12.3 The Acute Red Eye: Glaucoma, Uveitis & Keratitis

The Acute Red Eye: Glaucoma, Uveitis & Keratitis

The acute red eye is a common presenting complaint across acute medical, emergency, and primary care settings. In accordance with NICE Clinical Knowledge Summaries (CKS) and Royal College of Ophthalmologists guidance, whilst most presentations reflect self-limiting conditions such as viral conjunctivitis or minor subconjunctival haemorrhage, acute clinicians must rapidly identify sight-threatening pathologies that demand immediate emergency intervention.

---

Systematic Clinical Triage of the Acute Red Eye

When evaluating a patient with an acute red eye, the clinical assessment must immediately establish the presence of cardinal red flag features:

1. Severe, deep ocular or peri-orbital pain (indicates corneal ulceration, uveitis, scleritis, or acute glaucoma; superficial conjunctivitis causes only grittiness or burning).
2. True photophobia (characteristically severe in anterior uveitis and keratitis).
3. Diminished visual acuity (almost never occurs in uncomplicated conjunctivitis or episcleritis).
4. Haloes around lights (indicative of corneal epithelial oedema in acute angle-closure glaucoma).
5. Pupillary abnormality (fixed mid-dilated in glaucoma; small, sluggish, or irregular in uveitis).
6. Ciliary injection (ciliary flush): Violaceous circumcorneal ring of deep episcleral vessel engorgement, contrasting with the diffuse, superficial brick-red injection of conjunctivitis that moves with the conjunctiva and blanches with phenylephrine.

---

The Acute Red Eye Differential Spectrum

---

Acute Angle-Closure Glaucoma (AACG)

Acute angle-closure glaucoma is an ophthalmic emergency where mechanical apposition of the peripheral iris against the trabecular meshwork abruptly halts aqueous humour drainage through the canal of Schlemm, precipitating an explosive rise in intraocular pressure.

• Risk Factors & Pathophysiology: Predominantly occurs in individuals with an anatomically narrow anterior chamber angle: hypermetropes (long-sighted), elderly patients with age-related lens thickening, and females of East Asian descent.
• Precipitating Triggers: Dilatation of the pupil moves the peripheral iris root into the narrow drainage angle. Triggers include entering a dimly lit room or cinema, emotional stress, and medications with mydriatic properties (anticholinergics such as tropicamide, atropine, tricyclic antidepressants, and nebulised ipratropium bromide delivered via ill-fitting facemask; sympathomimetics).
• Clinical Presentation: Rapid onset of excruciating, severe unilateral peri-orbital and ocular pain that radiates across the ipsilateral hemicranium. Patients frequently present with intense frontal headache, nausea, and profuse vomiting, leading to frequent misdiagnoses of acute migraine or intra-abdominal pathology. Visual acuity drops precipitously, accompanied by the classic pathognomonic symptom of coloured rainbow haloes around streetlights.
• Physical Signs:
  • Cornea: Appears hazy, cloudy, or "steamy" (ground-glass appearance) due to corneal epithelial edema.
  • Pupil: Fixed, mid-dilated (5–6 mm), oval, and completely unreactive to direct or consensual light.
  • Vascular Injection: Prominent ciliary injection (violaceous circumcorneal flush).
  • Palpation: Gentle digital palpation through closed upper eyelids demonstrates a stony-hard / rock-hard globe compared to the fellow eye.
  • Tonometry: Intraocular pressure is markedly elevated, typically 40–80 mmHg (normal physiological range: 10–21 mmHg).
• Emergency Medical Management Protocol:
  • Aim: Rapidly lower IOP to prevent irreversible ischemic necrosis of the optic nerve head and permanent blindness.
  1. Topical Pilocarpine 2% Drops: Parasympathomimetic miotic agent; stimulates pupillary sphincter contraction, pulling the peripheral iris away from the trabecular meshwork to reopen the drainage angle. Instil 1 drop into the affected eye every 15 minutes for 2 doses, then QDS. Critical action: Also instil 1 drop of pilocarpine 1% into the unaffected fellow eye to prevent contralateral angle closure.
  2. Intravenous Acetazolamide 500 mg Stat: Potent carbonic anhydrase inhibitor; rapidly suppresses aqueous humour production by the ciliary body epithelium.
  3. Topical Beta-Blocker (Timolol 0.5% Drops): Suppresses aqueous secretion (contraindicated in severe asthma, COPD, or high-degree heart block).
  4. Topical Alpha-2 Agonist (Apraclonidine 1% Drops): Dual action: decreases aqueous synthesis and enhances uveoscleral outflow.
  5. Systemic Hyperosmotic Agents: Intravenous mannitol 20% (1–2 g/kg over 45 minutes) if IOP remains refractory >50 mmHg after 1–2 hours.
• Definitive Treatment: Bilateral Nd:YAG Laser Peripheral Iridotomy (LPI): Once medical therapy clears corneal edema, a laser creates a microscopic full-thickness hole in the superior peripheral iris. This creates a permanent fluid bypass channel connecting the posterior and anterior chambers, curing pupillary block. Both eyes must be treated because the anatomical predisposition is bilateral.

