip/side of the nose (nasociliary nerve involved) → high risk of ocular involvement ^[1]^[2]^[5]
Can cause keratitis (pseudodendritic — no terminal bulbs, unlike HSV), anterior uveitis, scleritis, optic neuritis, cranial nerve palsies
Pathophysiology: VZV reactivation → neuronal inflammation → dermatomal rash + direct viral involvement of ocular structures innervated by V₁

Can occur with autoimmune conditions (e.g. RA → peripheral ulcerative keratitis/PUK), severe dry eye, neurotrophic keratopathy

13. Anterior Uveitis (Iritis / Iridocyclitis)

Anterior uveitis is the most common form of uveitis. ^[1]^[2]^[3]

Definition: Inflammation of the iris (iritis) and/or ciliary body (iridocyclitis)
"Uveitis" = "uvea" (grape, referring to the pigmented vascular coat) + "-itis" (inflammation)
Aetiology:
- Idiopathic (most common — ~50%)
- HLA-B27–associated: ankylosing spondylitis, reactive arthritis, psoriatic arthritis, IBD (Crohn's, UC) ^[1]^[2]
- Sarcoidosis (granulomatous uveitis with mutton-fat KPs)
- Behçet's disease (oral + genital ulcers + uveitis with hypopyon — common in East Asian and Middle Eastern populations — relevant for HK exams)
- Infections: TB, syphilis, HSV, VZV, toxoplasmosis, CMV (immunocompromised) ^[1]
- JIA (juvenile idiopathic arthritis) — important in paediatrics
Pathophysiology: Immune-mediated inflammation of iris/ciliary body → disruption of blood-aqueous barrier → leakage of proteins (flare) and inflammatory cells into the anterior chamber → cells and flare visible on slit lamp. Inflammatory mediators also cause:
- Ciliary spasm → deep, aching pain, photophobia (contraction of inflamed ciliary muscle is painful)
- Miosis (small pupil) → sphincter pupillae spasm from prostaglandin release
- Posterior synechiae → inflammatory adhesions between iris and anterior lens capsule → irregular pupil → risk of pupil block glaucoma if 360° synechiae (seclusio pupillae)
Key features: Unilateral painful red eye, photophobia (consensual — even when light shone in the OTHER eye, because bilateral ciliary muscle contraction occurs), blurred vision, ciliary (circumcorneal) injection, miosis (small pupil), cells and flare in anterior chamber on slit lamp ^[1]^[2]
- Keratic precipitates (KPs): Inflammatory cell deposits on the corneal endothelium
  - Small, fine KPs → non-granulomatous (HLA-B27, Behçet's)
  - Large, greasy "mutton-fat" KPs → granulomatous (sarcoidosis, TB, syphilis, VKH) ^[1]
- Hypopyon: Layering of white cells in the anterior chamber — seen in severe uveitis (especially Behçet's disease, HLA-B27, endophthalmitis)

The triad of anterior uveitis: pain + photophobia + circumcorneal injection. Look for cells and flare on slit lamp. ^[1]^[2]

14. Acute Angle-Closure Glaucoma (AACG)

This is an ophthalmological EMERGENCY — delay in treatment can result in permanent blindness. ^[1]^[2]^[4]

Definition: Sudden obstruction of aqueous humour outflow through the trabecular meshwork due to apposition of the peripheral iris against the trabecular meshwork → acute rise in intraocular pressure (IOP)
"Glaucoma" from Greek "glaukos" (blue-green) — ancient descriptions of the hazy, greenish appearance of the cornea in acute attacks
Risk factors: East Asian ethnicity (Chinese), hypermetropia (short axial length → shallow anterior chamber), female sex, age > 60, family history, precipitants: dim lighting, pupil-dilating drugs (anticholinergics, sympathomimetics), emotional stress ^[1]^[2]^[4]
Pathophysiology (Pupillary block mechanism — most common):
1. The lens sits behind the iris. Aqueous humour is produced by the ciliary body in the posterior chamber → flows through the pupil into the anterior chamber → drains via the trabecular meshwork at the iridocorneal angle.
2. In a predisposed eye (shallow anterior chamber, thick lens, narrow angle), the iris can come into contact with the anterior lens surface → blocks aqueous flow through the pupil (pupillary block).
3. Aqueous builds up behind the iris → pushes the peripheral iris forward (iris bombé) → occludes the trabecular meshwork → IOP rises acutely (often > 60 mmHg; normal 10–21).
4. Precipitant: mid-dilation of the pupil (e.g. dim room, mydriatic drops) → maximal pupillary block occurs at mid-dilation because the iris has maximal contact with the lens at this position.
Key features: Acute onset severe eye pain, headache (may be mistaken for migraine or intracranial pathology), nausea and vomiting (vagal response to severe pain / raised IOP), blurred vision, haloes around lights (corneal oedema → light scattering), fixed mid-dilated pupil (sphincter pupillae ischaemia from raised IOP), ciliary injection, hazy/steamy cornea (oedematous), rock-hard globe on palpation, markedly raised IOP ^[1]^[2]^[4]

AACG vs Migraine

Acute angle-closure glaucoma can mimic a migraine or acute abdomen (due to N/V). Always check the eyes (pupil, cornea, IOP) in any patient presenting with severe headache + nausea/vomiting, especially elderly East Asian females. A missed AACG leads to irreversible optic nerve damage. ^[1]^[4]

G. Orbital / Periorbital Causes

Definition: Infection of the tissues posterior to the orbital septum (cf. preseptal/periorbital cellulitis = anterior to septum)
Pathophysiology: Usually secondary to sinusitis (especially ethmoid sinusitis in children) → direct spread through the thin lamina papyracea → orbital fat/muscle infection → proptosis, ophthalmoplegia, pain, reduced vision
Key features: Proptosis, painful/restricted eye movements, reduced vision, afferent pupillary defect (if optic nerve compressed), periorbital oedema, fever, red eye ^[5]
This is an emergency — risk of cavernous sinus thrombosis, intracranial spread, permanent vision loss ^[5]
Preseptal cellulitis: Infection anterior to septum → lid swelling, redness, but NO proptosis, NO ophthalmoplegia, NO visual loss → less dangerous but can progress to orbital cellulitis

Rare but life-threatening; usually from spreading infection (facial, orbital, sinus)
CN III, IV, V₁, V₂, VI pass through or near cavernous sinus → multiple cranial nerve palsies + proptosis + chemosis + red eye

H. Traumatic Causes

Can cause subconjunctival haemorrhage, hyphaema (blood in anterior chamber), lens dislocation, vitreous haemorrhage, retinal detachment, globe rupture
Hyphaema: blood in the anterior chamber — forms a fluid level. Risk of rebleeding (day 3–5), raised IOP, corneal blood staining ^[5]

Signs of globe rupture: irregular pupil (teardrop pupil pointing toward wound), shallow anterior chamber, hypotony (low IOP), positive Seidel test (streaming fluorescein from wound site), 360° subconjunctival haemorrhage, exposed uveal tissue ^[5]

Alkali burns are MORE dangerous than acid burns — alkali penetrates deeper (saponification of cell membranes → liquefactive necrosis), acid causes coagulative necrosis which limits penetration ^[5]
Immediate copious irrigation with saline/water is the FIRST and most important step — do NOT delay to check pH first ^[5]

Classification

Red eye can be classified in multiple ways:

Category	Conditions	Key Features
Non-urgent (Safe red eye)	Subconjunctival haemorrhage, bacterial/viral conjunctivitis (mild), allergic conjunctivitis, episcleritis, blepharitis, pterygium/pinguecula	Normal vision, no significant pain, no corneal opacity, normal pupil
Urgent (Dangerous red eye)	Acute angle-closure glaucoma, microbial keratitis/corneal ulcer, anterior uveitis, scleritis, gonococcal conjunctivitis, orbital cellulitis, chemical injury, penetrating trauma, endophthalmitis	Reduced vision, significant pain, photophobia, ciliary injection, corneal opacity, abnormal pupil, raised IOP

(As detailed above: eyelid → conjunctiva → episclera → sclera → cornea → anterior chamber/uvea → orbit)

Pattern	Suggests
Diffuse conjunctival injection	Conjunctivitis
Sectoral redness	Episcleritis, inflamed pterygium/pinguecula
Circumcorneal (ciliary) injection	Keratitis, anterior uveitis, AACG
Localised, flat, bright red patch	Subconjunctival haemorrhage
Deep violaceous hue	Scleritis

Clinical Features

The key history elements for red eye are: onset, laterality, pain character, vision changes, discharge character, photophobia, contact lens wear, trauma, and systemic associations. ^[1]^[2]

History Element	Significance
Onset	Acute → trauma, AACG, chemical injury, SCH; Subacute → uveitis, keratitis; Chronic → blepharitis, dry eye
Laterality	Unilateral → trauma, keratitis, uveitis, AACG, SCH; Bilateral → conjunctivitis (allergic, viral), blepharitis
Pain	No pain → SCH, conjunctivitis, episcleritis; Mild → episcleritis, mild keratitis; Severe, deep, boring → scleritis, AACG; Foreign body sensation → corneal abrasion/FB
Vision	Normal → conjunctivitis, SCH, episcleritis, blepharitis; Reduced → keratitis, uveitis, AACG, scleritis, endophthalmitis
Discharge	Watery → viral conjunctivitis, allergic; Mucopurulent → bacterial conjunctivitis; Purulent → gonococcal; None → uveitis, AACG, scleritis
Photophobia	Present → keratitis, uveitis (corneal/uveal inflammation → ciliary spasm → pain on pupil constriction)
Itching	Hallmark of allergic conjunctivitis
Contact lens wear	Risk for microbial keratitis (especially Pseudomonas, Acanthamoeba)
Trauma	Corneal abrasion, FB, chemical injury, globe rupture
Haloes around lights	AACG (corneal oedema diffracts light)
N/V	AACG (vagal response)
Systemic disease	RA → scleritis; HLA-B27 → uveitis; atopy → allergic conjunctivitis

Symptom	Pathophysiological Basis
Redness	Vasodilation of conjunctival/episcleral/scleral vessels in response to inflammation, infection, or mechanical irritation
Pain (deep, boring)	Scleral inflammation (scleritis), acute IOP rise (AACG) — sclera is richly innervated; AACG pain also from corneal oedema stretching corneal nerves
Pain (sharp, foreign body sensation)	Corneal epithelial disruption → exposed subepithelial nerve plexus (CN V₁ — one of the most densely innervated tissues in the body)
Photophobia	Ciliary muscle spasm — inflamed ciliary body contracts painfully when the pupil constricts in response to light (hence photophobia in uveitis, keratitis); consensual photophobia occurs because both ciliary muscles contract
Tearing (epiphora)	Reflex lacrimation from corneal nerve stimulation (CN V₁ → CN VII efferent pathway to lacrimal gland)
Discharge (watery)	Serous exudation from inflamed conjunctival vessels (viral/allergic conjunctivitis)
Discharge (mucopurulent/purulent)	Neutrophilic infiltrate + bacterial debris + dead epithelial cells (bacterial conjunctivitis)
Itching	Histamine release from mast cell degranulation → stimulates H₁ receptors on conjunctival nerve endings (allergic conjunctivitis)
Blurred vision	Corneal oedema (AACG, keratitis), cells/flare in AC (uveitis), corneal opacity (scar, infiltrate)
Haloes around lights	Corneal oedema → prismatic dispersion of light → coloured haloes (AACG)
Nausea / vomiting	Vagal stimulation from severe pain OR direct effect of acutely raised IOP on autonomic centres (AACG)
Headache	Referred pain from CN V₁ (AACG, scleritis, HZO)
Decreased corneal sensation	HSV keratitis — virus damages corneal nerves in CN V₁

Sign	What It Means	Pathophysiological Basis
Conjunctival injection (diffuse)	Conjunctivitis	Superficial posterior conjunctival vessel dilation; worst in fornices, spares limbus
Ciliary (circumcorneal) injection	Keratitis, uveitis, AACG	Deep anterior ciliary artery dilation around the limbus — indicates corneal, uveal, or IOP-related pathology
Subconjunctival haemorrhage	SCH	Vessel rupture under conjunctiva — flat, bright red, well-demarcated
Violaceous (blue-purple) hue	Scleritis	Deep scleral vessel inflammation — does not blanch with phenylephrine
Pupil: miotic (small)	Anterior uveitis	Prostaglandin-induced sphincter pupillae spasm
Pupil: fixed, mid-dilated	AACG	Iris sphincter ischaemia from extremely high IOP → cannot constrict; dilator still partially functions
Pupil: irregular	Posterior synechiae (uveitis) or globe rupture (teardrop pupil)	Adhesions between iris and lens (uveitis) OR iris prolapse through wound (trauma)
Cornea: hazy/steamy	AACG	Corneal epithelial and stromal oedema from acutely elevated IOP pushing fluid into the cornea
Cornea: white infiltrate/opacity	Microbial keratitis (corneal ulcer)	Neutrophilic infiltration and necrosis of corneal stroma
Cornea: dendritic ulcer (fluorescein)	HSV keratitis	Viral replication in corneal epithelium → branching pattern of epithelial cell death
Cornea: fluorescein uptake (linear)	Subtarsal FB	Foreign body under upper lid → repeated abrasion with each blink → vertical linear scratches
Anterior chamber: cells and flare	Anterior uveitis	Breakdown of blood-aqueous barrier → proteins (flare) and WBCs (cells) leak into AC
Anterior chamber: hypopyon	Severe uveitis, endophthalmitis, keratitis	WBCs sediment inferiorly in AC, forming visible white layer
Anterior chamber: hyphaema	Trauma	Blood in AC from torn iris/ciliary body vessels
Keratic precipitates (KPs)	Uveitis	Inflammatory cells (macrophages, lymphocytes) deposit on corneal endothelium
Raised IOP (hard globe)	AACG	Blocked aqueous outflow → pressure builds
Proptosis	Orbital cellulitis, posterior scleritis, cavernous sinus thrombosis	Infection/inflammation of orbital contents → mass effect pushing eye forward
Lid swelling/erythema	Preseptal/orbital cellulitis, allergic reaction, blepharitis, stye	Inflammation/infection of periorbital tissues
Pre-auricular lymphadenopathy	Viral conjunctivitis (also chlamydial, adenoviral keratoconjunctivitis)	Lymphatic drainage of conjunctiva → pre-auricular and submandibular lymph nodes
Papillae on palpebral conjunctiva	Bacterial conjunctivitis, allergic conjunctivitis, GPC	Epithelial hyperplasia with central fibrovascular core over conjunctival septae
Follicles on palpebral conjunctiva	Viral conjunctivitis, chlamydial infection	Lymphoid aggregates (germinal centres) in conjunctival substantia propria
Chemosis	Allergic conjunctivitis, orbital cellulitis	Oedema of the conjunctiva from increased vascular permeability
Hutchinson's sign	HZO with ocular involvement risk	Vesicles on nose tip/side = nasociliary nerve (V₁ branch) involved → same nerve supplies the eye

This is the single most high-yield table for red eye exams:

Feature	Conjunctivitis	Acute Uveitis	Acute Glaucoma	Keratitis	Scleritis	Episcleritis	SCH
Pain	Gritty/FB sensation	Aching	Severe	Sharp, FB	Deep, boring	Mild	None
Vision	Normal	↓	↓↓↓	↓	May ↓	Normal	Normal
Discharge	Yes (watery/purulent)	No	No	Watery	No	No	No
Photophobia	No/mild	Yes	No	Yes	No	No	No
Pupil	Normal	Small (miosis)	Fixed, mid-dilated	Normal	Normal	Normal	Normal
Cornea	Clear	KPs ± clear	Hazy/steamy	Opacity/infiltrate/ulcer	Clear	Clear	Clear
IOP	Normal	Normal/low	↑↑↑	Normal	Normal	Normal	Normal
Injection	Diffuse conjunctival	Ciliary	Ciliary + mixed	Ciliary	Deep, violaceous	Sectoral	Flat red patch
Phenylephrine test	Blanches	Does not blanch	Does not blanch	Does not blanch	Does not blanch	Blanches	N/A
AC	Normal	Cells + flare	Shallow	May have hypopyon	Normal	Normal	Normal

