Discuss the etiology and clinical features of keratitis, corneal ulcers and corneal abrasions.

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Keratitis, Corneal Ulcers, and Corneal Abrasions


1. KERATITIS

Keratitis is inflammation of the cornea, which may involve the epithelium, stroma, or endothelium. It is the leading infectious cause of corneal blindness worldwide.

A. Bacterial Keratitis

Etiology

Bacterial keratitis almost always requires prior compromise of the corneal epithelial barrier. Notable exceptions include Neisseria gonorrhoeae, N. meningitidis, Corynebacterium diphtheriae, and Haemophilus influenzae, which can penetrate an intact epithelium - typically in association with severe conjunctivitis. Infections may be polymicrobial (including bacterial-fungal co-infection).
Common pathogens:
  • Pseudomonas aeruginosa - Gram-negative bacillus; responsible for >60% of contact lens-related keratitis. Typically aggressive.
  • Staphylococcus aureus - Gram-positive, coagulase-positive; tends to present as a focal, fairly well-defined white or yellow-white infiltrate.
  • Streptococci (S. pyogenes, S. pneumoniae) - Often run an aggressive course.
Risk factors:
  • Contact lens wear - the most important risk factor, especially extended-wear soft lenses. Even daily disposables and apparently meticulous hygiene are not fully protective.
  • Trauma (including refractive surgery, particularly LASIK)
  • Agricultural injury (especially in developing countries, where fungal co-infection should be considered)
  • Ocular surface disease: herpetic keratitis, bullous keratopathy, dry eye, chronic blepharitis, trachoma/entropion, exposure keratopathy, severe allergy, corneal anaesthesia
  • Systemic: immunosuppression, diabetes, vitamin A deficiency

Clinical Features

  • Symptoms: Unilateral pain, photophobia, blurred vision, mucopurulent or purulent discharge
  • Signs:
    • Epithelial defect with infiltrate involving a larger area + significant circumcorneal (ciliary) injection
    • Stromal oedema, Descemet membrane folds
    • Anterior uveitis, commonly with a hypopyon and posterior synechiae in moderate-to-severe cases
    • Plaque-like keratic precipitates on the endothelium contiguous with affected stroma
    • Chemosis and eyelid swelling in severe cases
    • Severe ulceration may lead to descemetocoele formation and perforation (especially in Pseudomonas and Staphylococcus infections)
"Bacterial corneal ulceration should be excluded in a patient who wears contact lenses and presents with a painful red eye and blurred vision." - Kanski's Clinical Ophthalmology, 10th ed.

B. Fungal Keratitis

Etiology

  • Yeasts (e.g., Candida spp.) - responsible for most cases in temperate climates; typical in immunocompromised patients.
  • Filamentous fungi (e.g., Fusarium, Aspergillus) - the dominant pathogens in tropical climates; frequently follow agricultural trauma involving plant matter or gardening tools.
Predisposing factors: chronic ocular surface disease, long-term topical steroids (often post-corneal transplantation), contact lens wear, systemic immunosuppression, diabetes.

Clinical Features

  • Symptoms have a gradual onset: pain, grittiness, photophobia, blurred vision, watery or mucopurulent discharge.
  • Diagnosis is frequently delayed because fungal infection mimics bacterial disease.
  • Candida keratitis: yellow-white densely suppurative infiltrate.
  • Filamentous keratitis:
    • Grey or yellow-white stromal infiltrate with indistinct, fluffy margins
    • Progressive infiltration, often with satellite lesions or a ring-shaped infiltrate
    • Endothelial plaque and hypopyon may develop
  • Corneal perforation is common and prognosis for vision is frequently poor.

C. Herpes Simplex Keratitis (HSK)

Etiology

HSK is the most common infectious cause of corneal blindness in developed countries; up to 60% of corneal ulcers in developing countries may be herpetic. HSV-1 is the predominant causative agent (HSV-2 can be transmitted neonatally or venereally). After primary infection, latent virus resides in the trigeminal ganglion and cannot be eradicated. Reactivation is triggered by fever, hormonal change, UV radiation, trauma, or trigeminal injury.

Clinical Features - Epithelial Keratitis (active viral replication)

  • Dendritic ulcer: a branching, linear corneal ulcer with characteristic terminal bulbs at the ends; stains with fluorescein at the base and rose bengal at the edges. This is the hallmark of active HSV.
  • Geographic ulcer: a large irregular "map-shaped" epithelial ulcer representing coalescence of multiple dendrites, often triggered by inappropriate topical steroid use.
  • Symptoms: unilateral eye pain, photophobia, reduced visual acuity, tearing, foreign body sensation.
  • Corneal sensation is characteristically reduced or absent (due to viral neurotrophic damage).

Clinical Features - Stromal Keratitis (immune-mediated)

  • Disc-shaped (disciform) stromal oedema with overlying Descemet folds
  • Mild anterior uveitis; raised IOP may occur
  • No epithelial ulceration in immune stromal keratitis
  • Recurrence rate: ~10% at 1 year, ~50% at 10 years after first episode

D. Acanthamoeba Keratitis

Etiology

Caused by free-living protozoa (Acanthamoeba spp.) found in soil and water. Strongly associated with contact lens wear (especially use of tap water to rinse lenses or lens cases), swimming with lenses in, and corneal trauma.

Clinical Features

  • Severe, disproportionate pain - often out of proportion to the clinical signs (a hallmark feature).
  • Ring-shaped stromal infiltrate is characteristic (though not universal).
  • Radial keratoneuritis - infiltration along corneal nerves - is a highly specific early sign.
  • Slowly progressive course; initially often misdiagnosed as HSV keratitis.
  • Hypopyon and scleritis may develop.

