Red Eye and Painful Eye

Conjunctivitis

Definition, pathobiology and classification

Conjunctivitis is inflammation of the bulbar and/or palpebral conjunctiva, producing conjunctival hyperaemia with preserved visual acuity and absence of significant corneal, anterior chamber, or pupillary abnormality. In MRCP-style red-eye questions, the key discriminator is that conjunctivitis is usually diffuse, superficial, relatively painless, and not photophobic; pain, reduced vision, ciliary flush, corneal opacity, fixed mid-dilated pupil, or severe headache should prompt consideration of keratitis, uveitis, or acute angle-closure glaucoma rather than simple conjunctivitis.

The conjunctiva is a mucosa-associated lymphoid tissue surface with goblet cells, resident dendritic cells, IgA, lysozyme, lactoferrin, and complement. Conjunctivitis results from microbial invasion, toxin-mediated inflammation, type I hypersensitivity, delayed hypersensitivity, toxic irritation, or tear-film instability. Hyperaemia reflects dilation of superficial conjunctival vessels, which move with the conjunctiva and blanch with topical vasoconstrictor; this contrasts with the deeper perilimbal injection of intraocular inflammation.

Type	Typical mechanism	Characteristic clinical clues	Exam-relevant associations
Viral	Usually adenovirus; direct epithelial infection and lymphoid follicular response	Watery discharge, gritty discomfort, follicles, preauricular lymphadenopathy; often starts unilateral then bilateral	Highly contagious; epidemic keratoconjunctivitis associated with adenovirus serotypes 8, 19, 37, 53, 54
Bacterial	Surface colonisation/invasion; neutrophilic exudate	Purulent or mucopurulent discharge, eyelids stuck on waking; papillae more than follicles	Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae; contact lens wear raises concern for Gram-negative infection
Hyperacute bacterial	Neisseria gonorrhoeae penetrates intact epithelium	Profuse purulent discharge, chemosis, marked lid oedema, rapid progression	Ophthalmic emergency due to corneal perforation risk; assess for STI coinfection
Chlamydial adult inclusion conjunctivitis	Chlamydia trachomatis serovars D–K; chronic follicular inflammation	Subacute/chronic unilateral or bilateral conjunctivitis, follicles, mucopurulent discharge, poor response to topical antibiotics	Concurrent urethritis/cervicitis; treat patient and sexual partners
Allergic	IgE-mediated mast-cell degranulation; late eosinophilic inflammation	Itching is dominant; bilateral watery discharge, chemosis, papillary reaction	Seasonal/perennial atopy; vernal/atopic forms may threaten cornea
Toxic/irritative	Medication preservative toxicity, chemical exposure, dry eye, foreign material	Burning, diffuse redness, temporal relation to drops/cosmetics/occupational exposure	Benzalkonium chloride toxicity; topical vasoconstrictor rebound

Clinical assessment and diagnostic thresholds

Assess visual acuity, pupils, corneal clarity, fluorescein staining, contact lens use, photophobia, trauma/chemical exposure, immunosuppression, and sexually transmitted infection risk. Conjunctivitis should have normal visual acuity apart from tear-film blurring, no corneal epithelial defect, and no consensual photophobia. Preauricular lymphadenopathy favours viral or chlamydial disease. Follicles are dome-shaped lymphoid elevations, classically viral/chlamydial; papillae have central vascular cores and occur in bacterial, allergic, and contact lens-related disease.

Routine culture is unnecessary in uncomplicated acute conjunctivitis. Swab for Gram stain/culture and nucleic acid amplification testing when disease is hyperacute, severe, recurrent, neonatal, immunocompromised, contact lens-associated, or not improving after 7–10 days, and when gonococcal or chlamydial infection is suspected. Adenoviral point-of-care immunoassays have reported sensitivities around 40–90% and specificities often above 90%, depending on kit and reference standard; they are not required for routine MRCP-level management decisions.

Management principles and pharmacology

Most uncomplicated conjunctivitis is self-limiting. Supportive measures include ocular lubricants, cold compresses, avoidance of contact lenses, meticulous hand hygiene, and no sharing of towels. Viral conjunctivitis typically resolves within 1–3 weeks; infectivity is greatest while tearing and discharge persist, commonly for 10–14 days. Topical corticosteroids are not used empirically because they may exacerbate herpetic epithelial disease and delay viral clearance; they require ophthalmology supervision.