---

Anterior Uveitis (Acute Iritis / Iridocyclitis)

Anterior uveitis represents acute intraocular inflammation involving the iris and anterior ciliary body.

• Systemic Associations: Approximately 50% of cases are associated with the HLA-B27 major histocompatibility antigen: ankylosing spondylitis (young males, morning back stiffness), reactive arthritis (urethritis, arthritis, uveitis: "can't see, can't pee, can't climb a tree"), psoriatic arthritis, and inflammatory bowel disease (Crohn's disease, ulcerative colitis). Non-HLA-B27 associations include sarcoidosis, Behçet's disease, and syphilis.
• Clinical Presentation: Deep, dull, aching ocular pain, accompanied by intense photophobia that is characteristically aggravated when light is shone into the unaffected fellow eye (consensual photophobia, triggered by bilateral consensual pupillary constriction causing traction on the inflamed iris/ciliary body). Visual acuity is mildly blurred, accompanied by watery lacrimation.
• Examination Findings:
  • Vascular Injection: Violaceous circumcorneal ciliary flush.
  • Pupillary Signs: The pupil is small (miotic), sluggish, and frequently distorted or irregular due to posterior synechiae (inflammatory fibrinous adhesions binding the pupillary border of the iris to the anterior lens capsule).
  • Slit-Lamp Hallmarks: Flare (protein leakage into aqueous) and circulating leukocytes ("cells") resembling dust motes in a projector beam; keratic precipitates (inflammatory cell deposits on the lower corneal endothelium); severe inflammation may precipitate a sterile hypopyon (fluid level of layered white blood cells in the anterior chamber).
• Emergency Treatment:
  • Urgent same-day referral to an ophthalmologist.
  • Topical Cycloplegic / Mydriatic Agent (Cyclopentolate 1% or Atropine 1% Drops): Dual therapeutic mechanism: (1) paralyses the ciliary muscle and pupillary sphincter, abolishing painful ciliary spasm and photophobia; (2) dilates the pupil, pulling the iris border away from the lens, thereby preventing or breaking posterior synechiae.
  • Topical Corticosteroid Drops (Prednisolone Acetate 1% Drops): Administered intensively (e.g. hourly) to suppress intraocular inflammation.
  • Caution: Never commence topical corticosteroids until slit-lamp examination definitively excludes herpes simplex dendritic ulceration.

---

Microbial Keratitis: Bacterial & Herpetic

Bacterial Keratitis

Bacterial keratitis is a sight-threatening infectious ulceration of the corneal stroma with loss of the overlying corneal epithelium.

