Lucan · Conditions

The red eye: approach

Australian guidance: WA HealthPathways Red Eye + RANZCO position statements + RACGP acute red eye guidance + eTG (empirical antimicrobial and ophthalmic principles)

1. Definition and epidemiology

A red eye is any presentation in which vascular congestion of the conjunctiva, episclera, sclera, or anterior uveal tract produces visible hyperaemia of the globe, and it is one of the most common presenting complaints in Australian general practice, optometry, and emergency departments. The overwhelming majority of red eyes are benign and self-limiting, dominated by infective and allergic conjunctivitis, but a small minority represent one of a handful of sight-threatening or globe-threatening emergencies, namely microbial keratitis, anterior uveitis, scleritis, and acute angle closure glaucoma.

The entire clinical task in a red eye consultation is therefore not to name every possible cause but to run a structured bedside filter that reliably separates this small dangerous minority from the safe majority, because the consequences of missing one of the four emergencies (permanent vision loss from corneal perforation, synechial angle closure, scleral necrosis, or ischaemic optic nerve damage) are far greater than the cost of over-referring a benign case, and this is the framing used by WA HealthPathways and RANZCO in structuring the primary care approach to red eye.

2. Pathophysiology: patterns of injection

The single most useful physical sign in a red eye is the pattern of vascular injection, because it reflects which vascular plexus is inflamed and therefore how deep the pathology sits. Conjunctivitis, subconjunctival haemorrhage, and episcleritis inflame the superficial conjunctival and episcleral vessels, producing a bright red, diffuse or sectoral injection that is most intense peripherally, fades toward the limbus, and is mobile when the conjunctiva is gently moved over the sclera with a cotton bud; this superficial plexus also blanches transiently with a drop of topical phenylephrine, a bedside test used to confirm episcleritis and exclude scleritis. Keratitis, anterior uveitis, and acute angle closure instead inflame the deep episcleral and scleral vascular plexus immediately surrounding the cornea, producing a dusky, violaceous ring of injection concentrated at the limbus (ciliary flush or circumlimbal injection) that does not blanch with phenylephrine and does not move with the conjunctiva, because these vessels lie fixed within the deeper sclera. Circumlimbal injection is the anatomical signature of anterior segment inflammation and is treated as a red flag in its own right, prompting the examiner to specifically look for the pain, photophobia, pupil change, and visual loss that accompany the four sight-threatening causes.

3. Clinical presentation and diagnostic criteria

Every red eye is triaged with five bedside questions: is visual acuity reduced, is there significant pain rather than mere grittiness or itch, is there photophobia, is the pupil abnormal in size, shape, or reactivity, and is the injection conjunctival or circumlimbal in pattern. A red eye with normal vision, no pain beyond mild discomfort, no photophobia, a normal pupil, and conjunctival injection is almost always benign; any deviation from this pattern raises concern for one of the emergencies below.

Conjunctivitis is the commonest cause and is subdivided by aetiology. Viral conjunctivitis, usually adenoviral, presents with watery discharge, a follicular reaction on the tarsal conjunctiva, and often a tender preauricular lymph node; it is highly contagious, frequently starts unilaterally before spreading to the fellow eye, and runs a course of one to three weeks. Bacterial conjunctivitis produces a mucopurulent discharge with lids stuck together on waking and a papillary conjunctival reaction, and is usually self-limiting even without treatment. Allergic conjunctivitis is bilateral, intensely itchy rather than painful, and associated with chemosis (conjunctival oedema) and a history of atopy or seasonal exposure. In all three, vision, pupil, and pattern of injection remain normal, which is what allows conjunctivitis to be managed without ophthalmology referral.

Episcleritis and scleritis both inflame the outer coat of the eye but differ sharply in severity and significance, and the two are distinguished at the bedside rather than by imaging. Episcleritis causes a sectoral patch of bright, superficial redness with only mild ache or foreign body sensation, blanches with topical phenylephrine, and is a benign, usually idiopathic, self-limiting condition that requires no systemic work-up in a typical case.

Scleritis instead causes severe, boring pain that characteristically wakes the patient at night and radiates to the jaw, forehead, or periorbital region, does not blanch with phenylephrine, is tender to palpation through the closed lid, may reduce vision, and is frequently the presenting feature of an underlying systemic autoimmune disease such as rheumatoid arthritis or granulomatosis with polyangiitis; necrotising scleritis can progress to scleral thinning and globe perforation if untreated, which is why the phenylephrine blanching test is taught as the single discriminator that separates a reassurance conversation from a same-day referral.

