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Ophthalmology – Central Corneal Ulcers (Keratitis)
Central corneal ulcers are characterized by a localized epithelial defect accompanied by inflammation and destruction of the underlying corneal stroma. They are commonly referred to as corneal infiltrates or keratitis and may be either infectious or noninfectious. These ulcers are clinically significant because involvement of the central visual axis can rapidly lead to vision loss if not treated promptly.
The incidence of bacterial keratitis is substantial, with tens of thousands of cases occurring annually, particularly among contact lens users. Risk factors include contact lens wear (especially poor hygiene or overwear), ocular surface disease, inadequate eyelid closure, corneal hypoesthesia, and systemic autoimmune conditions. Preventive strategies focus on maintaining proper contact lens hygiene, preserving epithelial integrity, ensuring adequate lubrication, correcting eyelid abnormalities, and controlling underlying inflammatory or autoimmune diseases.
The pathophysiology begins with disruption of the corneal epithelium, which allows microorganisms or inflammatory processes to penetrate the stroma. This triggers a strong inflammatory response dominated by neutrophils, along with enzymatic degradation of the extracellular matrix through proteolytic enzymes such as matrix metalloproteinases. This process can lead to stromal thinning, ulceration, and even perforation if untreated.
Etiologically, central corneal ulcers may be infectious—caused by bacteria, fungi, viruses, or Acanthamoeba—or noninfectious, such as neurotrophic keratitis, exposure keratopathy, or autoimmune-related corneal melting. Infectious ulcers are frequently associated with contact lens misuse or trauma, whereas sterile ulcers are more commonly linked to systemic autoimmune diseases like rheumatoid arthritis or systemic lupus erythematosus.
Patients typically present with pain, redness, tearing, photophobia, and decreased vision. A detailed history is essential, especially regarding contact lens use, hygiene practices, water exposure, trauma, and systemic disease. On examination, findings include conjunctival injection, epithelial defects visible with fluorescein staining, stromal infiltrates, corneal thinning, and anterior chamber inflammation such as cells, flare, or hypopyon. Eyelid abnormalities and tear film insufficiency should also be assessed.
Diagnosis relies on clinical examination and microbiological evaluation. Central ulcers should be cultured before initiating antibiotic therapy. Corneal scrapings are obtained from the ulcer margin and inoculated onto appropriate media to identify bacterial, fungal, or protozoal pathogens. Special stains such as Gram stain, Giemsa, acid-fast stain, and calcofluor white may aid in identifying organisms. Additional tools like confocal microscopy can be useful, particularly in suspected Acanthamoeba infections. If the ulcer does not respond to treatment, corneal biopsy may be necessary.
Management requires urgent and aggressive therapy. First-line treatment for suspected bacterial ulcers involves intensive topical antibiotics, typically fourth-generation fluoroquinolones administered frequently, even hourly. Severe or resistant cases may require fortified antibiotics such as vancomycin combined with tobramycin or ceftazidime. Therapy should be adjusted based on culture results. If the ulcer is unresponsive or atypical, alternative diagnoses such as fungal or Acanthamoeba keratitis must be considered, and appropriate antifungal or anti-protozoal agents initiated.
Adjunctive therapy includes cycloplegic agents to relieve pain and prevent synechiae, as well as lubricating ointments to support epithelial healing. Systemic therapy may be required in certain infections, such as Neisseria or severe fungal disease. Referral to a cornea specialist is indicated if the ulcer is central, progressive, unresponsive to treatment within 24–48 hours, or difficult to culture.
Close follow-up is essential, typically on a daily basis until the ulcer stabilizes. Signs of improvement include re-epithelialization, reduction in infiltrate density, resolution of hypopyon, stabilization of corneal thickness, and improvement in visual acuity and symptoms. Early and appropriate management is critical to prevent complications such as corneal scarring, perforation, and permanent vision loss.
Central corneal ulcers are characterized by a localized epithelial defect accompanied by inflammation and destruction of the underlying corneal stroma. They are commonly referred to as corneal infiltrates or keratitis and may be either infectious or noninfectious. These ulcers are clinically significant because involvement of the central visual axis can rapidly lead to vision loss if not treated promptly.
The incidence of bacterial keratitis is substantial, with tens of thousands of cases occurring annually, particularly among contact lens users. Risk factors include contact lens wear (especially poor hygiene or overwear), ocular surface disease, inadequate eyelid closure, corneal hypoesthesia, and systemic autoimmune conditions. Preventive strategies focus on maintaining proper contact lens hygiene, preserving epithelial integrity, ensuring adequate lubrication, correcting eyelid abnormalities, and controlling underlying inflammatory or autoimmune diseases.
The pathophysiology begins with disruption of the corneal epithelium, which allows microorganisms or inflammatory processes to penetrate the stroma. This triggers a strong inflammatory response dominated by neutrophils, along with enzymatic degradation of the extracellular matrix through proteolytic enzymes such as matrix metalloproteinases. This process can lead to stromal thinning, ulceration, and even perforation if untreated.
Etiologically, central corneal ulcers may be infectious—caused by bacteria, fungi, viruses, or Acanthamoeba—or noninfectious, such as neurotrophic keratitis, exposure keratopathy, or autoimmune-related corneal melting. Infectious ulcers are frequently associated with contact lens misuse or trauma, whereas sterile ulcers are more commonly linked to systemic autoimmune diseases like rheumatoid arthritis or systemic lupus erythematosus.
Patients typically present with pain, redness, tearing, photophobia, and decreased vision. A detailed history is essential, especially regarding contact lens use, hygiene practices, water exposure, trauma, and systemic disease. On examination, findings include conjunctival injection, epithelial defects visible with fluorescein staining, stromal infiltrates, corneal thinning, and anterior chamber inflammation such as cells, flare, or hypopyon. Eyelid abnormalities and tear film insufficiency should also be assessed.
Diagnosis relies on clinical examination and microbiological evaluation. Central ulcers should be cultured before initiating antibiotic therapy. Corneal scrapings are obtained from the ulcer margin and inoculated onto appropriate media to identify bacterial, fungal, or protozoal pathogens. Special stains such as Gram stain, Giemsa, acid-fast stain, and calcofluor white may aid in identifying organisms. Additional tools like confocal microscopy can be useful, particularly in suspected Acanthamoeba infections. If the ulcer does not respond to treatment, corneal biopsy may be necessary.
Management requires urgent and aggressive therapy. First-line treatment for suspected bacterial ulcers involves intensive topical antibiotics, typically fourth-generation fluoroquinolones administered frequently, even hourly. Severe or resistant cases may require fortified antibiotics such as vancomycin combined with tobramycin or ceftazidime. Therapy should be adjusted based on culture results. If the ulcer is unresponsive or atypical, alternative diagnoses such as fungal or Acanthamoeba keratitis must be considered, and appropriate antifungal or anti-protozoal agents initiated.
Adjunctive therapy includes cycloplegic agents to relieve pain and prevent synechiae, as well as lubricating ointments to support epithelial healing. Systemic therapy may be required in certain infections, such as Neisseria or severe fungal disease. Referral to a cornea specialist is indicated if the ulcer is central, progressive, unresponsive to treatment within 24–48 hours, or difficult to culture.
Close follow-up is essential, typically on a daily basis until the ulcer stabilizes. Signs of improvement include re-epithelialization, reduction in infiltrate density, resolution of hypopyon, stabilization of corneal thickness, and improvement in visual acuity and symptoms. Early and appropriate management is critical to prevent complications such as corneal scarring, perforation, and permanent vision loss.
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