For exams: the "dangerous red eye" features to look for are — reduced vision, severe pain, photophobia, ciliary injection, abnormal pupil, corneal opacity, raised IOP, cells/flare in AC. ^[1]^[2]

Refer urgently if ANY of the following are present ^[1]^[2]^[5]:

Reduced visual acuity
Severe eye pain
Photophobia
Corneal opacity or ulcer
Fixed, dilated or irregular pupil
Suspected penetrating injury or globe rupture
Chemical injury (after immediate irrigation)
Hypopyon or hyphaema
Proptosis ± restricted eye movements
Failure to improve with initial treatment / uncertain diagnosis

High Yield Summary

Red Eye — Key Concepts for Exams:

Most common cause: Conjunctivitis (viral > bacterial > allergic)
Pattern of injection is key: diffuse conjunctival = benign; circumcorneal/ciliary = dangerous (keratitis, uveitis, AACG)
Safe red eye features: normal vision, no significant pain, normal pupil, no corneal opacity
Dangerous red eye features: ↓ vision, severe pain, photophobia, abnormal pupil, corneal opacity, raised IOP, cells/flare
AACG: severe pain, N/V, haloes, hazy cornea, fixed mid-dilated pupil, ↑↑↑ IOP — more common in East Asians — emergency
Contact lens wearer with painful red eye: assume microbial keratitis until proven otherwise → stop CL, urgent referral
HSV keratitis: dendritic ulcer — NEVER give topical steroids alone (enhances viral replication)
Anterior uveitis: pain, photophobia (consensual), miosis, ciliary injection, cells + flare
Scleritis: deep boring pain, violaceous hue, does NOT blanch with phenylephrine, associated with RA
Chemical injury: irrigate FIRST, check pH later; alkali > acid in severity
Hypopyon = WBC layer in AC → severe keratitis, endophthalmitis, Behçet's
Hutchinson's sign (nose vesicles) → HZO with ocular involvement
SCH without visible posterior border → suspect globe rupture

Active Recall - Red Eye

^[1] Lecture slides: GC 125. The Red Eye.pdf; 2024 General Clerkship - The Red Eye_Student Copy.pdf ^[2] Lecture slides: CFB (OPHTH01) Common Eye Diseases.pdf ^[3] Senior notes: Ryan Ho Opthalmology.pdf (p. 4, Ophthalmic History — Red Eye) ^[4] Lecture slides: GC 122. Chronic Visual Loss.pdf; GC 121. Acute Visual Loss.pdf (AACG content) ^[5] Lecture slides: GC 126. Trauma and Ocular Emergency.pdf

Differential Diagnosis of Red Eye

The differential diagnosis of red eye is best approached systematically by anatomical structure (outside → inside), cross-referenced against the key clinical discriminators: pain, vision, discharge, pupil, cornea, IOP, and injection pattern. This approach ensures you never miss a diagnosis and can rapidly risk-stratify at the bedside.

Before diving into individual diagnoses, the most important clinical task is triage — can this patient be managed in primary care, or do they need urgent ophthalmology referral?

The "dangerous red eye" has one or more of: reduced vision, severe pain, photophobia, ciliary (circumcorneal) injection, corneal opacity, abnormal pupil, raised IOP, cells/flare in the anterior chamber. Any of these features mandates urgent ophthalmology referral. ^[1]^[2]

Comprehensive Differential Diagnosis List (by Anatomical Structure)

Condition	Key Discriminating Features	Why It Causes Red Eye
Blepharitis	Lid margin crusting, burning, FB sensation, chronic course. Vision normal.	Chronic lid margin inflammation → meibomian gland dysfunction → unstable tear film → secondary conjunctival irritation and hyperaemia
Stye (hordeolum)	Tender, red, localised swelling at lid margin. External = lash follicle; Internal = meibomian gland	Acute Staph. aureus infection of lid gland → localised abscess → periorbital erythema and oedema
Chalazion	Painless, firm, non-tender lid nodule; chronic. Red only if secondarily inflamed	Chronic granulomatous inflammation of obstructed meibomian gland — not a true infection
Dacryocystitis	Tender swelling at medial canthus (over lacrimal sac), tearing, purulent discharge from punctum on pressure	Obstruction of nasolacrimal duct → stagnant tears → bacterial infection of lacrimal sac → localised inflammation and redness medially

Condition	Key Discriminating Features	Why It Causes Red Eye
Viral conjunctivitis	Watery discharge, follicular reaction on palpebral conjunctiva, pre-auricular lymphadenopathy, highly contagious. Often starts unilateral then spreads to other eye. Vision normal. ^[1]^[2]	Adenovirus (most common) invades conjunctival epithelium → lymphocytic immune response → follicle formation. Posterior conjunctival vessel dilation → diffuse injection. No purulence because no significant neutrophilic response.
Bacterial conjunctivitis	Mucopurulent discharge (lids stuck in morning), papillary reaction. Vision normal. ^[1]^[2]	Bacteria (Staph., Strep., H. influenzae) → neutrophilic infiltration → purulent exudate. Papillae form from non-specific inflammatory hyperplasia of conjunctival epithelium over existing septae.
Hyperacute (gonococcal) conjunctivitis	Copious purulent discharge, rapid onset (< 12 hours), lid swelling. Can perforate cornea within 24–48 hours → EMERGENCY. ^[1]^[2]	N. gonorrhoeae is uniquely virulent — can penetrate intact corneal epithelium (unlike most bacteria) → rapid stromal necrosis → perforation. The overwhelming neutrophilic response produces the profuse pus.
Allergic conjunctivitis	Bilateral, ITCHING is the hallmark, watery/mucoid discharge, chemosis, papillary reaction. Vision normal. ^[1]^[2]	Type I hypersensitivity → mast cell degranulation → histamine → H₁ receptor activation on conjunctival nerves (itching) and vessel dilation (redness). Why bilateral? Allergens contact both eyes.
Vernal keratoconjunctivitis (VKC)	Giant cobblestone papillae on upper tarsal conjunctiva, Horner-Trantas dots (limbal eosinophilic infiltrates), shield ulcer. Young males, seasonal. ^[1]	Chronic allergic inflammation with eosinophilic predominance → giant papillae form from chronic remodelling of conjunctival substantia propria. Eosinophil major basic protein damages corneal epithelium → shield ulcer.
Chlamydial conjunctivitis (adult inclusion)	Chronic follicular conjunctivitis, mucopurulent discharge, concurrent STI symptoms (urethritis/cervicitis). Must treat systemically (oral azithromycin/doxycycline). ^[1]	Chlamydia trachomatis (serotypes D–K) is an obligate intracellular pathogen → chronic lymphocytic response → follicles. Topical treatment alone is insufficient because the organism resides intracellularly and may also infect the genital tract.
Subconjunctival haemorrhage	Painless, bright red, well-demarcated, flat patch. NO vision loss, NO discharge, NO pain. ^[1]^[2]	Rupture of a small conjunctival/episcleral vessel → blood trapped under the transparent conjunctiva. Resolves spontaneously via macrophage phagocytosis (1–2 weeks).
Pterygium / Pinguecula	Wing-shaped growth encroaching onto cornea (pterygium) or yellowish nodule near limbus not crossing cornea (pinguecula). Intermittent redness.	UV-induced elastotic degeneration → fibrovascular proliferation. Inflammation of the lesion causes localised redness.

Follicles vs Papillae — How to Tell Them Apart

This is a classic exam question. Evert the upper lid and look at the palpebral conjunctiva:

Follicles: Small, round, pale/yellowish elevations with vessels running OVER them (no central vessel). Represent lymphoid germinal centres. → Think viral, chlamydial (lymphocyte-driven).
Papillae: Red, polygonal, flat-topped elevations with a central vascular core. Represent epithelial hyperplasia with fibrovascular septae. → Think bacterial, allergic (neutrophil/mast cell–driven).

Memory aid: "Follicles = Flat-topped? No! Follicles are round like a Follicle (hair follicle shape). Papillae have Polygonal shape with a Point (central vessel)."

^[1]^[2]

Condition	Key Discriminating Features	Why It Causes Red Eye
Episcleritis	Sectoral (localised) bright red injection, mild discomfort (NOT severe pain), vision normal, blanches with phenylephrine 2.5%. Self-limiting. ^[1]^[2]	Inflammation of the superficial episcleral vascular plexus — because the vessels are superficial, they are bright red and constrict with topical vasoconstrictors (phenylephrine). The inflammation does not extend to the sclera → no deep pain, no vision threat.
Scleritis	Severe, deep, boring pain (wakes from sleep), radiating to forehead/jaw. Violaceous (blue-purple) hue. Does NOT blanch with phenylephrine. Vision may be affected. 50% have systemic autoimmune disease (especially RA). ^[1]^[2]	Deep scleral vessel inflammation → vasculitis with immune complex deposition → tissue destruction. The deep vessels do not respond to phenylephrine. The violaceous colour comes from the deep, engorged scleral plexus seen through the overlying tissue. Scleral necrosis can lead to perforation (necrotising scleritis).

The phenylephrine 2.5% test is the key bedside test to distinguish episcleritis from scleritis. Episcleritis blanches (superficial vessels constrict); scleritis does NOT blanch (deep vessels unresponsive). ^[1]^[2]

Condition	Key Discriminating Features	Why It Causes Red Eye
Corneal abrasion	Acute pain after trauma, FB sensation, tearing, photophobia. Positive fluorescein staining (epithelial defect). Ciliary injection. ^[1]^[5]	Loss of epithelium → exposed subepithelial nerve plexus (CN V₁ — cornea is one of the most densely innervated tissues in the body) → intense nociceptive signalling → reflex tearing, blepharospasm. The ciliary injection occurs because the anterior ciliary arteries (which supply the limbal cornea) dilate reflexively.
Corneal foreign body	History of grinding/metalwork, visible FB, rust ring if metallic. Always evert upper lid for subtarsal FB. ^[1]^[5]	Same mechanism as abrasion + ongoing mechanical irritation from embedded material. Metallic FBs oxidise → rust ring → chemical keratitis from iron deposition → ongoing inflammation even after FB removal unless rust ring is debrided.
Microbial keratitis (corneal ulcer)	Contact lens wearer, white corneal infiltrate/opacity, mucopurulent discharge, hypopyon possible. Severe pain, reduced vision, ciliary injection. ^[1]^[2]	Breach in corneal epithelium (usually from CL micro-trauma or overwear) → bacterial/fungal/protozoal invasion of stroma → neutrophilic infiltrate (visible as white opacity) → corneal necrosis → if WBCs settle in AC by gravity → hypopyon. Pseudomonas produces exotoxins and proteases that cause rapid stromal dissolution.
Herpes simplex keratitis	Dendritic ulcer (branching pattern with terminal bulbs) on fluorescein staining. Reduced corneal sensation. History of recurrent episodes. Do NOT give topical steroids alone. ^[1]^[2]	HSV-1 reactivation from trigeminal ganglion → virus travels along CN V₁ → infects corneal epithelial cells → cell death in branching dendritic pattern (follows corneal nerve distribution). Terminal bulbs represent clusters of virus-laden cells. Corneal nerve damage → reduced sensation.
Herpes zoster ophthalmicus	Dermatomal vesicular rash in V₁ distribution. Hutchinson's sign (nose tip vesicles) = high risk of ocular involvement. ^[1]^[2]^[5]	VZV reactivation in V₁ ganglion → dermatomal inflammation. The nasociliary branch of V₁ supplies both the nose tip/side and the eye — so if vesicles appear on the nose (Hutchinson's sign), there is ~76% chance of ocular involvement (keratitis, uveitis, scleritis).
Marginal keratitis	Peripheral corneal infiltrates at 10, 2, 4, 8 o'clock positions (where lids cross limbus), with clear interval between infiltrate and limbus. Associated with blepharitis.	This is NOT an infection — it is a hypersensitivity reaction to staphylococcal exotoxins from lid margin colonisation. Toxins diffuse from the tear film into the peripheral cornea → localised immune response → sterile infiltrates. Important to distinguish from infectious keratitis (which requires scraping/culture).

Condition	Key Discriminating Features	Why It Causes Red Eye
Anterior uveitis (iritis/iridocyclitis)	Pain, photophobia (including consensual photophobia), blurred vision, circumcorneal (ciliary) injection, miotic pupil, cells and flare on slit lamp. Keratic precipitates on corneal endothelium. ^[1]^[2]	Inflammation of iris/ciliary body → breakdown of blood-aqueous barrier → protein leakage (flare) and WBC infiltration (cells) into AC. Ciliary muscle spasm → aching pain exacerbated by pupil constriction (photophobia). Prostaglandins cause sphincter spasm → miosis. Posterior synechiae form from fibrinous adhesions between inflamed iris and lens.
Acute angle-closure glaucoma (AACG)	Severe pain, N/V, haloes around lights, blurred vision, fixed mid-dilated pupil, hazy cornea, rock-hard globe, markedly raised IOP. More common in East Asians. ^[1]^[2]^[4]	Pupillary block → aqueous trapped behind iris → pushes peripheral iris forward → occludes trabecular meshwork → IOP rises acutely → corneal endothelial pump overwhelmed → corneal oedema (hazy cornea, haloes). Iris sphincter ischaemia from high IOP → fixed mid-dilated pupil. Pain from corneal nerve stretching and ciliary body ischaemia. Vagal response to pain → N/V.
Endophthalmitis	Severe pain, markedly reduced vision, hypopyon, lid swelling, chemosis. History of recent ocular surgery or penetrating trauma. ^[1]^[5]	Intraocular infection (bacteria > fungi) → overwhelming inflammatory response within the vitreous and anterior chamber. Post-operative endophthalmitis (most common) typically presents 2–7 days after cataract surgery. Endogenous endophthalmitis results from haematogenous spread (e.g. IV drug use, endocarditis).

Consensual Photophobia — Why?

In anterior uveitis, shining light in the unaffected eye also causes pain in the affected eye. Why? Because the pupillary light reflex is consensual — light in one eye causes bilateral pupil constriction. When the inflamed ciliary muscle in the affected eye contracts, it hurts. This is a useful clinical sign to confirm uveitis: if the patient winces when you shine light in the contralateral eye, suspect anterior uveitis. ^[1]^[2]

Condition	Key Discriminating Features	Why It Causes Red Eye
Orbital cellulitis	Proptosis, painful/restricted eye movements, reduced vision, RAPD (if optic nerve compressed), fever, lid swelling. Usually secondary to sinusitis. ^[5]	Infection posterior to orbital septum → inflammatory oedema and abscess in orbital fat → mass effect pushes globe forward (proptosis), compresses extraocular muscles (ophthalmoplegia), and may compress optic nerve (visual loss, RAPD). Venous congestion → conjunctival chemosis and redness.
Preseptal (periorbital) cellulitis	Lid swelling and redness, BUT no proptosis, no ophthalmoplegia, no visual loss. Typically from lid wound, insect bite, or sinusitis.	Infection anterior to orbital septum — does not involve orbital contents. Less dangerous but can progress to orbital cellulitis, especially in children.
Cavernous sinus thrombosis	Bilateral proptosis, multiple CN palsies (III, IV, V₁, V₂, VI), chemosis, fever, rapid deterioration. Usually from spreading facial/sinus infection.	Infection spreads to cavernous sinus → thrombosis → venous congestion → bilateral orbital findings. CN III, IV, V₁, V₂, VI all pass through/near the cavernous sinus.

Condition	Key Discriminating Features	Why It Causes Red Eye
Chemical injury	History of chemical exposure. ALKALI worse than acid. Immediate copious irrigation is the FIRST step — do NOT delay to check pH. ^[5]	Alkali: saponification of cell membranes → liquefactive necrosis → deep penetration → can damage limbal stem cells, anterior chamber, even lens. Acid: coagulative necrosis → protein precipitation limits further penetration (except HF acid).
Hyphaema	Blood visible in anterior chamber (fluid level). History of blunt trauma. Risk of rebleeding at day 3–5. ^[5]	Blunt force → tears iris root or ciliary body vessels → blood enters AC. Settles inferiorly by gravity. Rebleeding occurs when the initial clot retracts and friable new vessels at the tear site re-open. Raised IOP can occur from trabecular meshwork obstruction by blood/clot.
Globe rupture (open globe injury)	Irregular/teardrop pupil (pointing toward wound), shallow AC, hypotony, positive Seidel test (fluorescein streaming), 360° SCH without visible posterior border, exposed uveal tissue. ^[5]	Full-thickness breach of the corneoscleral wall → aqueous/vitreous leak out → IOP drops (hypotony) → AC collapses → pupil distorts as iris prolapses toward wound (teardrop). 360° SCH masks the wound site. Seidel test: fluorescein over wound → streaming green rivulet as aqueous leaks through.