• Etiology & Risk Factors: Contact lens wear is the predominant predisposing risk factor (>60% of cases), particularly extended overnight wear or washing lenses in domestic tap water. Pseudomonas aeruginosa is the most notorious pathogen in contact lens wearers, capable of secreting virulent proteases that produce rapid liquefactive stromal necrosis and corneal perforation within 24–48 hours. Other common culprits include Staphylococcus aureus and Streptococcus pneumoniae.
• Clinical Presentation: Severe sharp pain, foreign body sensation, marked photophobia, reduced visual acuity, and purulent discharge. Slit-lamp or penlight examination reveals a visible focal white/opaque corneal infiltrate or ulcer with an overlying epithelial defect that stains with fluorescein. A layered hypopyon is frequently present.
• Emergency Management Protocol:
  • Emergency same-day ophthalmological consultation.
  • Immediate corneal scrapings for Gram stain, microscopy, and culture prior to starting antibiotics.
  • Intensive Topical Fluoroquinolone Monotherapy: Topical ofloxacin 0.3% or levofloxacin 0.5% eye drops instilled every hour around the clock for the first 24–48 hours.
  • CRITICAL CONTRAINDICATION — NEVER PATCH A CONTACT LENS ULCER: Applying an eye patch creates a warm, dark, hypoxic, anaerobic chamber that accelerates Pseudomonas proliferation, leading to rapid corneal melting and permanent visual loss.

---

Herpes Simplex Keratitis (Epithelial Keratitis)

Caused by the reactivation of latent Herpes Simplex Virus Type 1 (HSV-1) within the sensory ophthalmic division (V1) of the trigeminal ganglion.

• Clinical Features: Unilateral ocular redness, mild-to-moderate aching discomfort, foreign body sensation, photophobia, and watery lacrimation. A key diagnostic examination sign is reduced corneal sensation (corneal hypoaesthesia), elicited by gently touching the peripheral cornea with a wisp of sterile cotton.
• Pathognomonic Examination Sign: Instillation of fluorescein dye examined under a cobalt blue light reveals a classic branching, arborising dendritic ulcer with linear branching patterns and terminal rounded bulbs that stain bright yellow-green.
• Medical Treatment: Topical aciclovir 3% eye ointment applied 5 times daily (or topical ganciclovir 0.15% gel) for 10–14 days.

---

Scleritis vs Episcleritis

• Episcleritis: Benign, self-limiting inflammation of the superficial episcleral vascular plexus, predominantly affecting young to middle-aged adults (female > male). Manifests with acute mild ocular redness, foreign body grittiness, or burning discomfort. Visual acuity is normal, and there is no severe deep pain. Examination reveals localized salmon-pink sectoral vascular engorgement. The Phenylephrine Test: Instillation of 1 drop of topical phenylephrine 2.5% causes complete blanching of the superficial episcleral vessels within 10–15 minutes, confirming episcleritis. Management requires simple reassurance, artificial lubricants, and oral NSAIDs if symptomatic.
• Scleritis: Severe, destructive, sight-threatening chronic granulomatous inflammation of the deep sclera, carrying a >50% association with underlying systemic autoimmune connective tissue diseases, predominantly rheumatoid arthritis, granulomatosis with polyangiitis (GPA / Wegener's), and systemic lupus erythematosus (SLE). Manifests with severe, deep, boring, excruciating ocular pain that characteristically radiates to the temple, forehead, and jaw, and classically wakes the patient from sleep at night. The globe is exquisitely tender to touch. Examination demonstrates a deep violaceous (bluish-red) scleral injection that DOES NOT blanch following topical phenylephrine 2.5% instillation. Complications include scleral thinning (scleromalacia perforans), globe perforation, and blindness. Management mandates urgent ophthalmology referral, high-dose oral NSAIDs, systemic oral corticosteroids (prednisolone), and DMARDs / biologic therapies.

---

Orbital Cellulitis vs Preseptal Cellulitis

The orbital septum—a fibrous sheet of connective tissue originating from the orbital periosteum and inserting into the tarsal plates of the eyelids—acts as a crucial physical barrier separating superficial periorbital tissues from the internal orbital cone.