Scenario	Preferred treatment	Key dosing	Comments
Uncomplicated bacterial conjunctivitis	Topical chloramphenicol or fusidic acid where local policy permits	Chloramphenicol 0.5% drops: 1 drop every 2 hours for 48 hours, then 4 times daily; continue 48 hours after resolution. Ointment 1% at night. Fusidic acid 1% gel: 1 drop twice daily.	UK practice commonly uses chloramphenicol; avoid soft contact lenses during therapy.
Contact lens wearer with suspected bacterial conjunctivitis	Urgent same-day ophthalmic assessment if pain, photophobia, reduced vision, or staining; consider antipseudomonal topical fluoroquinolone under local guidance	Ofloxacin 0.3%: commonly 1–2 drops 4 times daily; more intensive regimens if keratitis suspected	Do not dismiss as simple conjunctivitis; discard lenses/case.
Gonococcal conjunctivitis	Systemic ceftriaxone plus urgent ophthalmology/sexual health input	Ceftriaxone 1 g intramuscularly as a single dose is commonly recommended for uncomplicated gonococcal conjunctivitis in adults; irrigate saline if copious discharge	Test/treat chlamydia according to STI guidance; corneal perforation risk.
Adult chlamydial conjunctivitis	Systemic antichlamydial therapy	Doxycycline 100 mg orally twice daily for 7 days, or azithromycin 1 g orally once where appropriate	Topical therapy alone is inadequate; partner notification and STI screening.
Allergic conjunctivitis	Topical dual-action antihistamine/mast-cell stabiliser; lubricants	Olopatadine 0.1% 1 drop twice daily, ketotifen 0.025% 1 drop twice daily, or sodium cromoglicate 2% 1 drop 4 times daily	Oral non-sedating antihistamines may help rhinitis but can worsen dry eye.

Evidence for topical antibiotics in acute bacterial conjunctivitis shows modest benefit rather than dramatic cure. Cochrane reviews report increased early clinical remission compared with placebo, but high spontaneous resolution: approximately 60% of placebo-treated cases improve by days 2–5, and antibiotics shorten symptom duration by about 1–2 days in culture-positive disease. Therefore, delayed prescribing or no antibiotic is reasonable for mild cases, while immediate treatment is appropriate for purulent discharge, occupational need for rapid recovery, frailty, immunocompromise, or higher-risk presentations.

Red flags and examination traps

• Pain, photophobia, reduced acuity, ciliary flush, corneal opacity, abnormal pupil, nausea/vomiting, or headache are not typical of conjunctivitis and require urgent alternative diagnosis.
• Unilateral chronic conjunctivitis suggests chlamydia, molluscum contagiosum, lacrimal obstruction, masquerade malignancy, or retained foreign body.
• Membranous or pseudomembranous conjunctivitis occurs with severe adenovirus, Corynebacterium diphtheriae, Stevens–Johnson syndrome, ligneous conjunctivitis, or chemical injury and warrants specialist review.
• Itching is the most useful symptom favouring allergic conjunctivitis; purulence alone has limited diagnostic accuracy for bacterial disease.

Keratitis

Keratitis is inflammation of the cornea and is an ophthalmic emergency when infective, because stromal collagenolysis can progress to thinning, descemetocele, perforation and permanent visual loss within hours to days. In MRCP-style questions, the key discriminator is corneal involvement: pain, photophobia, foreign-body sensation, reduced visual acuity, ciliary injection and a fluorescein-staining epithelial defect or corneal opacity.

Pathophysiology and risk stratification

The corneal epithelium is a tight-junction barrier over an avascular stroma; breach of epithelium permits microbial adherence, toxin-mediated injury and neutrophil-driven stromal digestion. Contact lenses are the major modifiable risk factor: hypoxia, microtrauma and biofilm formation predispose particularly to Pseudomonas aeruginosa, which produces proteases and elastases causing rapidly progressive liquefactive necrosis. Other risks include topical corticosteroids, ocular surface disease, trauma with vegetable matter, diabetes, immunosuppression, lagophthalmos/exposure and reduced corneal sensation from trigeminal disease or herpes simplex.