Condition	Key Features	Mechanism
Dry eye syndrome	Chronic bilateral grittiness, FB sensation, worse at end of day or with prolonged screen use. Tear film breakup time < 10 seconds.	Tear film instability → ocular surface inflammation → conjunctival hyperaemia. Paradoxical tearing may occur (reflex lacrimation from corneal irritation).
Contact lens–related problems	FB sensation, redness, tearing after CL wear. Ranges from mild irritation to sight-threatening keratitis.	CL-induced hypoxia, mechanical irritation, allergic response (giant papillary conjunctivitis from CL protein deposits), or microbial keratitis.
Drug-induced red eye	Topical prostaglandin analogues (e.g. latanoprost for glaucoma) cause chronic conjunctival hyperaemia as a side effect.	Prostaglandins cause vasodilation of conjunctival vessels — this is a pharmacological side effect, not pathology.
Thyroid eye disease (Graves' ophthalmopathy)	Proptosis, lid retraction, lid lag, exposure keratopathy, diplopia, optic neuropathy.	Autoimmune inflammation of extraocular muscles and orbital fat → expansion of orbital contents → proptosis → incomplete lid closure → exposure of cornea → dryness and keratopathy → secondary redness.
Carotid-cavernous fistula	Pulsating proptosis, corkscrew episcleral vessels (arterialized conjunctival vessels), bruit on auscultation.	Abnormal communication between carotid artery and cavernous sinus → arterial blood flows retrograde into ophthalmic veins → engorgement of episcleral/conjunctival veins.

This table is the single most high-yield reference for exam questions on red eye. It allows pattern-based diagnosis by cross-referencing key features:

Feature	Conjunctivitis	Anterior Uveitis	AACG	Keratitis	Scleritis	Episcleritis	SCH
Pain severity	Gritty/mild	Moderate ache	Severe	Moderate–severe	Severe, boring	Mild	None
Vision	Normal	↓	↓↓↓	↓	± ↓	Normal	Normal
Discharge	Present	Absent	Absent	± watery	Absent	Absent	Absent
Photophobia	Absent/mild	Present	±	Present	Absent	Absent	Absent
Pupil	Normal	Miotic	Fixed mid-dilated	Normal	Normal	Normal	Normal
Cornea	Clear	± KPs	Hazy/oedematous	Opacity/infiltrate	Clear	Clear	Clear
IOP	Normal	Normal/↓	↑↑↑	Normal	Normal	Normal	Normal
Injection pattern	Diffuse conjunctival	Ciliary	Mixed/ciliary	Ciliary	Deep violaceous	Sectoral, bright	Flat red patch
AC findings	Normal	Cells + flare	Shallow	± Hypopyon	Normal	Normal	Normal
Phenylephrine	Blanches	No	No	No	No	Yes	N/A
N/V	No	No	Yes	No	No	No	No
Systemic assoc.	—	HLA-B27, sarcoid, Behçet	Hypermetropia	CL wear	RA, GPA, SLE	± autoimmune	HTN, anticoag

The following questions help you rapidly narrow the differential at the bedside: ^[1]^[2]^[3]

Step 1: Is vision affected?

Yes → Dangerous red eye (keratitis, uveitis, AACG, scleritis, endophthalmitis, orbital cellulitis)
No → Likely safe (conjunctivitis, SCH, episcleritis, blepharitis)

Step 2: Is there pain? What character?

No pain → SCH (painless), mild conjunctivitis
Gritty/FB sensation → corneal abrasion, FB, dry eye, blepharitis
Deep, boring, radiating → scleritis, AACG
Aching with photophobia → anterior uveitis

Step 3: What is the pattern of redness?

Diffuse, worst in fornices → conjunctivitis
Circumcorneal → uveitis, keratitis, AACG
Sectoral → episcleritis, pinguecula
Deep violaceous → scleritis
Well-demarcated flat red patch → SCH

Step 4: Is there discharge?

Watery → viral conjunctivitis, allergic
Mucopurulent/purulent → bacterial conjunctivitis
Hyperacute purulent → gonococcal → emergency
None → uveitis, AACG, scleritis, SCH

Step 5: Is the pupil normal?

Small (miotic) → anterior uveitis
Fixed mid-dilated → AACG
Irregular → posterior synechiae (uveitis) or globe rupture

Step 6: Is the cornea clear?

Hazy → AACG (oedema)
White infiltrate → microbial keratitis
Dendritic pattern → HSV keratitis

Step 7: Are there relevant systemic associations?

HLA-B27 conditions → anterior uveitis
RA, GPA → scleritis
Atopy → allergic conjunctivitis
Contact lens wear → microbial keratitis
Recent surgery → endophthalmitis

Do Not Miss These Diagnoses

The following diagnoses carry risk of permanent vision loss or serious systemic disease if not identified promptly:

Acute angle-closure glaucoma — irreversible optic nerve damage within hours
Microbial keratitis (corneal ulcer) — corneal perforation, endophthalmitis
Gonococcal conjunctivitis — corneal perforation within 24–48 hours (even through intact epithelium)
Anterior uveitis — posterior synechiae, secondary glaucoma, CMO, band keratopathy
Scleritis — scleral perforation; marker of systemic vasculitis (e.g. RA, GPA)
Orbital cellulitis — cavernous sinus thrombosis, intracranial abscess, optic nerve compression
Chemical injury (especially alkali) — limbal stem cell destruction, corneal melting
Open globe injury — endophthalmitis, sympathetic ophthalmia
Endophthalmitis — devastating intraocular infection → loss of eye possible
Neonatal gonococcal ophthalmia — corneal perforation → blindness in newborn

^[1]^[2]^[5]

Special Populations

Ophthalmia neonatorum (first 28 days): chemical (day 1), gonococcal (days 2–5), chlamydial (days 5–14), other bacterial, HSV
Orbital cellulitis from sinusitis — more common in children (ethmoid sinusitis → thin lamina papyracea)
Congenital glaucoma — presents with tearing, photophobia, buphthalmos (enlarged globe), cloudy cornea
JIA-associated uveitis — often asymptomatic (white, quiet eye) → screen all JIA patients regularly; bilateral, chronic, insidious anterior uveitis with band keratopathy

Always assume microbial keratitis until proven otherwise
Most common organism: Pseudomonas aeruginosa (CL wearers) — characteristically rapid, aggressive, central ulcer
Acanthamoeba keratitis: severe pain out of proportion to signs, ring infiltrate, history of swimming/tap water exposure with CLs
Giant papillary conjunctivitis: allergic response to CL protein deposits → giant papillae on upper tarsal conjunctiva

Endophthalmitis — severe pain, hypopyon, visual loss, typically days 2–7 post-cataract surgery
Wound leak (positive Seidel test)
Corneal graft rejection (circumcorneal injection, KPs on graft endothelium)

High Yield Summary — Differential Diagnosis of Red Eye

Approach: Triage first → safe vs dangerous. Key discriminators: vision, pain, pupil, cornea, IOP.
Most common cause overall: Viral conjunctivitis (adenovirus) — watery discharge, follicles, pre-auricular LN.
Most common cause of painful red eye with corneal ulcer: Microbial keratitis — especially in CL wearers (Pseudomonas).
Most dangerous "mimicker": AACG can mimic migraine or acute abdomen (N/V) — always check pupils and IOP.
Pattern recognition: Diffuse injection = conjunctivitis; ciliary injection = uveitis/keratitis/AACG; sectoral = episcleritis; violaceous = scleritis; flat red patch = SCH.
Phenylephrine test: Blanches = episcleritis (superficial); Does NOT blanch = scleritis (deep).
Abnormal pupil narrows DDx: Miotic = uveitis; Fixed mid-dilated = AACG; Irregular = synechiae or globe rupture.
Systemic associations: RA → scleritis; HLA-B27 → uveitis; Atopy → allergic conjunctivitis; CL wear → keratitis.
HSV keratitis: Dendritic ulcer — NEVER topical steroids alone.
Gonococcal conjunctivitis: Can perforate intact corneal epithelium — ophthalmological emergency.

Active Recall - DDx of Red Eye

References

Diagnostic Criteria, Algorithm, and Investigations for Red Eye

Red eye is a clinical sign, not a single disease. There are no universal "diagnostic criteria" in the way we have, say, the Jones criteria for rheumatic fever. Instead, the diagnosis relies on pattern recognition — matching a constellation of history and examination findings to a specific condition. Each individual cause of red eye has its own diagnostic features and investigation pathway.

The approach is therefore:

Structured clinical assessment (history + examination) → pattern-based diagnosis
Targeted investigations when the clinical picture demands further information or confirmation
Referral criteria for when bedside assessment alone is insufficient

For most cases of red eye, the diagnosis is clinical — made at the bedside with history, inspection, and a few key examination manoeuvres. Investigations are reserved for specific indications (e.g. corneal scraping in suspected microbial keratitis, IOP measurement in suspected AACG, blood tests for systemic associations in uveitis/scleritis). ^[1]^[2]

Diagnostic Criteria for Key Conditions

While there is no single set of "red eye diagnostic criteria," each major cause has characteristic diagnostic features. Here are the diagnostic criteria/hallmarks for the most important conditions:

Clinical diagnosis — requires all of the following ^[1]^[2]^[4]:

Criterion	Finding
Symptoms	Acute onset severe eye pain, headache, nausea/vomiting, blurred vision, haloes around lights
Pupil	Fixed, mid-dilated, non-reactive to light
Cornea	Hazy/steamy (oedematous)
Anterior chamber	Shallow (van Herick grading on slit lamp)
IOP	Markedly elevated ( > 40 mmHg, often > 60 mmHg; normal 10–21 mmHg)
Injection	Circumcorneal (ciliary) ± mixed conjunctival injection
Gonioscopy	Closed angle (appositional closure of iridocorneal angle) — this is the definitive confirmation but may be deferred in the acute setting

Why each criterion makes sense from first principles:

Hazy cornea: IOP so high that corneal endothelial pump is overwhelmed → stromal oedema → light scatter → haloes
Fixed mid-dilated pupil: IOP > 40–50 mmHg → iris sphincter ischaemia → pupil cannot constrict; dilator muscle still partially functions → mid-dilation
N/V: Oculocardiac reflex (trigeminal-vagal pathway) or direct autonomic response to extreme IOP

Van Herick Test

The van Herick test is a slit lamp–based screening test for narrow angles. A narrow slit beam is shone at the temporal limbus at 60°. The ratio of the peripheral anterior chamber depth to the corneal thickness is graded:

Grade 4: AC depth ≥ corneal thickness (wide open)
Grade 3: AC depth = 1/4–1/2 corneal thickness
Grade 2: AC depth = 1/4 corneal thickness (narrow)
Grade 1 or less: AC depth < 1/4 corneal thickness → occludable angle → risk of AACG

This is a quick, non-contact screening method; gonioscopy remains the gold standard for angle assessment. ^[1]^[4]

Clinical diagnosis based on slit lamp findings ^[1]^[2]:

Criterion	Finding
Symptoms	Pain, photophobia (including consensual), blurred vision
Injection	Ciliary (circumcorneal) injection
Pupil	Miotic (small), may be irregular if posterior synechiae present
Slit lamp — Anterior chamber	Cells (individual white cells visible in the slit beam, like dust particles in a beam of light) and flare (diffuse haziness from protein in aqueous, like a "Tyndall effect")
Slit lamp — Corneal endothelium	Keratic precipitates (KPs): fine = non-granulomatous; large, greasy "mutton-fat" KPs = granulomatous
Optional	Hypopyon (severe cases), posterior synechiae (adhesions between iris and lens)

Grading of anterior chamber cells (SUN Working Group criteria):

Grade	Cells per field (1 mm × 1 mm slit beam)
0	< 1
0.5+	1–5
1+	6–15
2+	16–25
3+	26–50
4+	> 50

Flare grading: 0 (none), 1+ (faint), 2+ (moderate — iris/lens details clear), 3+ (marked — iris/lens details hazy), 4+ (intense — fibrin clot/plastic aqueous)

Cells and flare on slit lamp examination is the hallmark diagnostic finding of anterior uveitis. Without a slit lamp, the diagnosis cannot be confirmed — this is why referral is essential. ^[1]^[2]

Clinical diagnosis + microbiological confirmation ^[1]^[2]:

Feature	Finding
History	Contact lens wear, corneal trauma, immunosuppression
Symptoms	Pain, photophobia, tearing, reduced vision
Slit lamp	Corneal epithelial defect with underlying stromal infiltrate (white opacity), ± hypopyon
Fluorescein staining	Positive uptake over the ulcer/epithelial defect (stains exposed stroma bright green under cobalt blue light)
Microbiological confirmation	Corneal scraping for Gram stain, culture and sensitivity (C/S) — this is the gold standard for identifying the causative organism

Specific patterns that suggest certain organisms ^[1]^[2]:

Organism	Characteristic Corneal Finding
Pseudomonas aeruginosa	Rapidly progressive, central, suppurative ulcer with mucopurulent discharge; "soupy" stromal melt
Staphylococcus aureus	Well-defined, round, grey-white infiltrate
Fungal (Fusarium, Aspergillus)	Feathery/satellite lesions at the edges, raised infiltrate, slower progression
Acanthamoeba	Ring infiltrate (pathognomonic), severe pain out of proportion to signs, history of CL + tap water/swimming
HSV	Dendritic ulcer — branching epithelial defect with terminal bulbs

Diagnosed clinically by the pathognomonic dendritic ulcer ^[1]^[2]:

Feature	Finding
Fluorescein staining	Dendritic ulcer: branching linear epithelial defect with terminal bulbs (swollen virus-laden cells at the ends)
Rose bengal staining	Stains devitalised cells at the margins of the dendrite (highlights the full extent better than fluorescein)
Corneal sensation	Reduced (hypoaesthesia) — virus damages corneal nerves. Test with a wisp of cotton wool before instilling anaesthetic drops.
Confirmation (if needed)	PCR for HSV DNA from corneal swab — rarely needed as clinical diagnosis is usually sufficient

The diagnosis is clinical — based on the character of discharge, type of conjunctival reaction, and associated features ^[1]^[2]:

Feature	Viral	Bacterial	Allergic
Discharge	Watery	Mucopurulent	Watery/mucoid
Conjunctival reaction	Follicles	Papillae	Papillae (± giant)
Laterality	Often unilateral → bilateral	Unilateral or bilateral	Bilateral
Itching	Mild/absent	Mild/absent	Prominent (hallmark)
Pre-auricular LN	Present	Usually absent	Absent
Associated features	URTI, contact history	Lids stuck in morning	Atopy, seasonal

Routine microbiological testing is NOT needed for most conjunctivitis. Culture is indicated for: (1) hyperacute/severe cases (suspected gonococcal), (2) neonatal conjunctivitis, (3) conjunctivitis unresponsive to empirical treatment. ^[1]^[2]

Clinical diagnosis — characterised by: ^[1]^[2]

Feature	Finding
Pain	Severe, deep, boring pain; may wake patient from sleep; radiates to forehead/jaw
Colour	Violaceous (blue-purple) hue under natural daylight
Phenylephrine test	Does NOT blanch
Vision	May be reduced (posterior scleritis or complications)
Scleral examination	Nodules (nodular type), thinning (necrotising), uveal show-through (scleromalacia)
Systemic workup	Essential — ~50% have underlying systemic autoimmune disease

The following algorithm represents the systematic approach to a patient presenting with a red eye in an emergency department or primary care setting:

Investigation Modalities

Investigations in red eye are targeted, not routine. Most diagnoses are clinical. Investigations are ordered when:

The clinical picture is uncertain
A sight-threatening diagnosis is suspected and needs confirmation
An underlying systemic cause needs to be identified
Microbiological identification is required to guide treatment

A. Bedside Examination Techniques

These are the "investigations" performed at the bedside — critical to red eye assessment:

This is the FIRST and most important "investigation" in any eye complaint. ^[1]^[2]^[7]

