Herpes simplex keratitis

Non-herpetic viral keratitis, overwhelmingly adenoviral, produces copious watery discharge, severe irritation, and preauricular lymphadenopathy that starts unilateral and spreads to the second eye. Management is supportive and infection-control focused; chronic subepithelial infiltrates are the vision-affecting sequela that sometimes needs ophthalmology-directed topical corticosteroid.

Bacterial keratitis is a corneal epithelial and stromal infection, most often Pseudomonas or Staphylococcus in soft contact lens wearers, that is a sight-threatening emergency treated with same-day corneal culture followed by hourly topical moxifloxacin 0.5% (small ulcer) or alternating fortified vancomycin and tobramycin (large or central ulcer). Delay or misdiagnosis as a benign red eye risks stromal melt, perforation, and permanent vision loss.

Acanthamoeba keratitis is a corneal infection by a free-living amoeba, strongly linked to soft contact lens wear combined with freshwater exposure, diagnosed by microscopic examination of corneal scrapings and treated with prolonged topical antiamoebic/antifungal therapy that often fails to prevent progressive corneal destruction. Any contact lens wearer with a painful, non-healing keratitis that is not responding to antibacterial therapy needs this diagnosis considered and an urgent corneal scraping sent.

Microbial keratitis (infectious corneal ulcer) is the unifying vision-threatening syndrome of a painful red eye with a corneal infiltrate, produced by bacterial, viral, fungal, or amebic invasion of a breached corneal epithelium, managed by the same urgent pathway regardless of organism: emergent scraping for smear and culture before any drug is given, then broad empiric coverage narrowed once results return. Delay, misdiagnosis as simple conjunctivitis, or premature corticosteroid use converts a treatable ulcer into stromal melt, perforation, and permanent vision loss.

Herpes zoster ophthalmicus is reactivation of latent varicella-zoster virus in the ophthalmic (V1) division of the trigeminal ganglion, producing a dermatomal vesicular rash that can involve the cornea, uvea, and optic nerve. Diagnosis is clinical, and first-line treatment is oral valacyclovir or famciclovir started within 72 hours of rash onset, with intravenous acyclovir for severe or immunocompromised disease.

A corneal abrasion is a traumatic or foreign-body-related defect of the corneal epithelium diagnosed by fluorescein uptake under cobalt-blue light. Uncomplicated cases heal in days with lubrication and pain control, but contact-lens wear mandates antipseudomonal coverage and any red flag (rust ring, infiltrate, Seidel sign, hypopyon) demands same-day ophthalmology referral.

Conjunctivitis is inflammation of the conjunctiva from viral, bacterial, or allergic causes presenting with red eye, discharge, and preserved vision, diagnosed clinically by discharge character and managed with supportive care, targeted topical antibiotics, or topical antihistamine/mast-cell-stabilizer therapy.

Uveitis is inflammation of the uveal tract, classified by anatomic location as anterior, intermediate, posterior, or panuveitis and by systemic association such as HLA-B27 spondyloarthritis, sarcoidosis, or Behcet disease. Anterior uveitis presents with a painful red eye and photophobia diagnosed at the slit lamp, while posterior uveitis presents with painless floaters or vision loss, and treatment is topical corticosteroid for anterior disease escalating to systemic corticosteroid and steroid-sparing immunosuppression for recurrent, severe, or posterior-segment disease.

Acute angle-closure glaucoma is a pupillary-block emergency in which sudden closure of the iridocorneal angle blocks aqueous outflow, causing severe eye pain, halos, and rapidly rising intraocular pressure that can blind the eye within hours if not treated. Diagnosis is clinical plus tonometry and gonioscopy; treatment is immediate topical and systemic IOP-lowering therapy followed by laser peripheral iridotomy.

Chemical burns are tissue injury from external skin or eye contact with a caustic agent: alkalis cause deep liquefaction necrosis and acids cause self-limiting coagulation necrosis. Diagnosis is clinical, guided by agent identity and, for the eye, conjunctival pH. First-line treatment is brushing off dry powder, then prolonged copious water irrigation, with calcium gluconate as the specific antidote for hydrofluoric acid.