Type	Typical clues	Fluorescein / slit-lamp findings	Exam-relevant danger
Bacterial keratitis	Contact lens wear, trauma, purulent discharge, severe pain	Focal epithelial defect with underlying stromal infiltrate; possible hypopyon	Pseudomonas may perforate rapidly; urgent same-day ophthalmology
HSV epithelial keratitis	Recurrent unilateral red painful eye, reduced corneal sensation	Branching dendritic ulcer with terminal bulbs staining with fluorescein/rose bengal	Topical steroid monotherapy worsens epithelial viral replication
HSV stromal/endothelial keratitis	Pain, photophobia, blurred vision; may have previous HSV	Stromal haze, disciform oedema, keratic precipitates; epithelial defect may be absent	Immune-mediated scarring; treatment requires ophthalmic steroid plus antiviral cover
Acanthamoeba keratitis	Contact lens exposure to tap water/swimming; pain disproportionate to signs	Early punctate keratitis; radial keratoneuritis; late ring infiltrate	Often misdiagnosed as HSV; prolonged intensive therapy required
Fungal keratitis	Trauma with vegetable matter, agricultural exposure, steroid use	Feathery-edged infiltrate, satellite lesions, dry surface, hypopyon	Deep stromal invasion; poor response to antibacterial drops

Assessment, staging and when to culture

Assess visual acuity before drops, contact lens history, onset rate, trauma, immunosuppression and steroid exposure. Examine for epithelial defect size, stromal infiltrate size/depth, distance from visual axis, anterior chamber reaction, hypopyon and corneal thinning. Fluorescein is essential; a cobalt-blue light reveals epithelial loss, while Seidel positivity indicates aqueous leak and possible perforation.

Microbiological scraping is recommended before antibiotics when keratitis is severe, central, large, atypical or treatment-resistant. A practical rule is the 1-2-3-ACT approach: culture if there is ≥1+ anterior chamber cells, an infiltrate ≥2 mm, or the infiltrate edge lies within 3 mm of the corneal centre; culture also for contact lens-related, fungal, Acanthamoeba or immunocompromised cases. Contact lenses, case and solution should be sent for culture when relevant.

Management principles

All suspected microbial keratitis requires urgent ophthalmology assessment. Initial management includes stopping contact lens wear, avoiding eye patching, analgesia, antiemetics if needed, and cycloplegia for ciliary spasm. Topical anaesthetics should not be prescribed for home use because they delay epithelial healing and can cause toxic keratopathy.

Condition	Typical treatment	Key pharmacological points
Small peripheral bacterial ulcer	Topical fluoroquinolone, e.g. ofloxacin 0.3% or levofloxacin 0.5% hourly initially, then tapered according to response	Good gram-negative cover; monotherapy often adequate for low-risk ulcers
Severe, central or sight-threatening bacterial keratitis	Fortified antibiotics such as cefazolin 5% plus gentamicin 1.4% or tobramycin 1.3% hourly, including overnight initially	Broader high-concentration cover; aminoglycosides cover Pseudomonas but are epithelial-toxic
HSV epithelial keratitis	Aciclovir 3% ointment five times daily or ganciclovir 0.15% gel five times daily until healed, then usually for several further days	Avoid topical corticosteroids unless directed by ophthalmology; debriding infected epithelium may reduce viral load
HSV stromal keratitis	Topical corticosteroid under ophthalmology supervision plus antiviral cover; oral aciclovir commonly 400 mg five times daily for active disease	Inflammation is largely immune-mediated; antiviral cover prevents epithelial recrudescence
Acanthamoeba keratitis	PHMB 0.02% and/or chlorhexidine 0.02% very frequently initially, often hourly, then prolonged taper over months	Cysts are resistant; early diagnosis improves outcome
Fungal keratitis	Natamycin 5% hourly for filamentous fungi; voriconazole 1% topical or systemic therapy may be used for deep or resistant disease	MUTT I showed natamycin superior to topical voriconazole for filamentous keratitis, especially Fusarium

Cycloplegics such as cyclopentolate 1% two to three times daily reduce painful ciliary spasm and help prevent posterior synechiae when there is associated anterior chamber inflammation. Oral analgesia is often required. Topical corticosteroids are nuanced: they may reduce immune-mediated scarring in selected bacterial or stromal herpetic disease, but only after organism-directed antimicrobial therapy has been established and under specialist supervision. The SCUT trial found no overall 3-month visual acuity benefit from adjunctive topical corticosteroid in bacterial keratitis, although possible benefit was seen in severe central ulcers and early-treated cases; harm is a concern in fungal, Acanthamoeba and untreated HSV epithelial keratitis.