Method: Snellen chart at 6 metres (or LogMAR chart). Test each eye separately. If patient cannot read letters: count fingers (CF) → hand movements (HM) → light perception (LP) → no light perception (NLP).
Why first? VA is the "vital sign" of the eye. Reduced VA immediately categorises the red eye as "dangerous" and mandates urgent referral. It also provides a baseline for monitoring.
Key findings:
- Normal (6/6 or better) → conjunctivitis, SCH, episcleritis, blepharitis
- Mildly reduced (6/9–6/18) → anterior uveitis, early keratitis
- Severely reduced (6/36 or worse) → AACG, severe keratitis, endophthalmitis

Always document visual acuity BEFORE any intervention (including drops). It is a medicolegal requirement and essential for monitoring. ^[1]^[2]

The single most useful bedside test for corneal pathology. ^[1]^[2]^[5]

Method: Instil fluorescein sodium 2% (orange dye) into the lower fornix → examine with cobalt blue light (on slit lamp or with a Wood's lamp/pen torch with blue filter)
Principle: Fluorescein is a hydrophilic dye that does not penetrate intact, hydrophobic corneal epithelium. When the epithelium is breached (abrasion, ulcer, dendritic lesion), fluorescein fills the defect and fluoresces bright green under blue light.
Key findings:

Pattern	Diagnosis
Focal green uptake (round/irregular)	Corneal abrasion or ulcer
Branching pattern with terminal bulbs	HSV dendritic ulcer (pathognomonic)
Vertical linear scratches	Subtarsal foreign body (FB abrades with each blink)
Punctate uptake (multiple tiny dots)	Dry eye, UV keratitis, toxic keratopathy
Streaming green rivulet (Seidel test positive)	Corneal/scleral wound with aqueous leak → globe perforation

The Seidel Test

The Seidel test detects a corneal or scleral wound with aqueous leak. Apply a concentrated fluorescein strip directly over the suspected wound site. If aqueous humour is leaking through the wound, it dilutes and washes away the fluorescein → you see a bright green rivulet streaming from the wound site against the dark orange background of undiluted fluorescein. A positive Seidel test = globe perforation → emergency. ^[5]

Size: Compare both pupils in ambient and dim light
- Miotic (small) → anterior uveitis (prostaglandin-induced sphincter spasm)
- Fixed mid-dilated → AACG (sphincter ischaemia)
- Irregular → posterior synechiae (uveitis) or globe rupture (iris prolapse)
Reactivity: Direct and consensual light reflex
- Non-reactive → AACG (iris sphincter too ischaemic to respond)
RAPD (Relative Afferent Pupillary Defect): Swinging flashlight test
- Present in optic nerve disease (e.g. orbital cellulitis compressing ON), severe retinal disease
- NOT expected in conjunctivitis, uveitis, or keratitis (these don't affect the optic nerve)

Essential to exclude a subtarsal foreign body — must be performed in ALL cases of corneal abrasion/FB sensation. ^[1]^[5]

Method: Patient looks down → grasp upper lid lashes → press a cotton bud at the upper tarsal crease → flip the lid upward over the cotton bud → inspect the everted tarsal conjunctiva
Why? A foreign body lodged under the upper lid causes repetitive corneal abrasion with every blink → produces characteristic vertical linear corneal scratches seen on fluorescein

Used to distinguish episcleritis from scleritis. ^[1]^[2]

Method: Instil phenylephrine 2.5% (a topical alpha-adrenergic agonist/vasoconstrictor) → observe the redness after 10–15 minutes
Interpretation:
- Blanches (redness clears) → EPISCLERITIS (superficial episcleral vessels constrict with alpha-agonist)
- Does NOT blanch → SCLERITIS (deep scleral vessels are not affected by topical vasoconstrictors)
Why does this work? Phenylephrine causes vasoconstriction of superficial vessels via alpha-1 receptors. The episcleral plexus is superficial enough to respond. The deep scleral plexus is buried within the scleral stroma → topical drug cannot reach these vessels in sufficient concentration.

Critical in suspected AACG. ^[1]^[2]^[4]

Methods:
- Goldmann applanation tonometry (GAT): Gold standard. Mounted on slit lamp. Measures the force needed to flatten a fixed area (3.06 mm diameter) of cornea. Requires fluorescein + topical anaesthetic.
- Non-contact tonometry ("air puff"): Screening tool; less accurate.
- Tono-Pen / iCare: Portable handheld devices — useful in ED settings.
- Digital palpation: Rough assessment — in AACG, the globe feels "rock-hard" like a golf ball compared to the normal eye. Unreliable for exact measurement but useful when instruments are unavailable.
Normal IOP: 10–21 mmHg
Key findings:
- IOP > 40–60 mmHg → strongly suggests AACG ^[1]^[4]
- IOP slightly raised → consider secondary glaucoma (e.g. from uveitis, hyphaema, lens-related)
- IOP low (hypotony) → suspect globe rupture (aqueous leaking out)

When NOT to Measure IOP

Do NOT attempt tonometry (or apply any pressure to the globe) if there is suspected globe rupture or penetrating injury. Applying pressure can extrude intraocular contents through the wound. Instead, shield the eye with a rigid eye shield (NOT a pressure patch) and arrange emergency surgery. ^[5]

The slit lamp is the single most important instrument in ophthalmology for red eye assessment. ^[1]^[2]

The slit lamp provides magnified, stereoscopic examination of all anterior segment structures. It generates a thin slit beam of light that can be varied in width, height, angle, and colour (white vs cobalt blue for fluorescein).

Structures examined and key findings:

Structure	What to Look For	Significance
Lids and lashes	Crusting, lash loss (madarosis), meibomian gland plugging, trichiasis	Blepharitis, meibomian gland disease, trachoma
Conjunctiva	Injection pattern (conjunctival vs ciliary), follicles, papillae, chemosis, membranes/pseudomembranes, foreign bodies	Conjunctivitis type, episcleritis, SCH
Cornea	Clarity, epithelial defects (fluorescein), stromal infiltrates, oedema, KPs on endothelium, Descemet's folds, neovascularisation	Keratitis (opacity/infiltrate), AACG (oedema), uveitis (KPs), old inflammation (scars, neovasc)
Anterior chamber	Depth (shallow in AACG), cells (individual WBCs in beam), flare (protein haze), hypopyon (WBC layer), hyphaema (blood layer)	Uveitis (cells + flare), AACG (shallow AC), keratitis/endophthalmitis (hypopyon), trauma (hyphaema)
Iris	Synechiae (posterior = iris-lens adhesions; anterior = iris-cornea), atrophy, rubeosis (new vessels — neovascular glaucoma), heterochromia	Uveitis (synechiae), ischaemia (atrophy), proliferative retinopathy (rubeosis)
Lens	Cataract, subluxation, pseudoexfoliation material on capsule	Trauma (subluxation), pseudoexfoliation glaucoma

The slit lamp exam can detect: (1) cells and flare confirming uveitis, (2) corneal ulcer/infiltrate in keratitis, (3) shallow AC in AACG, (4) KPs on endothelium, (5) hypopyon, (6) dendritic ulcer with fluorescein. Without it, many serious diagnoses would be missed. ^[1]^[2]

What it is: Direct visualisation of the iridocorneal angle using a goniolens (contact lens with mirrors) on the slit lamp
Why needed? The iridocorneal angle is normally hidden behind the limbal sclera — you cannot see it on direct examination. Gonioscopy uses total internal reflection with a mirror to view the angle.
Indication: Suspected angle-closure glaucoma, secondary glaucoma, angle tumours
Key findings:
- Open angle (Shaffer grade III–IV): Normal
- Narrow angle (Shaffer grade I–II): At risk for angle closure
- Closed angle (Shaffer grade 0): Diagnostic of angle closure in AACG

D. Microbiological Investigations

This is the gold standard investigation for microbial keratitis and must be performed BEFORE starting empirical antibiotics whenever possible. ^[1]^[2]

Method: Under topical anaesthesia and slit lamp magnification, use a sterile blade (e.g. No. 15 Bard-Parker) or sterile spatula to scrape the base and leading edge of the corneal ulcer
Specimens sent for:
- Gram stain — rapid (within minutes); identifies Gram-positive cocci (Staph, Strep), Gram-negative rods (Pseudomonas)
- Culture — blood agar, chocolate agar, Sabouraud's agar (fungi), thioglycolate broth, non-nutrient agar with E. coli overlay (Acanthamoeba)
- KOH preparation / calcofluor white — for fungal hyphae
- PCR — for atypical organisms (Acanthamoeba, HSV, VZV, Chlamydia)
Key findings:
- Gram-negative rods → Pseudomonas (CL-related)
- Gram-positive cocci in clusters → Staph. aureus
- Branching hyphae on KOH → fungal keratitis
- Double-walled cysts on calcofluor white → Acanthamoeba

Indicated in: Hyperacute/purulent conjunctivitis (suspected gonococcal), neonatal conjunctivitis, chronic/recurrent conjunctivitis unresponsive to treatment, suspected chlamydial infection ^[1]^[2]
Tests: Gram stain, culture and sensitivity, PCR/NAAT for N. gonorrhoeae and C. trachomatis
Key findings:
- Gram-negative intracellular diplococci → N. gonorrhoeae
- Intracytoplasmic inclusions on Giemsa stain → Chlamydia trachomatis

E. Blood Investigations (for Systemic Associations)

Blood tests are NOT routine for red eye. They are specifically indicated when anterior uveitis, scleritis, or other features suggest an underlying systemic condition. ^[1]^[2]

Investigation	Looking For	Interpretation
HLA-B27	Seronegative spondyloarthropathies	Positive in ~50% of anterior uveitis; associated with acute, unilateral, recurrent, non-granulomatous uveitis
ESR / CRP	Inflammatory markers	Raised in sarcoidosis, Behçet's, vasculitis, infections
Serum ACE + Chest X-ray	Sarcoidosis	Elevated ACE (~60% sensitivity); bilateral hilar lymphadenopathy on CXR
VDRL / RPR + FTA-ABS	Syphilis	Must exclude syphilis in all uveitis cases (treatable cause!)
QuantiFERON-TB Gold / T-SPOT	Tuberculosis	Especially important in Hong Kong given the intermediate TB prevalence
ANA, anti-dsDNA	SLE	If clinical features suggest lupus
Toxoplasma serology	Toxoplasmosis	More relevant in posterior uveitis (retinochoroiditis)

The "standard uveitis workup" typically includes: CBC, ESR/CRP, HLA-B27, VDRL/FTA-ABS, QuantiFERON/T-SPOT, serum ACE, chest X-ray, and urinalysis. Tailor further tests to clinical suspicion. ^[1]^[2]

Investigation	Looking For
Rheumatoid factor + anti-CCP	Rheumatoid arthritis (most common systemic association)
ANCA (c-ANCA / p-ANCA)	GPA (Wegener's) / microscopic polyangiitis
ANA, anti-dsDNA, complement	SLE
ESR / CRP	General inflammation
Urea, creatinine, urinalysis	Renal involvement (vasculitis)
Chest X-ray	Sarcoidosis, GPA (pulmonary nodules/cavities)
VDRL, QuantiFERON	Syphilis, TB (infective scleritis)

F. Imaging Investigations

Indication: Posterior scleritis (cannot be directly visualised), vitreous haemorrhage obscuring fundal view, suspected retinal detachment, intraocular foreign body
Key finding in posterior scleritis: "T-sign" — fluid in sub-Tenon's space at the junction of the sclera and optic nerve, creating a T-shaped echo ^[1]^[2]
Also useful for measuring axial length (short axial length → hypermetropic → AACG risk)

Non-contact, high-resolution imaging of the anterior chamber angle and depth
Indication: Assessment of angle width in suspected angle closure — can quantify anterior chamber angle (supplement to gonioscopy)
Useful for monitoring corneal thickness and pathology

Indication: Orbital cellulitis (to identify subperiosteal/orbital abscess and guide drainage), orbital trauma (bony fractures, FB localisation), suspected intraocular/orbital foreign body (especially metallic)
CT is superior to MRI for detecting bony fractures and metallic foreign bodies ^[5]^[7]

Metallic FB and MRI

NEVER perform MRI if a metallic intraocular foreign body is suspected. The magnetic field can cause the metal to move within the eye, causing catastrophic further damage. Use CT for foreign body detection. Plain X-ray can also detect metallic FBs. ^[5]

Indication: Posterior scleritis evaluation, optic neuritis, orbital tumour, cavernous sinus pathology
Superior soft tissue contrast compared to CT; better for optic nerve and intracranial extension

High-frequency ultrasound (35–50 MHz) providing detailed images of the anterior segment, including the ciliary body and angle — structures not visible on slit lamp
Indication: Detailed angle assessment, ciliary body lesions, plateau iris configuration, angle recession after trauma

Test	Indication	Method	Key Finding
Schirmer's test	Dry eye assessment	Filter paper strip in lower fornix for 5 minutes	< 5 mm wetting = aqueous-deficient dry eye
Tear film breakup time (TBUT)	Dry eye (lipid layer deficiency)	Fluorescein → observe time until first break in tear film under slit lamp	< 10 seconds = unstable tear film
Amsler grid	Macular pathology (if visual blur accompanies red eye)	Patient fixates on central dot, reports distortion/scotoma	Metamorphopsia = macular oedema
Pachymetry	Corneal thickness measurement	Ultrasonic or optical device	Thick cornea may overestimate IOP; thin cornea may underestimate IOP
Corneal topography	Corneal curvature mapping	Placido disc / Scheimpflug imaging	Irregular astigmatism from corneal pathology (keratoconus, post-keratitis)
Fundoscopy (dilated)	Posterior segment evaluation	Direct/indirect ophthalmoscopy through dilated pupil	CONTRAINDICATED if AACG suspected (dilation worsens angle closure). Useful for posterior uveitis, retinal pathology

Do NOT Dilate in Suspected AACG

Pupil dilation with mydriatic drops (e.g. tropicamide, phenylephrine) is CONTRAINDICATED in suspected acute angle-closure glaucoma. Dilation worsens pupillary block by bringing the iris into closer contact with the lens → exacerbates the attack. Paradoxically, pilocarpine (a miotic) is part of the acute treatment — it constricts the pupil and pulls the iris away from the trabecular meshwork. ^[1]^[4]

Condition	Key Investigations
Conjunctivitis (viral/bacterial/allergic)	Usually none (clinical diagnosis); conjunctival swab + C/S only if hyperacute, neonatal, or refractory
SCH	Check BP, bleeding profile (PT/APTT/CBC) if recurrent
Episcleritis	Phenylephrine test (blanches); autoimmune screen only if recurrent
Scleritis	Phenylephrine test (does NOT blanch); full autoimmune/vasculitis screen; B-scan USS for posterior scleritis
Corneal abrasion/FB	Fluorescein staining, eyelid eversion
Microbial keratitis	Corneal scraping for Gram stain + C/S + KOH/PCR; fluorescein staining
HSV keratitis	Fluorescein staining (dendritic ulcer); corneal sensation testing; PCR if uncertain
Anterior uveitis	Slit lamp (cells, flare, KPs, synechiae); IOP; uveitis blood workup (HLA-B27, VDRL, IGRA, ACE, CXR)
AACG	IOP measurement (Goldmann/Tono-Pen); slit lamp (shallow AC, corneal oedema); gonioscopy (closed angle); van Herick test
Chemical injury	pH testing (litmus paper) AFTER irrigation; fluorescein staining; assess limbal ischaemia (blanching = stem cell damage)
Orbital cellulitis	CT orbit with contrast (abscess detection); CBC, blood culture; CT sinuses
Penetrating trauma/globe rupture	CT orbit (FB localisation, globe integrity); Seidel test; do NOT press on globe; NO MRI if metallic FB suspected

High Yield Summary — Diagnostics for Red Eye

Visual acuity is the FIRST and most important assessment — reduced VA = dangerous red eye
Fluorescein staining is the most useful bedside test for corneal pathology (abrasion, dendritic ulcer, Seidel test)
Slit lamp biomicroscopy is essential for: cells/flare (uveitis), corneal infiltrate (keratitis), AC depth (AACG), KPs, hypopyon
IOP measurement is critical in suspected AACG — IOP often > 40–60 mmHg
Phenylephrine 2.5% distinguishes episcleritis (blanches) from scleritis (does not blanch)
Corneal scraping is the gold standard for identifying the causative organism in microbial keratitis — perform BEFORE starting antibiotics
Blood tests are indicated for uveitis workup (HLA-B27, VDRL, IGRA, ACE, CXR) and scleritis workup (RF, ANCA, ANA)
CT orbit for orbital cellulitis, trauma, and metallic FB (never MRI for metallic FB)
B-scan USS for posterior scleritis (T-sign) and when fundal view is obscured
Always evert the upper lid to look for subtarsal FB in any patient with corneal scratches
Do NOT dilate in suspected AACG; do NOT press on globe in suspected rupture; do NOT delay irrigation in chemical injury

Active Recall - Diagnostics for Red Eye

References

Management of Red Eye

The management of red eye follows directly from the diagnostic approach: triage first, treat accordingly. The golden rule is to separate the "safe" from the "dangerous" — and for dangerous causes, initiate appropriate treatment immediately while arranging ophthalmology referral.

