19.1 The Acute Red Eye & Ophthalmic Emergencies

Ophthalmic emergencies and vision-threatening disorders frequently present to primary care, urgent care, and inpatient internal medicine services. An internist must be adept at rapidly distinguishing benign, self-limiting superficial conditions from sight-threatening emergencies requiring immediate intraocular pressure reduction, antimicrobial pharmacotherapy, high-dose systemic corticosteroids, or emergent vitreoretinal surgery.

1. Acute Red Eye Triage & Differential Diagnosis

The initial evaluation of the acute red eye begins with four critical triage questions:

1. Is there vision loss or decreased visual acuity? (Suggests keratitis, anterior uveitis, acute glaucoma, or endophthalmitis)
2. Is there severe, deep, aching, or boring eye pain? (Suggests scleritis, anterior uveitis, acute angle-closure glaucoma, or corneal ulceration)
3. Is there marked photophobia? (Suggests corneal epithelial defect, keratitis, or anterior uveitis)
4. Is the pupil abnormal (fixed, mid-dilated, or irregular/constricted)? (Suggests acute angle-closure glaucoma or anterior uveitis with posterior synechiae)

2. In-Depth Management of Specific Ophthalmic Conditions

Acute Angle-Closure Glaucoma (AACG)

• Pathophysiology: Narrowing or closure of the anterior chamber angle between the peripheral iris and trabecular meshwork, preventing aqueous humor outflow through the canal of Schlemm. Most commonly triggered by pupillary dilation (mydriasis in dim lighting, emotional stress, or pharmacologic mydriatics/anticholinergics such as atropine, ipratropium, oxybutynin, tricyclic antidepressants, topiramate, or sympathomimetics) in anatomically predisposed eyes (hyperopia, shallow anterior chambers, advancing age, Asian or Inuit ancestry).
• Diagnostic Confirmation: Tonometry revealing Intraocular Pressure (IOP) markedly elevated above normal (10–21 mmHg), typically reaching 40 to 70 mmHg. Direct visualization of shallow anterior chamber and closed angle via gonioscopy (performed by ophthalmology).
• Emergency IOP-Lowering Pharmacotherapy Protocol:
  1. Topical Beta-Blocker: Timolol 0.5% ophthalmic solution (1 drop) — suppresses aqueous humor production by ciliary epithelium.
  2. Topical Alpha-2 Adrenergic Agonist: Apraclonidine 1% or Brimonidine 0.2% (1 drop) — dual action: reduces aqueous humor production and increases uveoscleral outflow.
  3. Topical Cholinergic / Miotic Agent: Pilocarpine 2% (1 drop every 15 minutes for 2 doses) — stimulates pupillary sphincter muscle contraction to physically pull the peripheral iris away from the trabecular meshwork, opening the filtration angle. Clinical Pearl: Pilocarpine is ineffective when IOP >40–50 mmHg due to pressure-induced ischemia of the pupillary sphincter; administer after initiating pressure-lowering systemic agents.
  4. Systemic Carbonic Anhydrase Inhibitor: Acetazolamide 500 mg IV or PO (followed by 250 mg PO QID) — rapidly halts aqueous humor production via carbonic anhydrase inhibition. (Check for severe sulfonamide allergy and avoid in sickle cell disease where acetazolamide induces sickling in the anterior chamber).
  5. Systemic Hyperosmotic Agent (for refractory IOP): Intravenous Mannitol 1.0–2.0 g/kg IV over 30–45 minutes — increases serum osmolality to draw water out of the vitreous humor, reducing intraocular volume.
• Definitive Treatment: Laser Peripheral Iridotomy (LPI) to create a full-thickness bypass hole in the peripheral iris, restoring aqueous flow. Prophylactic LPI is mandatory in the unaffected contralateral eye due to high rates (>50%) of subsequent angle-closure.

Herpes Simplex Keratitis vs Herpes Zoster Ophthalmicus

• Herpes Simplex Keratitis (HSV-1):
  • Reactivation of latent HSV-1 from the trigeminal ganglion migrating down the ophthalmic branch (V1).
  • Hallmark Finding: Branching dendritic ulcer with rounded terminal bulbs on fluorescein staining, accompanied by reduced corneal sensation (neurotrophic cornea).
  • Treatment: Topical antivirals (Ganciclovir 0.15% ophthalmic gel 5 times daily or Trifluridine 1% drops 8–9 times daily) OR systemic oral antivirals (Valacyclovir 1000 mg PO TID or Acyclovir 400 mg PO 5 times daily for 10–14 days).
  • Critical Board Warning: NEVER USE TOPICAL CORTICOSTEROIDS in active epithelial dendritic keratitis. Corticosteroids potentiate viral replication, causing rapid transition into massive "geographic" corneal ulcers, corneal stromal melting, secondary bacterial superinfection, and permanent blindness.
• Herpes Zoster Ophthalmicus (HZO):
  • Reactivation of Varicella-Zoster Virus in the ophthalmic division of the trigeminal nerve (CN V1).
  • Hutchinson Sign: Vesicles involving the tip, side, or ala of the nose, indicating nasociliary branch involvement; correlates with a >75% risk of intraocular complications (keratitis, anterior uveitis, secondary glaucoma, acute retinal necrosis).
  • Slit-Lamp: "Pseudodendrites" (elevated mucous plaques without terminal bulbs that stain poorly with fluorescein).
  • Treatment: Oral Valacyclovir 1000 mg PO TID for 7–10 days initiated within 72 hours of rash onset, combined with urgent ophthalmologic evaluation.

Episcleritis vs Scleritis

• Episcleritis: Mild, self-limiting inflammation of the superficial episcleral vascular network. Features sectoral or diffuse salmon-pink injection. Phenylephrine 2.5% blanching test: Application of topical phenylephrine causes rapid blanching/constriction of episcleral vessels within 10–15 minutes, confirming superficial inflammation. Managed with cold compresses, artificial tears, or oral NSAIDs.
• Scleritis: Severe, destructive, full-thickness inflammation of the deep sclera. Features excruciating, deep, boring pain radiating to the periorbital region, temple, or jaw that wakes the patient from sleep. Sclera demonstrates a distinct violaceous or bluish-red hue under natural light. Vessels DO NOT blanch with topical 2.5% Phenylephrine. Strongly associated with underlying systemic autoimmune diseases in >50% of cases (Rheumatoid Arthritis [most common], Granulomatosis with Polyangiitis [GPA], Relapsing Polychondritis, Systemic Lupus Erythematosus). Complications include scleral thinning (scleromalacia perforans) and globe rupture. Managed with systemic high-dose NSAIDs, oral corticosteroids (Prednisone 1 mg/kg/day), and biologic immunosuppression (e.g., Rituximab, Infliximab).