Herpetic recurrence prevention is exam-relevant. The Herpetic Eye Disease Study showed oral aciclovir 400 mg twice daily for 12 months reduced ocular HSV recurrence from approximately 32% to 19%, and recurrent stromal keratitis in patients with previous stromal disease from about 28% to 14%. Long-term prophylaxis is considered after recurrent or sight-threatening HSV keratitis, particularly if topical steroids are required.

Uveitis

Definition, classification and pathobiology

Uveitis denotes intraocular inflammation involving the uveal tract, but clinically includes adjacent retina, vitreous and optic nerve inflammation. For MRCP, the key red painful eye phenotype is acute anterior uveitis: ciliary flush, photophobia, aching periocular pain, small or irregular pupil, and cells/flare in the anterior chamber. Mechanistically, breakdown of the blood–aqueous or blood–retinal barrier permits leukocyte trafficking and protein leakage, mediated by TNF-α, IL-6, IL-17, interferon-γ and prostaglandins. HLA-B27 disease is typically acute, unilateral or alternating, non-granulomatous and recurrent; sarcoidosis, tuberculosis and syphilis more often produce granulomatous inflammation with “mutton-fat” keratic precipitates.

Classification	Key features	Important associations
Anterior	Iritis/iridocyclitis; cells and flare; pain, photophobia, ciliary injection	HLA-B27 spondyloarthritis, reactive arthritis, psoriatic arthritis, IBD, JIA, HSV/VZV, sarcoidosis
Intermediate	Vitreous cells, “snowballs/snowbanking”; floaters more than pain	Multiple sclerosis, sarcoidosis, TB, idiopathic pars planitis
Posterior	Retinitis, choroiditis, retinal vasculitis; visual loss, floaters	Toxoplasmosis, CMV in immunosuppression, Behçet disease, sarcoidosis, syphilis
Panuveitis	Inflammation in anterior chamber, vitreous and retina/choroid	Behçet disease, Vogt–Koyanagi–Harada, sarcoidosis, TB, syphilis

Clinical assessment and grading

The Standardization of Uveitis Nomenclature (SUN) system grades anterior chamber cells using a 1 mm × 1 mm slit beam: 0 (<1 cell), 0.5+ (1–5), 1+ (6–15), 2+ (16–25), 3+ (26–50), 4+ (>50). Flare is graded 0 to 4+ according to protein scatter. Disease duration is limited if ≤3 months and persistent if >3 months; chronic implies relapse within 3 months of stopping therapy, while recurrent describes repeated episodes separated by inactive intervals ≥3 months off treatment.

• Symptoms: consensual photophobia is highly suggestive of iritis; reduced acuity suggests severe anterior disease, keratitis, glaucoma, macular oedema or posterior involvement.
• Signs: circumcorneal injection, keratic precipitates, aqueous cells/flare, posterior synechiae, hypopyon, raised or low intraocular pressure. A dendritic corneal ulcer suggests herpetic keratouveitis rather than idiopathic anterior uveitis.
• Red flags requiring same-day ophthalmology: reduced visual acuity, hypopyon, corneal opacity, irregular pupil, immunosuppression, suspected herpetic disease, or raised intraocular pressure.

Investigations and systemic associations

A first mild episode of unilateral acute anterior uveitis may need no extensive systemic work-up once infection and keratitis are excluded. Recurrent, bilateral, granulomatous, posterior, intermediate or severe disease warrants targeted investigation. Examination should actively seek inflammatory back pain, enthesitis, psoriasis, oral/genital ulceration, diarrhoea, pulmonary symptoms, neurological symptoms and sexually transmitted infection risk.