The management of red eye depends entirely on the underlying cause. There is no single "treatment for red eye." The priority is: (1) identify and manage immediate threats (chemical injury, globe rupture, AACG), (2) treat the specific condition, (3) refer urgently when indicated. ^[1]^[2]

Three principles underpin all red eye management:

Do no harm — avoid topical steroids unless the diagnosis is certain and under specialist supervision; never press on a ruptured globe; never dilate a pupil in AACG
Time-critical conditions first — chemical injury (irrigate NOW), AACG (lower IOP NOW), globe rupture (protect and refer NOW)
Treat the cause, not just the redness — treating surface redness with vasoconstrictors while missing uveitis or glaucoma is dangerous

Management by Condition

A. Immediate Emergencies (Minutes Matter)

Chemical injury is the ONE condition where you treat BEFORE doing anything else — even before checking visual acuity. ^[5]

Immediate management:

IRRIGATE IMMEDIATELY — copious saline (or tap water if saline unavailable) for at least 30 minutes. Use an IV giving set connected to a bag of normal saline, directing the stream across the ocular surface while holding the lids open. Do NOT delay for pH testing, VA testing, or history.
- Why irrigation first? Every second of chemical contact causes further tissue destruction. Dilution and removal of the chemical is the single most effective intervention. Nothing else matters until this is done.
Evert both lids — sweep fornices with a moist cotton bud to remove any retained solid particles (e.g. cement, plaster)
Check pH with litmus/pH paper AFTER irrigation. Continue irrigating until pH is neutral (7.0–7.4). Recheck pH 5 minutes after stopping irrigation to ensure it does not drift back (especially with alkali, which penetrates deeply and can continue to release from tissues).
Assess severity — document VA, degree of limbal ischaemia (blanching = limbal stem cell damage), corneal clarity, conjunctival involvement
Topical antibiotics (e.g. chloramphenicol) — prophylaxis against secondary infection
Topical cycloplegic (e.g. cyclopentolate 1%) — reduces ciliary spasm pain
Topical preservative-free lubricants — frequent, to maintain ocular surface hydration
Oral vitamin C (ascorbic acid) 1g QDS — promotes collagen synthesis in damaged corneal stroma
Topical citric acid 10% — chelates calcium to prevent calcium deposition in corneal stroma
Urgent ophthalmology referral for further assessment and grading (Roper-Hall or Dua classification)

Alkali burns are MORE dangerous than acid burns because alkali causes liquefactive necrosis — it saponifies cell membrane lipids, allowing deep penetration into corneal stroma, anterior chamber, and even the lens. Acid causes coagulative necrosis, which creates a barrier protein precipitate that limits further penetration (except hydrofluoric acid, which behaves like alkali). ^[5]

Key Principle

In chemical injury, the ONLY correct first step is IRRIGATION. Not checking pH. Not checking VA. Not taking a history. IRRIGATE FIRST. This is one of the most commonly examined points. ^[5]

An open globe injury requires immediate protection and emergency surgical repair. ^[5]

Management:

Shield the eye with a rigid eye shield (e.g. a plastic cup taped over the orbit) — do NOT use a pressure patch (this can extrude intraocular contents through the wound)
Do NOT press on the globe, do NOT remove any protruding foreign body — manipulation risks further extrusion of vitreous/uveal tissue
Nil by mouth — patient will need emergency surgery under general anaesthesia
Analgesia + antiemetic — vomiting raises IOP and can worsen extrusion
IV broad-spectrum antibiotics — prophylaxis against endophthalmitis (e.g. IV cefuroxime + IV gentamicin, or IV vancomycin + IV ceftazidime)
Check tetanus immunisation status — update if needed
CT orbit (NOT MRI) — to identify intraocular foreign body and assess extent of injury
Emergency surgical repair under general anaesthesia — primary wound closure, removal of intraocular FB if present, anterior chamber washout if needed

Signs of globe rupture to recognise ^[5]:

Teardrop (irregular) pupil pointing toward wound
Shallow anterior chamber (aqueous leak)
Positive Seidel test
360° subconjunctival haemorrhage with no visible posterior border
Hypotony (soft globe)
Exposed uveal tissue (dark brown/pigmented tissue visible)

This is a true ophthalmic emergency — permanent optic nerve damage can occur within hours if IOP is not lowered. ^[1]^[2]^[4]

Acute Medical Management (to lower IOP urgently):

The strategy is to reduce aqueous production and facilitate aqueous outflow simultaneously:

Step	Drug	Route	Mechanism	Why It Works
1	Timolol 0.5%	Topical (1 drop)	Non-selective beta-blocker → reduces aqueous production by ciliary body	Beta-2 receptors on ciliary epithelium mediate aqueous secretion; blocking them reduces production by ~25%
2	Apraclonidine 1% or Brimonidine 0.2%	Topical	Alpha-2 agonist → reduces aqueous production + increases uveoscleral outflow	Alpha-2 stimulation on ciliary epithelium suppresses cAMP-mediated aqueous secretion
3	Pilocarpine 2%	Topical (1 drop, repeat x1 after 15 min)	Cholinergic miotic → constricts pupil → pulls iris away from trabecular meshwork → opens drainage angle	This directly breaks the pupillary block mechanism. However, pilocarpine only works once IOP has been partially lowered (at very high IOP, the iris sphincter is too ischaemic to respond to pilocarpine) — hence give timolol FIRST to lower IOP, then pilocarpine
4	Acetazolamide 500 mg	IV (or oral if IV unavailable)	Carbonic anhydrase inhibitor → reduces aqueous production	Carbonic anhydrase in ciliary epithelium is essential for aqueous humour formation (facilitates Na⁺/HCO₃⁻ transport); inhibiting it reduces production by ~50%
5	Prednisolone acetate 1%	Topical, hourly	Topical corticosteroid → reduces secondary inflammation in the anterior segment	The acute IOP spike causes iris sphincter ischaemia and ciliary body congestion → secondary inflammation → further trabecular meshwork oedema. Steroids break this vicious cycle.
6	Mannitol 20% (1–2 g/kg)	IV infusion over 30–45 min	Osmotic agent → draws water from vitreous → reduces vitreous volume → lowers IOP	Used only if IOP remains uncontrolled despite above measures. Contraindicated in renal failure, heart failure (osmotic load). Also contraindicated in severe dehydration.

Positioning: Supine is often recommended (allows lens to fall back by gravity → may partially relieve pupillary block)

Definitive Management:

Treatment	Indication	Mechanism
Laser peripheral iridotomy (laser PI)	Definitive treatment for all angle-closure attacks ^[1]^[2]^[4]	A small hole is created in the peripheral iris with a Nd:YAG or argon laser → allows aqueous to flow directly from the posterior chamber to the anterior chamber, bypassing the pupil → eliminates pupillary block. Usually placed superiorly (covered by upper lid).
Prophylactic laser PI to the fellow eye	ALWAYS performed ^[1]^[4]	The fellow eye has the same anatomical predisposition (shallow AC, narrow angle) and is at high risk (~40–80% lifetime risk) of an acute attack → prophylactic PI prevents this.
Lens extraction (cataract surgery)	If persistent angle closure despite PI, or if significant cataract coexists	Removing the thickened lens deepens the anterior chamber and widens the angle → removes the anatomical substrate for pupillary block. Increasingly considered as primary treatment in some centres.

Why Pilocarpine AFTER Timolol?

When IOP is extremely high ( > 50–60 mmHg), the iris sphincter muscle is ischaemic and cannot respond to cholinergic stimulation. Giving pilocarpine as the first drug in this situation is futile. You must first lower IOP with timolol (and/or IV acetazolamide) to restore some blood flow to the iris sphincter — then pilocarpine can work effectively. This is a commonly examined point. ^[1]^[4]

Drugs That Can PRECIPITATE AACG

The following drugs are contraindicated (or used with extreme caution) in patients with narrow angles / known risk for angle closure ^[1]^[4]:

Anticholinergics (e.g. atropine, hyoscine, ipratropium inhaler, TCAs, antipsychotics) — cause pupil dilation → mid-dilation is the position of maximal pupillary block
Sympathomimetics (e.g. phenylephrine, adrenaline, pseudoephedrine) — also dilate the pupil
Topiramate, sulfonamides — can cause supraciliary effusion → forward rotation of ciliary body → secondary angle closure (mechanism different from pupillary block)
Mydriatic drops (tropicamide, cyclopentolate) — ophthalmological dilation drops; must assess angle before using

After laser PI, these drugs become safe because the iridotomy provides an alternative route for aqueous flow, bypassing the pupil.

Management is with topical steroids (to suppress inflammation) and cycloplegics (to relieve pain and prevent synechiae). ^[1]^[2]

Drug	Dose	Mechanism	Rationale
Topical prednisolone acetate 1%	Intensive: hourly during waking hours initially, then taper gradually over weeks based on cell count	Corticosteroid → suppresses inflammatory cascade (phospholipase A₂ inhibition → ↓prostaglandins, leukotrienes; ↓leukocyte migration; ↓vascular permeability)	Controls the intraocular inflammation, reduces cells and flare, prevents complications (synechiae, CMO, secondary glaucoma)
Topical cyclopentolate 1% or atropine 1%	2–3 times daily	Cycloplegic + mydriatic → relaxes ciliary muscle (relieves pain/photophobia) + dilates pupil (prevents/breaks posterior synechiae)	Two-fold benefit: (1) Pain relief — paralysing the inflamed, spasming ciliary muscle removes the source of the deep aching pain and photophobia; (2) Pupil dilation — keeps the iris away from the lens capsule, preventing inflammatory adhesions (posterior synechiae) that could cause pupil block glaucoma

Key management points:

Steroids must be tapered gradually, NOT stopped abruptly — sudden cessation causes rebound inflammation
Monitor IOP during steroid treatment — topical steroids can cause steroid-induced raised IOP (steroid responders) via increased trabecular meshwork resistance; this can lead to steroid-induced glaucoma
For recurrent or bilateral uveitis, investigate for underlying cause — HLA-B27, sarcoidosis, TB, syphilis, Behçet's
Systemic treatment is indicated for: posterior/panuveitis, sight-threatening uveitis, uveitis refractory to topical steroids, uveitis with systemic disease requiring treatment
- Systemic steroids (oral prednisolone)
- Steroid-sparing immunosuppressants: methotrexate, azathioprine, mycophenolate mofetil, ciclosporin
- Biologics: adalimumab (anti-TNF — first biologic licensed for non-infectious uveitis), infliximab, tocilizumab

The mnemonic for anterior uveitis treatment: "S + C" — Steroids (topical prednisolone to suppress inflammation) + Cycloplegics (cyclopentolate/atropine to relieve spasm and prevent synechiae). ^[1]^[2]

When Are Topical Steroids Safe vs Dangerous?

Topical steroids are INDICATED in anterior uveitis (to suppress inflammation) but CONTRAINDICATED as monotherapy in active epithelial HSV keratitis (enhances viral replication).

The rule is simple:

Uveitis = immune-mediated inflammation → steroids suppress the damaging immune response → beneficial
HSV epithelial keratitis = active viral infection → steroids suppress the immune response that is trying to clear the virus → virus replicates unchecked → ulcer enlarges → devastating

Steroids CAN be used in HSV stromal/disciform keratitis and HSV-related uveitis — but ONLY with concurrent antiviral cover (topical aciclovir) and under ophthalmologist supervision. ^[1]^[2]

This requires urgent ophthalmology referral and typically inpatient management with intensive topical antibiotics. ^[1]^[2]

Management steps:

Stop contact lens wear immediately — remove and keep lenses + case for microbiological analysis
Corneal scraping — for Gram stain + culture BEFORE starting antibiotics (as detailed in the diagnostics section)
Intensive topical fortified antibiotics — started empirically, then adjusted based on culture results:

Regimen	Coverage	Typical Agents
Dual fortified antibiotics (monotherapy with commercial drops is insufficient for severe ulcers)	Gram-positive + Gram-negative	Fortified cefuroxime 5% (or vancomycin 5%) + Fortified gentamicin 1.5% (or ceftazidime 5%)
Topical fluoroquinolone monotherapy	Broad-spectrum (acceptable for small, peripheral ulcers)	Ofloxacin 0.3% or moxifloxacin 0.5%

Why "fortified"? Commercial antibiotic drops have concentrations designed for conjunctivitis, which are insufficient for corneal stromal infection. Fortified drops are pharmacy-compounded at much higher concentrations to achieve therapeutic levels in the avascular corneal stroma.
Dosing: every 30 minutes to 1 hour, day AND night initially (e.g. alternating drops every 30 minutes) → gradually reduce frequency as ulcer improves ^[1]^[2]

Topical cycloplegic (e.g. cyclopentolate 1% TDS or atropine 1% BD) — reduces ciliary spasm pain
Do NOT patch the eye — a warm, moist, dark environment promotes bacterial growth
Do NOT use topical steroids initially — steroids impair corneal immune defences and can worsen infection. Steroids may be cautiously introduced later (after infection is controlled, under specialist supervision) to reduce corneal scarring.
Review frequently — daily slit lamp assessment for ulcer size, depth, hypopyon, visual acuity

Special cases:

Organism	Specific Treatment
Pseudomonas	Fortified gentamicin/tobramycin + fluoroquinolone; aggressive, frequent dosing
Fungal (Fusarium, Aspergillus)	Topical natamycin 5% (first-line for filamentary fungi) or topical amphotericin B 0.15%; oral voriconazole for deep infections
Acanthamoeba	Topical polyhexamethylene biguanide (PHMB) 0.02% + propamidine isethionate (Brolene) 0.1%; treatment required for months; very difficult to eradicate
HSV	See below

The hallmark dendritic ulcer is treated with topical antivirals. Topical steroids are CONTRAINDICATED in active epithelial disease. ^[1]^[2]

Type	Treatment	Rationale
Epithelial (dendritic/geographic)	Topical aciclovir 3% ointment, 5 times daily for 14 days (or topical ganciclovir 0.15% gel 5x/day)	Direct antiviral action — aciclovir is a guanosine analogue that is selectively phosphorylated by viral thymidine kinase → incorporated into viral DNA → chain termination. The selectivity for virus-infected cells (which express thymidine kinase) explains the low toxicity to normal cells.
Epithelial — alternative	Debridement — gentle removal of virus-laden epithelium with a sterile cotton bud under slit lamp	Physically removes viral reservoir from the corneal surface. Simple and effective for small dendrites. Often combined with antiviral.
Stromal/disciform (immune-mediated)	Topical steroid (e.g. prednisolone 0.5%) WITH concurrent topical aciclovir cover	The stromal disease is driven by immune-mediated inflammation (antigen-antibody complexes, T-cell response), not active viral replication. Steroids suppress the damaging immune response. BUT antiviral cover is mandatory to prevent viral reactivation while immune surveillance is suppressed.
Recurrent episodes	Oral aciclovir 400 mg BD prophylaxis (long-term)	The Herpetic Eye Disease Study (HEDS) showed oral aciclovir prophylaxis reduces recurrence rate by ~50%. Reduces both epithelial and stromal recurrences.