Keratitis is inflammation or infection of the cornea and presents with pain, marked photophobia, foreign body sensation, watering, and blurred vision, with an epithelial defect that stains with fluorescein under cobalt blue light; a branching, dendritic staining pattern is characteristic of herpes simplex keratitis.

Contact lens wear is a specific red flag in any painful red eye: overnight or extended wear, poor lens hygiene, and swimming or showering in lenses all predispose to microbial keratitis from Pseudomonas aeruginosa, which in severe or fulminant cases can progress to corneal perforation in as little as 24 to 48 hours, or to Acanthamoeba keratitis, which causes pain disproportionate to the clinical signs and a characteristic ring infiltrate; any contact lens wearer with a painful red eye is treated as microbial keratitis until proven otherwise and requires same-day ophthalmology assessment with the lenses, case, and solution brought for culture.

Anterior uveitis (iritis) presents with a painful, photophobic red eye, often with marked consensual photophobia (pain in the affected eye when light is shone into the unaffected eye), circumlimbal injection, a small, sluggish, or irregular pupil from posterior synechiae, and reduced vision from anterior chamber cellular activity or, in severe cases, a visible hypopyon. Roughly half of acute anterior uveitis in Australian practice is associated with HLA-B27-related spondyloarthropathy (ankylosing spondylitis, reactive arthritis, psoriatic arthritis, or inflammatory bowel disease), so a first presentation, particularly if recurrent or bilateral, prompts screening for these associations alongside urgent ophthalmology referral.

Acute angle closure glaucoma is the ophthalmic emergency that must never be missed. It presents with sudden, severe unilateral eye pain, headache, and often nausea and vomiting severe enough to mimic an acute abdomen, markedly reduced vision, and haloes seen around lights from corneal oedema. Examination shows a red eye with circumlimbal injection, a hazy or steamy cornea, and a fixed, mid-dilated, poorly reactive pupil, with the globe feeling firm or hard on gentle palpation through the closed lid; it is typically precipitated by pupillary dilation in a predisposed (hypermetropic, shallow anterior chamber) eye, including in dim light, emotional stress, or after pharmacological dilation with mydriatics or anticholinergic and sympathomimetic medications.

4. Investigations and AU-specific cutoffs

Visual acuity, measured with a Snellen chart, is the essential first step in every red eye assessment and functions as the ophthalmic vital sign; any reduction from baseline changes the presentation from routine to urgent regardless of the presumed diagnosis. Fluorescein staining under cobalt blue light is performed in any painful eye to detect corneal epithelial defects, abrasions, or the dendritic pattern of herpetic keratitis, and pupillary examination for size, shape, symmetry, and reactivity (including a relative afferent pupillary defect) is performed in every case with reduced vision or significant pain. Where slit lamp facilities are available, applanation tonometry measures intraocular pressure; normal pressure is roughly 10 to 21 mmHg, and acute angle closure classically presents with pressures well above 40 mmHg and sometimes above 60 mmHg, a level at which the diagnosis can be confirmed on the spot and treatment started before formal gonioscopy defines the angle anatomy in the ophthalmology clinic. Conjunctival or corneal swabs for bacterial culture or viral PCR are reserved for atypical, severe, recurrent, or neonatal conjunctivitis, since ophthalmia neonatorum from Neisseria gonorrhoeae or Chlamydia trachomatis is a notifiable, sight-threatening emergency in the first weeks of life. Recurrent or bilateral anterior uveitis and scleritis warrant a systemic work-up (inflammatory markers, HLA-B27, rheumatoid factor, ANCA, and a chest X-ray where sarcoidosis or granulomatosis with polyangiitis is suspected) to identify an underlying autoimmune or infective driver, consistent with RACGP and RANZCO guidance on investigating recurrent ocular inflammation. WA HealthPathways sets the referral thresholds used across primary care: optometry or community pharmacy review for uncomplicated conjunctivitis, GP review for atypical or persistent cases, and same-day ophthalmology or emergency department referral for any of the red flags described above.

5. Management

Viral conjunctivitis is managed supportively with cold compresses, lubricating drops, and strict hygiene advice given its high contagiousness; antibiotics have no role. Bacterial conjunctivitis is usually self-limiting, but topical chloramphenicol is first-line where treatment is desired, given the mild severity and rapid resolution expected. Allergic conjunctivitis responds to topical antihistamine or dual-action antihistamine and mast cell stabiliser drops alongside allergen avoidance.