E. Herpes Zoster (VZV) Keratitis

Etiology/Clinical Features

  • Results from reactivation of varicella-zoster virus in the trigeminal ganglion (ophthalmic division = herpes zoster ophthalmicus).
  • Can cause epithelial keratitis (pseudodendrite - a poorly staining mucous plaque, without true epithelial erosion, unlike HSV), stromal keratitis, uveitis, scleritis, and elevated IOP.
  • Hutchinson's sign (rash on the tip of the nose) predicts ocular involvement.
  • Anterior chamber shows cells and flare; consider immunocompromise if patient is <40 years old.

2. CORNEAL ULCER

A corneal ulcer is a serious infection involving multiple layers of the cornea (epithelium and underlying stroma), developing secondary to breaks in the epithelial barrier.

Etiology

The epithelial barrier may be disrupted by:
  • Desquamation (e.g., exposure keratitis from Bell's palsy causing corneal desiccation and sloughing)
  • Trauma (direct inoculation of organisms)
  • Direct microbial invasion (e.g., N. gonorrhoeae)
Causative organisms:
CategoryOrganisms
BacteriaPseudomonas aeruginosa (esp. contact lens users), S. pneumoniae, Staphylococcus spp., Moraxella spp.
VirusesHerpes simplex, Varicella zoster
FungiCandida, Aspergillus, Fusarium, Penicillium
ProtozoaAcanthamoeba
Soft contact lens wear - especially extended-wear - is the most common predisposing cause. Widespread use of topical and systemic immunosuppressants has made fungal and viral ulcers more frequent.

Clinical Features

  • History: contact lens use, prior ocular surgery or injury, recent trauma, history of genital herpes, topical or systemic steroids
  • Symptoms:
    • Eye redness and lid/conjunctival swelling
    • Ocular pain or foreign body sensation
    • Photophobia
    • Mucopurulent or purulent discharge
    • Blurred vision (especially if the ulcer is in the central visual axis or if uveal tract inflammation is present)
  • Signs on slit lamp:
    • Epithelial defect with underlying stromal opacity/infiltrate
    • Hypopyon (sterile pus in the anterior chamber) in severe cases
    • Descemetocoele (herniation of Descemet membrane) with risk of perforation
    • Fluorescein staining confirms the epithelial defect
    • Reduced or absent corneal sensation in herpetic or neurotrophic ulcers
"A corneal ulcer is a serious infection involving multiple layers of the cornea and develops secondary to breaks in the epithelial barrier, so that infectious agents invade the underlying corneal stroma." - Tintinalli's Emergency Medicine, 9th ed.

3. CORNEAL ABRASION

Etiology

A corneal abrasion is a superficial defect confined to the corneal epithelium (does not involve the stroma). The corneal epithelium is fragile and richly innervated, making abrasions very painful.
Causes:
  • Contact lens wear (most common)
  • Fingernails, makeup brushes
  • Foreign objects blown into the eye (wind, outdoor work)
  • Overhead work (mechanics, construction workers - objects falling into the eye)
  • High-speed machinery (grinders, lawn mowers, weed whackers, hammering metal) - important to note these carry risk of corneal laceration and globe perforation

Clinical Features

Symptoms:
  • Intense eye pain - may be delayed several hours after the inciting event
  • Foreign body sensation
  • Photophobia
  • Tearing/lacrimation
  • Decreased visual acuity if the abrasion is in the central visual axis or if iritis develops
Signs:
  • Conjunctival injection
  • Tearing and lid swelling
  • Blepharospasm (severe pain causing involuntary lid closure; may require topical anaesthetic to complete examination)
  • The abrasion may be visible to the naked eye as an irregular area of light reflection off the cornea
  • Relief of pain with topical anaesthesia is virtually diagnostic of corneal abrasion
Slit lamp findings:
  • Superficial, irregular corneal defect appearing bright green under cobalt blue light after fluorescein instillation
  • No corneal infiltrate (distinguishes it from keratitis/ulcer)
  • Multiple fine vertical linear abrasions suggest a foreign body embedded in the tarsal conjunctiva of the upper lid (evert the lid to check)
  • In large abrasions >24 hours old: flare and cells from iritis may appear, but still no stromal infiltrate
  • Seidel test negative (no aqueous leak = no perforation)
Healing: The corneal epithelium regenerates quickly; most abrasions heal within 24-48 hours. However, damaged epithelium is a portal of entry for bacteria, viruses, and fungi, and most untreated abrasions develop an associated iritis.

Summary Comparison

FeatureKeratitisCorneal UlcerCorneal Abrasion
DepthEpithelium ± stroma ± endotheliumEpithelium + stromaEpithelium only
InfiltratePresentPresent (stromal)Absent
HypopyonIn severe casesCommonAbsent
FluoresceinVariable pattern (dendrite, etc.)Stains defect + infiltrateBright green superficial defect
Corneal sensationReduced in HSV/VZVReduced in neurotrophicNormal
PainModerate-severeSevereSevere (richly innervated)
CauseMicrobial (bacterial, viral, fungal, protozoal)Microbial invasion of stromaPhysical trauma
HealingSlow; scarring riskSlow; perforation risk24-48 hours

Sources: Kanski's Clinical Ophthalmology: A Systematic Approach, 10th Edition; Tintinalli's Emergency Medicine: A Comprehensive Study, 9th Edition
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