Key rule: In HSV keratitis, NEVER give topical steroids without topical antiviral cover. In epithelial disease, steroids are contraindicated altogether. In stromal disease, steroids + antivirals are used together. ^[1]^[2]

Treatment is with systemic antivirals, started within 72 hours of rash onset. ^[1]^[2]^[5]

Drug	Dose	Duration
Oral aciclovir	800 mg, 5 times daily	7 days
Oral valaciclovir (preferred — better bioavailability)	1 g TDS	7 days
Oral famciclovir	500 mg TDS	7 days

Hutchinson's sign (vesicles on nose tip/side) = high risk of ocular involvement → lower threshold for ophthalmology referral ^[1]^[2]^[5]
Topical aciclovir added if corneal involvement (pseudodendritic keratitis)
Topical steroids for anterior uveitis or stromal keratitis associated with HZO — with concurrent antiviral cover
Topical cycloplegic for ciliary spasm/pain
Analgesics — HZO causes severe neuralgic pain; may require paracetamol, NSAIDs, gabapentin/pregabalin for post-herpetic neuralgia

G. Conjunctivitis

Most common cause of infective conjunctivitis. Self-limiting. Treatment is supportive. ^[1]^[2]

Measure	Rationale
Supportive care: cool compresses, artificial tears (lubricants)	Symptomatic relief of irritation and discomfort
Hand hygiene — frequent handwashing, avoid touching eyes, do not share towels	Adenovirus is HIGHLY contagious — transmitted by direct contact and fomites. The virus can survive on surfaces for weeks. Strict hygiene prevents epidemic spread (schools, hospitals).
No topical antibiotics (unless secondary bacterial infection suspected)	Antibiotics do not work against viruses; unnecessary use promotes resistance
Avoid contact lenses until fully resolved	CL wear can worsen epithelial disruption and prolong recovery
Advise patient: self-limiting in 1–3 weeks	Manage expectations; the second eye often becomes involved 2–5 days after the first

Epidemic keratoconjunctivitis (EKC) caused by adenovirus serotypes 8, 19, 37 may cause subepithelial infiltrates (corneal immune deposits) that persist for months → can cause glare and reduced vision. May require low-dose topical steroids under ophthalmologist supervision.

Mild cases are self-limiting; topical antibiotics shorten the course. ^[1]^[2]

Drug	Dose	Notes
Chloramphenicol 0.5% drops	Every 2 hours initially, then QDS for 5–7 days	First-line in Hong Kong and UK; broad-spectrum, good conjunctival penetration, cheap
Chloramphenicol 1% ointment	QDS or at night	Better for nighttime use (provides prolonged contact); useful in children
Fluoroquinolone drops (ofloxacin 0.3%, moxifloxacin 0.5%)	QDS for 5–7 days	Reserved for severe cases or where Gram-negative cover is specifically needed
Fusidic acid 1% gel	BD	Effective against Staph. aureus; good compliance (only BD dosing)

Contraindications/Cautions:

Chloramphenicol: Rarely causes idiosyncratic aplastic anaemia (not dose-related; Type B ADR). Risk is extremely low with topical use (~1 in 30,000–50,000) but worth knowing for exams.
Aminoglycosides (gentamicin, tobramycin): Corneal epithelial toxicity with prolonged use — avoid for routine conjunctivitis.

This is an ophthalmological EMERGENCY — can perforate the cornea within 24–48 hours. ^[1]^[2]

Treatment	Details
Systemic ceftriaxone	1 g IM or IV single dose (adults); treats the systemic gonococcal infection
Frequent saline lavage	Copious saline irrigation to remove purulent discharge mechanically
Topical antibiotics	Adjunctive (e.g. chloramphenicol or fluoroquinolone drops)
Screen and treat for concurrent STIs	Chlamydia co-infection is common (~30%) → add oral azithromycin 1 g single dose or doxycycline 100 mg BD for 7 days
Contact tracing	Partner notification and treatment

Neonatal gonococcal ophthalmia: Systemic ceftriaxone (25–50 mg/kg IV/IM single dose, max 125 mg) + frequent saline irrigation + topical antibiotics

Topical treatment alone is INSUFFICIENT — must treat systemically. ^[1]

Treatment	Details
Oral azithromycin 1 g single dose	First-line; treats the intracellular organism systemically
Alternative: oral doxycycline 100 mg BD for 7 days	For patients who cannot tolerate azithromycin
Screen and treat sexual partners	Chlamydia is sexually transmitted
Screen for concurrent STIs	Gonorrhoea, HIV, syphilis

Why systemic treatment? Chlamydia trachomatis is an obligate intracellular pathogen — topical antibiotics cannot achieve adequate intracellular concentrations. Additionally, the genital tract is almost always co-infected → topical eye drops cannot treat the reservoir.

Treatment is stepwise: allergen avoidance → topical antihistamines/mast cell stabilisers → topical steroids (short course, specialist only). ^[1]^[2]

Step	Drug Class	Examples	Mechanism
1. Non-pharmacological	—	Allergen avoidance, cold compresses, artificial tears	Cold compresses: vasoconstriction + soothing. Tears: dilute and wash out allergens.
2. Topical antihistamine	H₁ receptor antagonist	Olopatadine 0.1% BD (also has mast cell stabiliser activity — "dual-action")	Blocks histamine at H₁ receptors on conjunctival nerve endings → reduces itching, redness, and chemosis
3. Topical mast cell stabiliser	Prevents mast cell degranulation	Sodium cromoglicate 2% QDS, lodoxamide 0.1% QDS	Stabilises mast cell membranes → prevents release of histamine and other mediators. Takes 1–2 weeks to reach full effect → best as prophylaxis rather than acute treatment
4. Topical NSAIDs	COX inhibitor	Ketorolac 0.5% QDS	Reduces prostaglandin-mediated inflammation; adjunctive for itching
5. Topical steroids (short course)	—	Prednisolone acetate 1%, fluorometholone 0.1%	Reserved for severe flares unresponsive to the above; should be used for shortest possible duration under specialist supervision due to risks of steroid-induced glaucoma, cataract, and secondary infection
6. Oral antihistamines	Systemic H₁ blocker	Cetirizine 10 mg daily, loratadine 10 mg daily	For concurrent allergic rhinitis/systemic allergy

For vernal keratoconjunctivitis (VKC) and atopic keratoconjunctivitis (AKC) — severe, chronic forms that may cause corneal damage:

Topical ciclosporin A 0.05–2% — immunomodulator that inhibits T-cell activation → steroid-sparing agent
Supratarsal injection of steroids (triamcinolone) for severe giant papillae
Shield ulcer may require epithelial debridement ± amniotic membrane transplant

Scleritis requires SYSTEMIC treatment — topical treatment alone is insufficient. ^[1]^[2]

Severity	Treatment
Mild, non-necrotising	Oral NSAIDs (e.g. indomethacin 25–50 mg TDS, naproxen 500 mg BD, ibuprofen 600 mg TDS) — first-line
Moderate / refractory	Oral corticosteroids (prednisolone 1 mg/kg/day, taper over weeks–months)
Severe / necrotising	Systemic immunosuppressants: methotrexate, azathioprine, mycophenolate mofetil, cyclophosphamide (for GPA/necrotising)
Necrotising scleritis with GPA	Cyclophosphamide or rituximab — same as systemic vasculitis treatment
Scleromalacia perforans	Scleral patch graft if perforation is imminent; treat underlying RA

Why systemic, not topical?

The sclera is relatively avascular — topical drops cannot penetrate deeply enough to reach the inflamed tissue
The inflammation is often immune complex–mediated vasculitis → requires systemic immunosuppression
~50% of patients have an underlying systemic autoimmune disease → this itself needs systemic treatment

Always screen for underlying systemic disease in scleritis: RA (RF, anti-CCP), GPA (c-ANCA), SLE (ANA), and infections (syphilis, TB). Treatment of the underlying condition is essential. ^[1]^[2]

Self-limiting. Treatment is symptomatic. ^[1]^[2]

Treatment	Details
Reassurance	Benign and self-limiting; resolves in 1–3 weeks
Artificial tears (lubricants)	Symptomatic relief
Topical NSAIDs (e.g. ketorolac 0.5% QDS)	If discomfort persists; reduces mild inflammation
Oral NSAIDs (ibuprofen, naproxen)	For more symptomatic cases
Topical steroids	Rarely needed; only for refractory cases; avoid chronic use

No treatment is needed — resolves spontaneously in 1–2 weeks. ^[1]^[2]

Action	Details
Reassurance	Painless, no vision threat, will self-resolve. The blood is reabsorbed by macrophages; may change colour (red → orange → yellow → clear) over 1–2 weeks.
Check blood pressure	If recurrent SCH, exclude hypertension
Check bleeding profile	If on anticoagulants/antiplatelets, or if recurrent — CBC, PT/INR, APTT
Artificial tears	If mild surface irritation (optional)

Red flags in SCH ^[5]:

No visible posterior border → suspect globe rupture or orbital fracture (blood tracking from orbit)
Post-traumatic → assess for occult globe injury
Recurrent → exclude bleeding diathesis

Most corneal abrasions heal within 24–48 hours with appropriate management. ^[1]^[5]

Treatment	Details
Topical antibiotic (prophylactic)	Chloramphenicol 0.5% drops QDS or ointment QDS for 5 days — prevents secondary bacterial infection of the epithelial defect
Topical cycloplegic	Cyclopentolate 1% TDS or homatropine 2% BD — relieves ciliary spasm and associated pain
Oral analgesics	Paracetamol ± NSAIDs for pain
Do NOT patch the eye	Patching does NOT accelerate healing and may actually increase risk of secondary infection (warm, moist, dark environment). Studies (including Cochrane reviews) show no benefit of patching for simple abrasions.
Review at 24–48 hours	Ensure healing is progressing; if not improving, consider recurrent erosion, secondary infection, or retained FB

Foreign body management ^[5]:

Topical anaesthetic (e.g. proxymetacaine 0.5%) — for comfort during removal
Remove FB under slit lamp with a sterile 25G needle or cotton bud
Metallic FB → remove rust ring with a sterile needle or ophthalmic burr under slit lamp magnification — rust ring causes ongoing chemical keratitis from iron oxidation if left in situ
Evert upper lid — check for and remove subtarsal FB
Post-removal: treat as per corneal abrasion (topical antibiotic + cycloplegic)

Topical Anaesthetic Abuse

NEVER prescribe topical anaesthetic drops (e.g. proxymetacaine, tetracaine) for patients to take home. Repeated use inhibits corneal epithelial healing, causes corneal epithelial toxicity, and masks worsening symptoms. They are used ONLY in clinic for examination and procedures. This is a common error in emergency departments. ^[1]^[5]

This is a medical and potential surgical emergency requiring inpatient management. ^[5]

Treatment	Details
IV broad-spectrum antibiotics	IV amoxicillin-clavulanate (augmentin) ± IV metronidazole; or IV ceftriaxone + metronidazole — must cover Strep., Staph., H. influenzae, and anaerobes (from sinusitis)
CT orbit with contrast	To identify subperiosteal or orbital abscess
Surgical drainage	Indicated if: abscess identified on CT, vision deteriorating, no improvement after 48 hours of IV antibiotics, or IOP rising
ENT consultation	Often needed for concurrent sinusitis management (which is the usual source)
Close monitoring	VA, pupil reactions (RAPD), colour vision, IOP, eye movements — to detect optic nerve compromise early

Chronic conditions requiring long-term maintenance therapy ("lid hygiene"). ^[1]^[2]

Step	Treatment	Rationale
1. Warm compresses	Warm flannel applied to closed lids for 5–10 minutes, BD	Melts solidified meibomian secretions → restores meibomian gland flow → improves lipid tear layer
2. Lid scrubs	Gentle cleaning of lid margins with dilute baby shampoo or commercial lid wipes	Removes bacterial biofilm, crusts, and debris from lid margin
3. Artificial tears	Preservative-free lubricants (e.g. hypromellose, carboxymethylcellulose)	Supplements deficient tear film → reduces ocular surface irritation
4. Topical antibiotics	Chloramphenicol or fusidic acid ointment to lid margins	For anterior blepharitis with significant staphylococcal colonisation
5. Oral antibiotics	Oral doxycycline 50–100 mg daily for 6–12 weeks	For moderate-severe MGD — doxycycline has anti-inflammatory properties (inhibits MMPs) beyond its antibiotic activity → improves meibomian gland function
6. Topical ciclosporin 0.05%	For moderate-severe dry eye disease refractory to lubricants	Immunomodulator → reduces ocular surface inflammation
7. Punctal plugs	Silicone plugs inserted into puncta to block tear drainage	Increases tear film residence time on the ocular surface — for moderate-severe aqueous-deficient dry eye

Drug	Contraindication	Why
Topical steroids	Active epithelial HSV keratitis (without antiviral cover)	Suppresses immune clearance of virus → uncontrolled replication → worsening ulcer
Topical steroids (chronic)	Undiagnosed red eye	May mask a sight-threatening diagnosis; risk of steroid glaucoma, cataract, infection
Mydriatic drops	Suspected AACG / known narrow angles (pre-PI)	Pupil dilation worsens pupillary block → exacerbates angle closure
Topical anaesthetics (take-home)	Never prescribe for home use	Inhibits corneal epithelial healing, causes toxic keratopathy
Anticholinergics (systemic)	Known narrow angles (pre-PI)	Pupil dilation → may precipitate AACG
Aminoglycosides (prolonged topical)	Routine conjunctivitis	Corneal epithelial toxicity
IV mannitol	Renal failure, heart failure	Osmotic load → fluid overload, electrolyte disturbances
Contact lenses	Active keratitis, conjunctivitis, uveitis	CL wear worsens corneal hypoxia and traps organisms/inflammation

Condition	First-Line Treatment	Key Points
Chemical injury	Immediate copious irrigation	Do NOT delay for anything; alkali > acid severity
Globe rupture	Shield, NBM, IV Abx, emergency surgery	Do NOT press on globe; CT not MRI
AACG	Timolol → pilocarpine → IV acetazolamide → definitive laser PI	Pilocarpine only works AFTER partial IOP reduction; prophylactic PI to fellow eye
Anterior uveitis	Topical steroid + cycloplegic	Taper steroids gradually; monitor IOP
Microbial keratitis	Corneal scraping → intensive fortified topical Abx	Stop CL; no steroid initially; no eye patch
HSV keratitis	Topical aciclovir 3% 5x/day	NO topical steroids in epithelial disease
HZO	Oral valaciclovir/aciclovir within 72 hours	Hutchinson's sign → ophtho referral
Viral conjunctivitis	Supportive (lubricants, cold compress, hygiene)	Self-limiting; highly contagious
Bacterial conjunctivitis	Topical chloramphenicol	Self-limiting but Abx shorten course
Gonococcal conjunctivitis	Systemic ceftriaxone + saline lavage	Emergency — can perforate cornea in 24–48h
Allergic conjunctivitis	Topical antihistamine/mast cell stabiliser	Itching is hallmark; steroids only for severe flares
Scleritis	Oral NSAIDs → systemic steroids → immunosuppressants	Topical treatment insufficient; screen for systemic disease
Episcleritis	Reassurance ± lubricants ± topical NSAIDs	Self-limiting
SCH	Reassurance	Check BP and bleeding profile if recurrent
Corneal abrasion/FB	Topical Abx + cycloplegic; remove FB	No eye patch; review 24–48h
Orbital cellulitis	IV Abx ± surgical drainage	CT orbit; monitor for optic nerve compromise

High Yield Summary — Management of Red Eye

Chemical injury: IRRIGATE FIRST — before checking VA, pH, or history. Alkali > acid.
Globe rupture: Shield (rigid), do NOT press, NBM, IV antibiotics, CT (not MRI), emergency surgery.
AACG: Timolol first (lower IOP to restore iris sphincter blood flow), THEN pilocarpine (miosis to open angle), THEN IV acetazolamide. Definitive = laser PI. Always do prophylactic PI on the fellow eye.
Anterior uveitis: Topical steroids + cycloplegics. Taper steroids gradually. Monitor IOP (steroid response).
Microbial keratitis: Corneal scraping BEFORE Abx. Intensive fortified topical Abx (every 30–60 min). Stop CL. No steroids initially. No eye patch.
HSV keratitis: Topical aciclovir 3% x5/day. NEVER topical steroids alone in epithelial disease. Steroids + antivirals okay for stromal disease under specialist.
Gonococcal conjunctivitis: Emergency — systemic ceftriaxone + saline lavage. Screen for chlamydia.
Scleritis: Systemic treatment (oral NSAIDs → steroids → immunosuppressants). Screen for RA, GPA.
Topical steroids safe in: uveitis, post-op inflammation, allergic (short course). Dangerous in: undiagnosed red eye, active HSV epithelial keratitis, suspected infection.
Never prescribe topical anaesthetics for home use — toxic to corneal epithelium.