Episcleritis requires only reassurance, lubricants, and a topical NSAID if uncomfortable, and resolves without ophthalmology input in most cases. Scleritis requires same-day ophthalmology referral; oral NSAIDs are first-line for mild disease, while moderate to severe or necrotising scleritis requires systemic corticosteroids or steroid-sparing immunosuppression alongside investigation and treatment of the underlying systemic disease.

Suspected microbial keratitis requires same-day ophthalmology referral, cessation of contact lens wear, and intensive topical antibiotics (a fluoroquinolone such as ofloxacin is typical first-line empirical therapy pending culture), while a dendritic ulcer confirmed on fluorescein staining is treated with topical or oral aciclovir. Topical corticosteroids must never be started in an undiagnosed red eye in primary care, because they can accelerate progression of an unrecognised herpetic or bacterial keratitis to corneal perforation; steroid use in keratitis is an ophthalmology decision made only once the organism and epithelial status are known.

Anterior uveitis is managed with same-day ophthalmology referral, a topical cycloplegic (cyclopentolate or, for more severe disease, atropine) to relieve ciliary spasm pain and prevent posterior synechiae, and topical corticosteroids initiated and tapered under ophthalmology supervision, alongside treatment of any identified systemic association.

Acute angle closure glaucoma is a same-day ophthalmic emergency requiring immediate referral to an eye emergency department: initial pressure-lowering treatment combines a topical beta-blocker, a topical alpha-2 agonist, and intravenous or oral acetazolamide, with topical pilocarpine added once the pressure has fallen enough for the sphincter muscle to respond, plus analgesia and an antiemetic for symptomatic relief; in severe or refractory presentations that fail to settle with this combination, a hyperosmotic agent (intravenous mannitol or oral glycerol) is added to draw fluid osmotically from the vitreous and achieve a faster pressure reduction. Definitive treatment is laser peripheral iridotomy in the affected eye with prophylactic iridotomy of the fellow eye given its shared anatomical predisposition.

6. Pharmacology and AU PBS notes

Chloramphenicol 0.5% eye drops and 1% ointment are Schedule 2 pharmacy medicines in Australia, available over the counter without a prescription for presumed bacterial conjunctivitis, reflecting the low risk of serious adverse effects from short-course topical use; PBS-subsidised prescription supply also exists for patients who see a doctor first. Topical NSAIDs such as ketorolac or flurbiprofen are used for episcleritis discomfort. Cyclopentolate 1% and atropine 1% are the standard cycloplegic agents for anterior uveitis and are PBS-listed. Acetazolamide, a carbonic anhydrase inhibitor, is given intravenously or orally in acute angle closure to rapidly reduce aqueous humour production and is PBS-listed for glaucoma indications. Topical glaucoma agents used in the acute setting, including timolol (beta-blocker), apraclonidine or brimonidine (alpha-2 agonists), and pilocarpine (miotic), are all PBS-listed with glaucoma-specific restrictions. Topical corticosteroids (prednisolone acetate, dexamethasone) are PBS-listed but, as above, are an ophthalmology-initiated therapy in any undiagnosed or infective-appearing red eye because of the risk of worsening keratitis or precipitating steroid-induced glaucoma. Topical aciclovir 3% eye ointment is used for herpes simplex dendritic keratitis and is PBS-listed as a restricted benefit for this indication.

7. Complications and same-day referral

The organising principle of red eye triage in Australian primary care is that reduced vision, significant pain, photophobia, an abnormal pupil, or circumlimbal (rather than purely conjunctival) injection each independently mandates same-day ophthalmology or emergency department referral, as does any contact lens wearer with a painful eye, any corneal opacity or epithelial defect, a fixed mid-dilated pupil with a hard globe, and any red eye in a neonate, since all of these patterns point toward the small set of causes in which delay costs vision. Untreated acute angle closure causes permanent optic nerve damage and profound, often irreversible visual loss within hours if intraocular pressure is not urgently controlled, while an unrecognised or undertreated microbial keratitis can progress to corneal scarring, perforation, and endophthalmitis. Necrotising scleritis left untreated progresses to scleral thinning and globe perforation, and recurrent or poorly controlled anterior uveitis leads to posterior synechiae, secondary glaucoma, cataract, and cystoid macular oedema, all of which erode vision cumulatively over successive episodes. By contrast, conjunctivitis, episcleritis, and a benign subconjunctival haemorrhage carry essentially no risk to vision and are managed safely without same-day referral once the emergency features above have been actively excluded, which is precisely why the bedside filter, rather than the specific diagnosis, is the skill this topic is built to teach.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.