Clinical clue	Suggested tests	Rationale
Recurrent acute anterior uveitis, back pain	HLA-B27, CRP/ESR; sacroiliac imaging if indicated	Up to 50% of acute anterior uveitis is HLA-B27-associated in many European cohorts
Granulomatous, bilateral, pulmonary features	Chest radiograph/CT, serum ACE, calcium; consider TB testing	Sarcoidosis; ACE has limited specificity and is not diagnostic alone
Posterior uveitis or retinal vasculitis	Syphilis serology, HIV test; toxoplasma serology when focal retinochoroiditis	Infectious mimics must be excluded before immunosuppression
Oral/genital ulcers, hypopyon	Clinical diagnosis; HLA-B51 supportive only	Behçet uveitis is sight-threatening and often relapsing

Management principles

Initial management of acute anterior uveitis is ophthalmology-led but exam candidates should know the pharmacological logic. Treatment aims are rapid suppression of inflammation, analgesia, prevention of posterior synechiae and detection of complications. Topical corticosteroids reduce cytokine transcription via glucocorticoid receptor signalling; typical regimens include prednisolone acetate 1% one drop every 1–2 hours initially, then taper over weeks according to anterior chamber cell grade. Difluprednate 0.05% is more potent but has higher risk of steroid-induced ocular hypertension. Steroids are hazardous if epithelial HSV keratitis is missed.

Drug class	Examples and typical use	Key cautions
Cycloplegic/mydriatic	Cyclopentolate 1% one drop 2–3 times daily; atropine 1% once or twice daily in severe disease	Relieves ciliary spasm and prevents synechiae; avoid unnecessary prolonged mydriasis
Topical steroid	Prednisolone acetate 1% hourly to 2-hourly initially in severe anterior uveitis	Raises intraocular pressure, cataract risk, worsens untreated herpetic/fungal keratitis
Periocular/intravitreal steroid	Triamcinolone acetonide 40 mg sub-Tenon or intravitreal 4 mg/0.1 mL in selected posterior/intermediate disease	Ocular hypertension, cataract, infection; avoid if infectious uveitis possible
Systemic steroid	Prednisolone 0.5–1 mg/kg/day for severe bilateral, posterior or systemic disease, then taper	Exclude TB, syphilis, viral retinitis; bone, glucose and gastric protection as appropriate

Steroid-sparing immunomodulation is indicated for chronic, relapsing, bilateral, posterior or sight-threatening disease, or when prednisolone cannot be reduced below approximately 7.5–10 mg/day without relapse. Common agents include methotrexate 15–25 mg weekly with folic acid, mycophenolate mofetil 1 g twice daily, azathioprine 1–2.5 mg/kg/day and ciclosporin 2–5 mg/kg/day. In non-infectious intermediate, posterior and panuveitis, adalimumab 40 mg subcutaneously every 2 weeks after an 80 mg loading dose is evidence-based; VISUAL I and II showed significantly prolonged time to treatment failure versus placebo. Complications tested in exams include cataract, secondary glaucoma, cystoid macular oedema, posterior synechiae, band keratopathy and permanent visual loss.

Acute Angle-Closure Glaucoma

Acute angle-closure glaucoma is an ophthalmic emergency caused by sudden obstruction of aqueous outflow through the trabecular meshwork, producing a rapid rise in intraocular pressure (IOP), corneal oedema, iris ischaemia and risk of irreversible optic nerve damage. Normal IOP is approximately 10–21 mmHg; acute attacks commonly present with IOP 40–80 mmHg. For MRCP, the key is to distinguish it from conjunctivitis, keratitis and anterior uveitis: visual loss, severe pain, haloes, vomiting, a cloudy cornea and a mid-dilated fixed pupil are high-yield features.

Mechanism and classification

The commonest mechanism is relative pupillary block. Aqueous produced by the ciliary body cannot pass freely from posterior to anterior chamber through the pupil, creating a pressure gradient that bows the peripheral iris anteriorly (iris bombe) and apposes it to the trabecular meshwork. Predisposing anatomy includes a short axial length, hypermetropia, shallow anterior chamber, thick or anteriorly positioned lens, older age and female sex. East Asian and Inuit populations have particularly high prevalence. Attacks are precipitated by physiological or pharmacological mydriasis: dim light, stress, anticholinergics, sympathomimetics, tricyclics, selective serotonin reuptake inhibitors, topiramate and nebulised ipratropium/salbutamol in susceptible patients.