Active Recall - Management of Red Eye

References

^[1] Lecture slides: GC 125. The Red Eye.pdf; 2024 General Clerkship - The Red Eye_Student Copy.pdf ^[2] Lecture slides: CFB (OPHTH01) Common Eye Diseases.pdf ^[3] Senior notes: Ryan Ho Opthalmology.pdf (p. 4, Ophthalmic History — Red Eye; p. 130, Graves Ophthalmopathy Management) ^[4] Lecture slides: GC 122. Chronic Visual Loss.pdf; GC 121. Acute Visual Loss.pdf (AACG content) ^[5] Lecture slides: GC 126. Trauma and Ocular Emergency.pdf

Complications of Red Eye Conditions

The complications of "red eye" are really the complications of the individual conditions that cause it. The unifying theme is straightforward: complications arise when the pathological process is either untreated, inadequately treated, or inherently aggressive enough to damage ocular structures despite treatment. The most devastating complications lead to permanent visual loss — which is why rapid triage and appropriate referral are so critical.

The complications can be organised by:

Complications of the disease itself (if missed or inadequately treated)
Complications of treatment (iatrogenic — particularly from topical steroids and surgery)

A. Complications by Condition

AACG is inherently destructive because acutely raised IOP (often > 60 mmHg) damages multiple structures simultaneously:

Complication	Mechanism	Clinical Significance
Irreversible optic nerve damage (glaucomatous optic neuropathy)	IOP > 40–50 mmHg compresses retinal ganglion cell axons at the lamina cribrosa → ischaemia and mechanical deformation → axonal death. Unlike chronic open-angle glaucoma (which takes years), acute angle closure can cause permanent damage within hours. ^[1]^[4]	This is the main reason AACG is an emergency — if IOP is not lowered within hours, the optic nerve suffers irreversible cupping and visual field loss
Iris sphincter atrophy	Extremely high IOP → ischaemia of the iris sphincter muscle → permanent muscle damage	Pupil may remain permanently dilated or irregular (sector iris atrophy) even after the attack is resolved
Anterior subcapsular/glaukomflecken cataract	High IOP causes direct pressure necrosis of anterior lens epithelial cells → small, white, anterior subcapsular opacities ("glaukomflecken" — from German, "glaucoma spots")	Pathognomonic sign of a previous acute angle-closure attack. The lens epithelial cells, once necrosed, leave permanent opacities. Usually does not significantly affect vision unless extensive.
Posterior synechiae	Acute inflammation during the attack → fibrinous adhesions between iris and lens capsule	Can cause chronic angle closure or pupil block if extensive (seclusio pupillae)
Corneal decompensation	Prolonged IOP elevation → endothelial cell loss → permanent stromal oedema	Chronic corneal haze → reduced vision
Central retinal artery occlusion (CRAO)	If IOP exceeds central retinal artery perfusion pressure → complete retinal ischaemia	Rare but devastating — sudden, complete, painless visual loss. "Cherry red spot" on fundoscopy.
Chronic angle-closure glaucoma	Peripheral anterior synechiae (PAS) form during the attack → permanent closure of portions of the angle → chronically raised IOP even after the acute episode resolves	Requires long-term IOP-lowering treatment ± surgery (trabeculectomy, tube shunt)

The fellow (unaffected) eye has a ~40–80% lifetime risk of an acute attack if prophylactic laser peripheral iridotomy is NOT performed. This is why bilateral PI is standard of care. ^[1]^[4]

If undertreated or if chronic/recurrent, anterior uveitis causes cumulative structural damage:

Complication	Mechanism	Clinical Significance
Posterior synechiae	Inflammatory fibrinous adhesions between the posterior surface of the iris and the anterior lens capsule → iris adheres to the lens ^[1]^[2]	Irregular pupil (won't dilate properly); if 360° synechiae form (seclusio pupillae), aqueous cannot flow through the pupil → iris bows forward (iris bombé) → secondary angle-closure glaucoma
Secondary glaucoma	Multiple mechanisms: (1) Pupil block from seclusio pupillae (see above); (2) Inflammatory debris clogs trabecular meshwork → reduced outflow; (3) Steroid-induced (from treatment)	Any form of secondary glaucoma → elevated IOP → optic nerve damage if untreated
Band keratopathy	Chronic anterior segment inflammation → calcium deposition in Bowman's membrane of the cornea → horizontal band of white/grey opacity across the interpalpebral cornea	Characteristic of chronic uveitis (especially JIA-associated uveitis in children). Reduces vision if central. Treated by chelation (EDTA) or excimer laser.
Cystoid macular oedema (CMO)	Chronic inflammation → breakdown of blood-retinal barrier → fluid accumulates in cystoid spaces in the outer plexiform layer (Henle's layer) of the macula	Most common cause of visual loss in uveitis. Diagnosed on OCT (macular thickening with cystoid spaces). Treated with intensive anti-inflammatory therapy (steroids, periocular triamcinolone injection, intravitreal anti-VEGF).
Cataract (posterior subcapsular)	Two causes: (1) Direct effect of chronic inflammation on lens epithelium → posterior subcapsular opacification; (2) Chronic topical or systemic steroid use → steroid-induced posterior subcapsular cataract	Common in patients with chronic uveitis; may require cataract surgery (but surgery itself can trigger uveitis flares → must ensure quiet eye for ≥3 months before operating)
Hypotony	Chronic ciliary body inflammation → reduced aqueous production → low IOP	Can lead to phthisis bulbi (shrunken, non-functional eye) in severe, end-stage cases
Phthisis bulbi	End-stage complication of severe, chronic, uncontrolled uveitis → globe shrinks from chronic hypotony, inflammation, and tissue destruction	Irreversible loss of the eye

JIA-Associated Uveitis — The Silent Threat

Juvenile idiopathic arthritis (JIA), particularly the oligoarticular subtype, causes a chronic, bilateral, non-granulomatous anterior uveitis that is often ASYMPTOMATIC — the eye looks white and quiet. Children do not complain. This means it can go undetected for months, silently causing posterior synechiae, band keratopathy, cataracts, and CMO. This is why all JIA patients must have regular slit lamp screening by an ophthalmologist. ^[1]^[6]

Corneal infections can progress rapidly, especially with virulent organisms:

Complication	Mechanism	Clinical Significance
Corneal perforation	Aggressive organisms (especially Pseudomonas, N. gonorrhoeae) produce proteases → rapid stromal necrosis → full-thickness corneal melt → perforation	Ophthalmological emergency — aqueous leaks out (positive Seidel test), anterior chamber collapses, iris prolapses through the defect. Requires emergency tectonic corneal grafting or tissue glue + bandage CL.
Endophthalmitis	Organisms spread from the cornea through into the anterior chamber and vitreous → overwhelming intraocular infection	Devastating — can result in loss of the eye. Presents with severe pain, markedly reduced vision, hypopyon, vitritis (vitreous haze). Requires intravitreal antibiotics ± vitrectomy.
Corneal scarring	Even after infection is cleared, the inflammatory response causes fibrosis and permanent stromal opacification	Permanent reduction in visual acuity if the scar is central. May ultimately require corneal transplantation (penetrating keratoplasty or DALK) for visual rehabilitation.
Descemetocele	Deep ulceration erodes through all stromal layers, leaving only Descemet's membrane (the thinnest layer) bulging forward → imminent perforation	Positive Seidel test may not be present yet (Descemet's intact), but the thin membrane is at extreme risk of rupture. Urgent surgical intervention (tissue glue, patch graft).
Secondary glaucoma	Inflammatory debris, PAS, or pupillary block from synechiae → raised IOP	Requires IOP management alongside infection control
Irregular astigmatism	Uneven healing and scarring → irregular corneal surface	Reduced best-corrected VA; may require rigid contact lens fitting or corneal surgery

The key feature of HSK is its recurrent nature — the virus persists in the trigeminal ganglion for life:

Complication	Mechanism	Clinical Significance
Recurrent epithelial keratitis	HSV-1 reactivation from trigeminal ganglion → virus travels along CN V₁ → re-infects corneal epithelium → dendritic ulcer recurs	Each recurrence damages more corneal nerves → progressive neurotrophic keratopathy; each episode also risks stromal involvement
Stromal keratitis (disciform/interstitial)	Immune-mediated — antigen-antibody complexes and T-cell response in the stroma cause inflammation → oedema, neovascularisation, and scarring	Leading cause of corneal visual loss from HSV. Requires topical steroids WITH antiviral cover.
Neurotrophic keratopathy	Repeated viral damage to corneal nerves → progressive loss of corneal sensation → corneal epithelium loses its trophic support (corneal nerves release substance P and other neuropeptides that maintain epithelial health) → persistent epithelial defects → sterile ulceration → melting	"The cornea that can't feel, can't heal." Reduced corneal sensation is both a diagnostic clue (preceding HSK) and a complication (consequence of HSK).
Corneal scarring and neovascularisation	Chronic/recurrent stromal inflammation → fibrosis and ingrowth of blood vessels into the normally avascular cornea	Permanent visual reduction; may require corneal transplantation (but high risk of graft rejection due to neovascularisation and ongoing viral reactivation)
Geographic (amoeboid) ulcer	IATROGENIC — occurs when topical steroids are given for active epithelial HSV without antiviral cover → uncontrolled viral replication → dendrite expands into a large, irregularly-shaped geographic ulcer	This is the feared complication of inappropriate steroid use in HSV keratitis — a preventable disaster ^[1]^[2]

Complication	Mechanism
Post-herpetic neuralgia (PHN)	Most common complication of HZO. Viral damage to sensory neurons → persistent neuropathic pain in V₁ distribution lasting months to years after rash resolution. More common in elderly (> 60 years). Risk reduced by early antiviral treatment.
Keratitis (pseudodendritic, stromal, neurotrophic)	Direct viral damage to cornea and corneal nerves
Anterior uveitis	Viral-triggered intraocular inflammation → cells, flare, raised IOP
Cranial nerve palsies	VZV-related vasculitis affecting CN III, IV, or VI → diplopia. Usually self-limiting but may take months to recover.
Secondary glaucoma	Trabeculitis (viral inflammation of trabecular meshwork) → reduced outflow → raised IOP
Corneal anaesthesia → neurotrophic keratopathy	Similar mechanism to HSV — viral damage to corneal nerves
Acute retinal necrosis (ARN)	Rare but devastating — VZV (or HSV) causes necrotising retinitis → can lead to retinal detachment and blindness

Complication	Mechanism	Clinical Significance
Scleral thinning and perforation	Necrotising scleritis → destruction of scleral collagen by vasculitis and proteolytic enzymes → progressive thinning → uveal tissue (dark brown) visible through thin sclera → risk of spontaneous perforation ^[1]^[2]	Most severe complication of necrotising scleritis. May require scleral patch grafting.
Scleromalacia perforans	Necrotising scleritis without inflammation — seen in long-standing RA → gradual, painless scleral necrosis	Paradoxically painless because the inflammation is so minimal — but the sclera melts away silently
Peripheral ulcerative keratitis (PUK)	Scleral inflammation extends to adjacent cornea → peripheral corneal thinning/ulceration	Often co-occurs with scleritis in RA/GPA; can perforate
Secondary glaucoma	Inflammation of adjacent trabecular meshwork, or from steroid treatment	IOP monitoring required
Uveitis	Contiguous spread of inflammation from sclera to uvea	Cells and flare, hypotony, CMO
Cataract	Chronic inflammation ± chronic steroid use	Posterior subcapsular cataract
Exudative retinal detachment	Posterior scleritis → choroidal inflammation → subretinal fluid accumulation	Presents with visual loss; diagnosed by B-scan USS or MRI

Scleritis is not just an eye disease — it is often a manifestation of serious systemic vasculitis. The life-threatening complication is the SYSTEMIC disease itself (e.g. GPA can cause pulmonary haemorrhage, renal failure; RA causes multisystem disease). Up to 50% of patients with scleritis have or will develop a systemic autoimmune condition. ^[1]^[2]

Most conjunctivitis is self-limiting, but complications can occur:

Condition	Complication	Mechanism
Gonococcal conjunctivitis	Corneal perforation	N. gonorrhoeae can penetrate INTACT corneal epithelium (unique among bacteria) → rapid stromal necrosis → perforation within 24–48 hours ^[1]^[2]
Neonatal gonococcal ophthalmia	Blindness	Same mechanism — devastating in newborns if untreated
Adenoviral keratoconjunctivitis (EKC)	Subepithelial infiltrates	Immune reaction to viral antigens deposited in anterior stroma → white, round, anterior stromal opacities → glare, photophobia, reduced contrast sensitivity. May persist for months. Can be treated with low-dose topical steroids (under specialist supervision).
Adenoviral conjunctivitis	Pseudomembrane/membrane formation	Severe inflammation → fibrin exudation on palpebral conjunctiva → pseudomembrane (peels easily) or true membrane (bleeds when removed). True membranes can cause conjunctival scarring → symblepharon (adhesion between bulbar and palpebral conjunctiva) → restricted eye movements, forniceal shortening.
Chlamydial (trachoma)	Corneal scarring → blindness	Repeated infection → tarsal conjunctival scarring → entropion → trichiasis (lashes turn inward and rub cornea) → corneal abrasion, ulceration, vascularisation, and scarring → blindness. Leading infectious cause of blindness worldwide.
Allergic (VKC/AKC)	Shield ulcer	Eosinophilic major basic protein (MBP) released from giant papillae is directly toxic to corneal epithelium → large, oval, central/superior epithelial defect (shield ulcer). May require debridement and amniotic membrane graft.
Allergic (VKC/AKC)	Keratoconus	Chronic eye rubbing (in response to itching) → mechanical weakening of the corneal stroma → progressive corneal thinning and conical protrusion. Strong association between atopic eye disease and keratoconus.

Complication	Mechanism	Clinical Significance
Limbal stem cell deficiency (LSCD)	Chemical destruction of limbal stem cells (located at the corneoscleral junction) → cornea can no longer regenerate its epithelium → conjunctival epithelium grows over the cornea (conjunctivalisation) → opaque, vascularised corneal surface ^[5]	The most devastating long-term complication of chemical burns. Treatment requires limbal stem cell transplantation (autologous from fellow eye, or allogeneic from donor/ex vivo expanded cells).
Corneal scarring and opacification	Stromal necrosis followed by disorganised fibrotic healing	Permanent visual reduction; may require corneal transplantation (but graft survival is poor in eyes with LSCD)
Symblepharon	Conjunctival scarring → adhesions between bulbar and palpebral conjunctiva → forniceal shortening → restricted eye movements	Requires surgical lysis; may recur
Corneal neovascularisation	Loss of limbal barrier → blood vessels invade the normally avascular cornea	Contributes to opacity; increases risk of corneal graft rejection
Glaucoma	Chemical damage to trabecular meshwork → reduced outflow; or angle closure from synechiae	May be immediate or delayed; difficult to manage
Cataract	Alkali penetrates to the lens → lens epithelial damage → cortical cataract	Especially with alkali burns
Phthisis bulbi	Severe burns with extensive destruction → chronic inflammation → globe shrinkage	End-stage; non-functional eye

Complication	Mechanism
Rebleeding (hyphaema)	Occurs at day 3–5 post-injury — the initial clot undergoes fibrinolysis and retracts, and friable new vessels at the iris/ciliary body tear site re-bleed. The rebleed is often larger than the initial haemorrhage. ^[5]
Raised IOP (from hyphaema)	Blood and clot block the trabecular meshwork → reduced aqueous outflow → acutely raised IOP
Corneal blood staining	Prolonged contact of blood with corneal endothelium (especially if IOP is raised) → haemoglobin breakdown products penetrate into the stroma → permanent yellowish-brown corneal staining
Endophthalmitis (post-penetrating injury)	Organisms introduced through the wound → intraocular infection
Sympathetic ophthalmia	A rare but devastating bilateral granulomatous panuveitis that occurs after penetrating injury (or surgery) to one eye. The immune system becomes sensitised to uveal antigens exposed by the injury → autoimmune attack on BOTH the injured and the uninjured (sympathetic) eye. ^[5]
Siderosis bulbi	Retained iron-containing intraocular foreign body → iron disseminates into ocular tissues → toxic damage to retina, lens, trabecular meshwork

Sympathetic Ophthalmia

Sympathetic ophthalmia is the classic exam question on complications of penetrating eye trauma. The key concept: uveal antigens (melanin-containing cells of the iris, ciliary body, choroid) are normally sequestered from the immune system behind the blood-ocular barrier. A penetrating injury breaches this barrier → uveal antigens are exposed to systemic immune cells → sensitisation → the immune system attacks BOTH eyes (because both contain the same uveal antigens). It is an example of an autoimmune response triggered by breakdown of immune privilege. ^[5]

B. Complications of Treatment (Iatrogenic)

Topical steroids are the most commonly used anti-inflammatory agent in ophthalmology but carry significant risks with prolonged use ^[1]^[2]:

Complication	Mechanism	Prevention
Steroid-induced raised IOP / steroid glaucoma	Steroids alter the extracellular matrix of the trabecular meshwork — increase deposition of glycosaminoglycans (GAGs) and reduce phagocytic activity of trabecular endothelial cells → reduced aqueous outflow → raised IOP	Monitor IOP at every follow-up visit during steroid treatment. "Steroid responders" (~30% of population) show clinically significant IOP rise. Use the lowest effective dose for the shortest duration.
Posterior subcapsular cataract	Chronic steroid exposure → inhibition of Na⁺-K⁺ ATPase pump in lens epithelial cells → osmotic swelling and disruption → posterior subcapsular opacification	Use lowest effective dose; consider steroid-sparing alternatives for chronic conditions
Exacerbation of ocular infection	Steroids suppress local immune defences → bacterial, viral (HSV), or fungal infections can flourish	Never prescribe steroids for undiagnosed red eye; never use steroids in active epithelial HSV without antiviral cover
Corneal thinning / delayed wound healing	Steroids inhibit fibroblast activity and collagen synthesis → impaired corneal stromal repair	Avoid in active corneal infection or after corneal surgery

The rule of thumb: every patient on topical steroids needs regular IOP monitoring. Any "steroid responder" who develops raised IOP should have their steroid tapered or switched to a "soft steroid" (e.g. fluorometholone, loteprednol) that has less IOP-elevating effect. ^[1]^[2]

Complication	Mechanism
Transient IOP spike	Inflammatory debris from the laser treatment temporarily blocks trabecular meshwork
Iritis	Laser energy causes localised iris inflammation
Corneal endothelial damage	Laser energy can damage corneal endothelial cells if the PI is performed too centrally or with excessive energy
Dysphotopsia (glare/haloes)	Light entering through the iridotomy → unwanted light rays hitting the retina → glare symptoms. Minimised by placing the PI superiorly (covered by upper lid).
Closure of PI	Inflammatory membrane or pigment occludes the iridotomy → may require repeat procedure

Corneal transplantation may be needed after severe keratitis, corneal scarring, or chemical injury:

Complication	Mechanism
Graft rejection	Host immune system recognises donor corneal endothelial antigens → immune-mediated destruction → endothelial rejection line (Khodadoust line), graft oedema, KPs on graft endothelium. Treated with intensive topical steroids.
Graft failure	Endothelial cell loss → corneal oedema → permanent opacity
Infection	Suture-related infection, recurrence of original infection (especially HSV)
Suture-related problems	Loose sutures, suture abscess, suture-induced astigmatism
Raised IOP	Steroid use post-transplant, or peripheral anterior synechiae

Some red eye conditions are markers of systemic disease — the "complications" extend far beyond the eye:

Ocular Condition	Systemic Association	Systemic Complications
Scleritis	RA, GPA (Wegener's), SLE, relapsing polychondritis	GPA: pulmonary haemorrhage, rapidly progressive glomerulonephritis, saddle nose deformity. RA: joint destruction, interstitial lung disease. SLE: nephritis, serositis, cytopenias.
Anterior uveitis	Ankylosing spondylitis, Crohn's disease, sarcoidosis, Behçet's	AS: spinal fusion, aortitis. Crohn's: strictures, fistulae. Sarcoidosis: pulmonary fibrosis, cardiac sarcoid. Behçet's: cerebral venous thrombosis, intestinal ulceration.
HZO	VZV reactivation (immunocompromise)	May indicate underlying immunosuppression — consider HIV testing in young patients with HZO
Gonococcal conjunctivitis	Disseminated gonococcal infection	Septic arthritis, tenosynovitis, endocarditis, meningitis
Orbital cellulitis	Sinusitis, facial infection	Cavernous sinus thrombosis, intracranial abscess (subdural/extradural), meningitis, sepsis ^[5]

High Yield Summary — Complications of Red Eye Conditions

Most important sight-threatening complications to know for exams:

AACG → irreversible optic nerve damage within hours; glaukomflecken; iris atrophy; CRAO ^[1]^[4]
Anterior uveitis → posterior synechiae → seclusio pupillae → secondary angle-closure glaucoma; CMO (most common cause of visual loss in uveitis); band keratopathy; cataract ^[1]^[2]
Microbial keratitis → corneal perforation (Pseudomonas, gonococcus); endophthalmitis; corneal scarring requiring transplantation ^[1]^[2]
HSV keratitis → recurrent disease; stromal scarring; neurotrophic keratopathy; geographic ulcer from inappropriate steroid use ^[1]^[2]
Scleritis → scleral perforation (necrotising); scleromalacia perforans (RA); PUK; systemic vasculitis complications ^[1]^[2]
Chemical injury → limbal stem cell deficiency (most devastating long-term complication); corneal scarring; symblepharon; phthisis ^[5]
Penetrating trauma → endophthalmitis; sympathetic ophthalmia (autoimmune bilateral panuveitis); siderosis bulbi ^[5]
Gonococcal conjunctivitis → corneal perforation within 24–48h (even through intact epithelium) ^[1]
Topical steroid complications → steroid glaucoma; posterior subcapsular cataract; worsening of infection (HSV, fungal) ^[1]^[2]
Trachoma → entropion → trichiasis → corneal scarring → blindness (leading infectious cause of blindness worldwide)
Hyphaema → rebleeding (day 3–5); raised IOP; corneal blood staining ^[5]

Active Recall - Complications of Red Eye

References

^[1] Lecture slides: GC 125. The Red Eye.pdf; 2024 General Clerkship - The Red Eye_Student Copy.pdf ^[2] Lecture slides: CFB (OPHTH01) Common Eye Diseases.pdf ^[4] Lecture slides: GC 122. Chronic Visual Loss.pdf; GC 121. Acute Visual Loss.pdf (AACG content) ^[5] Lecture slides: GC 126. Trauma and Ocular Emergency.pdf ^[6] Lecture slides: GC 123. Eye problems in children.pdf

High Yield Summary

Red Eye — Key Concepts for Exams:

Most common cause: Conjunctivitis (viral > bacterial > allergic)
Pattern of injection is key: diffuse conjunctival = benign; circumcorneal/ciliary = dangerous (keratitis, uveitis, AACG)
Safe red eye features: normal vision, no significant pain, normal pupil, no corneal opacity
Dangerous red eye features: ↓ vision, severe pain, photophobia, abnormal pupil, corneal opacity, raised IOP, cells/flare
AACG: severe pain, N/V, haloes, hazy cornea, fixed mid-dilated pupil, ↑↑↑ IOP — more common in East Asians — emergency
Contact lens wearer with painful red eye: assume microbial keratitis until proven otherwise → stop CL, urgent referral
HSV keratitis: dendritic ulcer — NEVER give topical steroids alone (enhances viral replication)
Anterior uveitis: pain, photophobia (consensual), miosis, ciliary injection, cells + flare
Scleritis: deep boring pain, violaceous hue, does NOT blanch with phenylephrine, associated with RA
Chemical injury: irrigate FIRST, check pH later; alkali > acid in severity
Hypopyon = WBC layer in AC → severe keratitis, endophthalmitis, Behçet's
Hutchinson's sign (nose vesicles) → HZO with ocular involvement
SCH without visible posterior border → suspect globe rupture

High Yield Summary — Differential Diagnosis of Red Eye

Approach: Triage first → safe vs dangerous. Key discriminators: vision, pain, pupil, cornea, IOP.
Most common cause overall: Viral conjunctivitis (adenovirus) — watery discharge, follicles, pre-auricular LN.
Most common cause of painful red eye with corneal ulcer: Microbial keratitis — especially in CL wearers (Pseudomonas).
Most dangerous "mimicker": AACG can mimic migraine or acute abdomen (N/V) — always check pupils and IOP.
Pattern recognition: Diffuse injection = conjunctivitis; ciliary injection = uveitis/keratitis/AACG; sectoral = episcleritis; violaceous = scleritis; flat red patch = SCH.
Phenylephrine test: Blanches = episcleritis (superficial); Does NOT blanch = scleritis (deep).
Abnormal pupil narrows DDx: Miotic = uveitis; Fixed mid-dilated = AACG; Irregular = synechiae or globe rupture.
Systemic associations: RA → scleritis; HLA-B27 → uveitis; Atopy → allergic conjunctivitis; CL wear → keratitis.
HSV keratitis: Dendritic ulcer — NEVER topical steroids alone.
Gonococcal conjunctivitis: Can perforate intact corneal epithelium — ophthalmological emergency.

High Yield Summary — Diagnostics for Red Eye

Visual acuity is the FIRST and most important assessment — reduced VA = dangerous red eye
Fluorescein staining is the most useful bedside test for corneal pathology (abrasion, dendritic ulcer, Seidel test)
Slit lamp biomicroscopy is essential for: cells/flare (uveitis), corneal infiltrate (keratitis), AC depth (AACG), KPs, hypopyon
IOP measurement is critical in suspected AACG — IOP often > 40–60 mmHg
Phenylephrine 2.5% distinguishes episcleritis (blanches) from scleritis (does not blanch)
Corneal scraping is the gold standard for identifying the causative organism in microbial keratitis — perform BEFORE starting antibiotics
Blood tests are indicated for uveitis workup (HLA-B27, VDRL, IGRA, ACE, CXR) and scleritis workup (RF, ANCA, ANA)
CT orbit for orbital cellulitis, trauma, and metallic FB (never MRI for metallic FB)
B-scan USS for posterior scleritis (T-sign) and when fundal view is obscured
Always evert the upper lid to look for subtarsal FB in any patient with corneal scratches
Do NOT dilate in suspected AACG; do NOT press on globe in suspected rupture; do NOT delay irrigation in chemical injury

High Yield Summary — Management of Red Eye

Chemical injury: IRRIGATE FIRST — before checking VA, pH, or history. Alkali > acid.
Globe rupture: Shield (rigid), do NOT press, NBM, IV antibiotics, CT (not MRI), emergency surgery.
AACG: Timolol first (lower IOP to restore iris sphincter blood flow), THEN pilocarpine (miosis to open angle), THEN IV acetazolamide. Definitive = laser PI. Always do prophylactic PI on the fellow eye.
Anterior uveitis: Topical steroids + cycloplegics. Taper steroids gradually. Monitor IOP (steroid response).
Microbial keratitis: Corneal scraping BEFORE Abx. Intensive fortified topical Abx (every 30–60 min). Stop CL. No steroids initially. No eye patch.
HSV keratitis: Topical aciclovir 3% x5/day. NEVER topical steroids alone in epithelial disease. Steroids + antivirals okay for stromal disease under specialist.
Gonococcal conjunctivitis: Emergency — systemic ceftriaxone + saline lavage. Screen for chlamydia.
Scleritis: Systemic treatment (oral NSAIDs → steroids → immunosuppressants). Screen for RA, GPA.
Topical steroids safe in: uveitis, post-op inflammation, allergic (short course). Dangerous in: undiagnosed red eye, active HSV epithelial keratitis, suspected infection.
Never prescribe topical anaesthetics for home use — toxic to corneal epithelium.

High Yield Summary — Complications of Red Eye Conditions

Most important sight-threatening complications to know for exams:

AACG → irreversible optic nerve damage within hours; glaukomflecken; iris atrophy; CRAO ^[1]^[4]
Anterior uveitis → posterior synechiae → seclusio pupillae → secondary angle-closure glaucoma; CMO (most common cause of visual loss in uveitis); band keratopathy; cataract ^[1]^[2]
Microbial keratitis → corneal perforation (Pseudomonas, gonococcus); endophthalmitis; corneal scarring requiring transplantation ^[1]^[2]
HSV keratitis → recurrent disease; stromal scarring; neurotrophic keratopathy; geographic ulcer from inappropriate steroid use ^[1]^[2]
Scleritis → scleral perforation (necrotising); scleromalacia perforans (RA); PUK; systemic vasculitis complications ^[1]^[2]
Chemical injury → limbal stem cell deficiency (most devastating long-term complication); corneal scarring; symblepharon; phthisis ^[5]
Penetrating trauma → endophthalmitis; sympathetic ophthalmia (autoimmune bilateral panuveitis); siderosis bulbi ^[5]
Gonococcal conjunctivitis → corneal perforation within 24–48h (even through intact epithelium) ^[1]
Topical steroid complications → steroid glaucoma; posterior subcapsular cataract; worsening of infection (HSV, fungal) ^[1]^[2]
Trachoma → entropion → trichiasis → corneal scarring → blindness (leading infectious cause of blindness worldwide)
Hyphaema → rebleeding (day 3–5); raised IOP; corneal blood staining ^[5]

Red Eye

Definition

Epidemiology and Risk Factors

Epidemiology

Risk Factors (by condition)

Anatomy and Function

Layers of the Eye (Outside → Inside)

Vascular Supply and Patterns of Injection

The Tear Film

Aetiology and Pathophysiology

A. Eyelid and Adnexal Causes

1. Blepharitis

2. Stye (Hordeolum)

3. Chalazion

B. Conjunctival Causes

4. Conjunctivitis (Most Common Cause of Red Eye)

a) Viral Conjunctivitis

b) Bacterial Conjunctivitis

c) Allergic Conjunctivitis

d) Chlamydial Conjunctivitis

5. Subconjunctival Haemorrhage (SCH)

6. Pterygium and Pinguecula

C. Episcleral and Scleral Causes

7. Episcleritis

8. Scleritis

D. Corneal Causes

9. Corneal Abrasion

10. Corneal Foreign Body

11. Keratitis (Corneal Infection/Inflammation)

a) Microbial Keratitis

b) Herpes Simplex Keratitis (HSK)

c) Herpes Zoster Ophthalmicus (HZO)

12. Corneal Ulcer (Sterile)

E. Uveal Causes

F. Raised Intraocular Pressure

G. Orbital / Periorbital Causes

15. Orbital Cellulitis

16. Cavernous Sinus Thrombosis

H. Traumatic Causes

17. Blunt Trauma (Contusion)

18. Penetrating / Perforating Injury

19. Chemical Injury

Classification

By Urgency (Most Clinically Useful)

By Anatomical Structure

By Pattern of Redness

Clinical Features

Structured Approach to History

Symptoms (with pathophysiological basis)

Signs (with pathophysiological basis)

Key Distinguishing Features Table (Master Comparison)

Summary of Red Flags Requiring Urgent Ophthalmology Referral

Active Recall - Red Eye

References

Conceptual Framework: The "Safe" vs "Dangerous" Red Eye

Comprehensive Differential Diagnosis List (by Anatomical Structure)

A. Eyelid and Adnexal Causes

B. Conjunctival Causes

C. Episcleral and Scleral Causes

D. Corneal Causes

E. Anterior Chamber and Uveal Causes

F. Orbital and Periorbital Causes

G. Traumatic Causes

H. Other / Systemic Causes

Master Differential Diagnosis Comparison Table

Clinical Approach to Narrowing the Differential

Important "Do Not Miss" Diagnoses

Special Populations

Red Eye in Children [6]

Red Eye in Contact Lens Wearers [1][2]

Red Eye After Ocular Surgery [1][5]

Active Recall - DDx of Red Eye

Overarching Principle

Diagnostic Criteria for Key Conditions

1. Acute Angle-Closure Glaucoma (AACG)

2. Anterior Uveitis

3. Microbial Keratitis (Corneal Ulcer)

4. Herpes Simplex Keratitis

5. Conjunctivitis (Viral vs Bacterial vs Allergic)

6. Scleritis