Classification	Definition	Clinical implication
Primary angle-closure suspect	Iridotrabecular contact, typically ≥180°, without raised IOP, peripheral anterior synechiae or optic neuropathy	Risk stratification; prophylactic laser considered in high-risk eyes
Primary angle closure	Occludable angle with raised IOP and/or peripheral anterior synechiae, but no glaucomatous optic neuropathy	Requires definitive angle-opening treatment
Primary angle-closure glaucoma	Primary angle closure plus glaucomatous optic neuropathy and compatible visual field loss	Chronic disease control after acute management
Acute angle-closure crisis	Sudden symptomatic angle closure with marked IOP elevation	Same-day ophthalmology emergency

Clinical features and diagnosis

Patients typically report abrupt unilateral severe ocular pain, frontal headache, blurred vision, coloured haloes around lights, nausea and vomiting. Examination shows reduced visual acuity, circumcorneal injection, hazy oedematous cornea, shallow anterior chamber, hard globe and a mid-dilated poorly reactive pupil. IOP measurement confirms the diagnosis, but treatment should not be delayed if tonometry is unavailable. Slit-lamp examination may show corneal epithelial oedema and mild anterior chamber inflammation. Gonioscopy, once the cornea is sufficiently clear, confirms angle closure and assesses the fellow eye. Optic disc assessment is needed after pressure control.

Feature	Acute angle closure	Anterior uveitis	Keratitis
Pupil	Mid-dilated, fixed	Small/irregular, photophobic	Usually normal or reactive
Cornea	Diffuse oedema, haloes	Keratic precipitates may occur	Focal epithelial defect or infiltrate
IOP	Markedly raised, often >40 mmHg	Often low or mildly raised	Usually normal unless secondary glaucoma
Systemic symptoms	Nausea/vomiting common	Uncommon	Uncommon

Emergency management

Immediate aims are to lower IOP, reduce inflammation and reverse angle closure, followed by definitive laser treatment. Give analgesia and antiemetic therapy, keep the patient supine if tolerated, and avoid further mydriatics. Urgent ophthalmology referral is mandatory.

Drug/intervention	Typical adult regimen	Rationale and cautions
Acetazolamide	500 mg IV or orally stat, then 250 mg orally 6-hourly	Carbonic anhydrase inhibitor; reduces aqueous production. Half-life approximately 6–9 h. Avoid in severe renal/hepatic disease, sulfonamide hypersensitivity, Addison disease, significant hyponatraemia/hypokalaemia.
Topical beta-blocker	Timolol 0.5% 1 drop	Reduces aqueous production. Avoid in asthma/COPD with bronchospasm, bradycardia, second/third-degree heart block, decompensated heart failure.
Alpha-2 agonist	Apraclonidine 0.5–1% 1 drop or brimonidine 0.2% 1 drop	Reduces aqueous production and increases uveoscleral outflow; useful rapid adjunct.
Pilocarpine	2% 1 drop, repeated after 15–30 min once IOP begins to fall	Miosis pulls peripheral iris away from trabecular meshwork. Ineffective when IOP is very high, usually >40–50 mmHg, due to iris sphincter ischaemia; avoid in lens-induced or inflammatory secondary closure unless advised.
Topical corticosteroid	Prednisolone acetate 1% 1 drop hourly initially	Controls secondary anterior segment inflammation; ophthalmology-directed.
Hyperosmotic therapy	Mannitol 20% IV 1–2 g/kg over 30–60 min; oral glycerol 1–1.5 g/kg if appropriate	For very high or refractory IOP. Avoid/caution in heart failure, severe renal impairment, dehydration; glycerol worsens hyperglycaemia and nausea.

Definitive treatment and evidence

Once the cornea clears and IOP is controlled, definitive treatment is laser peripheral iridotomy, usually to the affected eye and prophylactically to the fellow eye, because the fellow eye is anatomically predisposed. Iridotomy bypasses pupillary block by equalising posterior and anterior chamber pressure. If laser is not possible, surgical iridectomy or lens extraction may be required. Persistent raised IOP after angle opening implies chronic trabecular damage, peripheral anterior synechiae or established primary angle-closure glaucoma, requiring long-term pressure-lowering therapy and optic nerve monitoring.

The EAGLE trial supported early clear-lens extraction in selected patients aged ≥50 years with primary angle closure and IOP ≥30 mmHg or primary angle-closure glaucoma, showing better health status and approximately 1.18 mmHg lower mean IOP than standard care at 36 months. The ZAP trial in primary angle-closure suspects found prophylactic laser peripheral iridotomy reduced incident angle-closure endpoints but with low absolute event rates, so population-wide prophylaxis in low-risk suspects is not justified. In an acute attack, however, same-day pressure reduction and definitive iridotomy remain non-negotiable.