Keratitis and corneal ulcer

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The transparent cornea supplies much of the eye's refractive power and provides a physical barrier to infection. When the epithelium breaks down, organisms may enter the stroma and provoke inflammation, tissue destruction and scarring. A small lesion near the visual axis can have major functional consequences, while a rapidly progressive peripheral lesion may threaten the integrity of the eye. Assess location, symptoms and progression rather than judging urgency only from the apparent surface area. Significant infection can deteriorate over hours.

Ask about the exact onset, contact-lens type and wearing pattern, overnight wear, swimming or showering in lenses, recent injury, previous ocular surgery, topical steroid use and immune compromise. Recurrent unilateral disease, lid vesicles or a branching epithelial lesion raises concern for herpes simplex. Soil or plant material suggests a possible fungal cause, while water exposure in a lens wearer raises concern for Acanthamoeba. These clues influence specialist testing and treatment but do not reliably identify an organism without examination.

Inspect visual acuity in both eyes before additional drops where practical, examine the cornea with suitable illumination and use fluorescein when trained and when an open-globe injury is not suspected. An epithelial defect stains, while the stromal infiltrate may appear as a white or grey opacity. Ophthalmology assesses lesion size, depth, position, thinning and anterior chamber reaction. The absence of dramatic discharge or severe pain is not reassuring when an infiltrate, visual reduction or reduced corneal sensation is present.

Key points

Keratitis means corneal inflammation; a corneal ulcer involves epithelial breakdown with underlying tissue involvement and may be infectious or non-infectious.
Pain, watering, photophobia and reduced vision are common, but reduced corneal sensation can make dangerous disease less painful.
A corneal infiltrate or ulcer is not uncomplicated conjunctivitis, even when there is associated discharge.
Contact lenses increase concern for microbial infection; injury involving soil or plant material broadens the pathogen differential.
Intensive topical antimicrobial treatment is prescribed by ophthalmology, with sampling and modification according to the clinical picture.
Steroids can aggravate microbial corneal disease and should only be considered by the corneal specialist after diagnosis and infection assessment.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Microbial entry

Bacterial infection can follow epithelial disruption, contact-lens wear or ocular-surface disease. Other organisms become more likely with particular exposures, immune compromise or an atypical clinical course.

Herpetic infection

Herpes simplex can recur in the cornea and affect epithelial or deeper layers. Previous episodes may alter sensation and leave scarring that complicates later assessment.

Non-infectious ulceration

Severe dryness, exposure, neurotrophic disease and systemic inflammatory disorders can damage corneal tissue without primary infection. Secondary infection may coexist, so ulcer appearance requires careful assessment.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Barrier failure
Disruption of the epithelial barrier allows organisms or inflammatory injury to reach the stroma. Local immune responses produce infiltrates, pain and loss of transparency.
2
Stromal destruction
Microbial products and host inflammatory enzymes can degrade corneal tissue. Progressive thinning can continue rapidly and lead to perforation if the destructive process is not controlled.
3
Optical scarring
Healing can replace transparent corneal architecture with scar tissue and irregular curvature. Even after the acute infection resolves, central opacity or distortion may reduce visual acuity.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Bacterial ulcer pattern

An acute painful red eye with an epithelial defect, stromal infiltrate and possible purulent discharge suggests bacterial keratitis; a contact-lens history increases concern.

Herpetic epithelial disease

A branching dendritic epithelial lesion, recurrent unilateral symptoms or reduced corneal sensation supports herpes simplex, although specialist examination is needed to classify the affected corneal layer.

Atypical organism clues

Water exposure, lens hygiene problems, organic trauma or an unexpectedly prolonged course should prompt consideration of amoebic or fungal disease rather than repeated routine antibiotic assumptions.

Advanced tissue damage

Thinning, an enlarging infiltrate, a hypopyon or rapidly declining acuity suggests severe disease that may need admission and more intensive specialist intervention.

Red flags requiring action

A focal corneal infiltrate with an epithelial defect, especially near the visual axis, requires emergency ophthalmic assessment.
Rapidly worsening pain, reduced vision, hypopyon or apparent corneal thinning indicates potentially advanced infection.
Contact-lens use, water exposure, organic-material injury or immunosuppression changes the likely pathogens and must be communicated during referral.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Acuity and slit-lamp assessmentFirst step
Why
Measure visual impact and map the corneal lesion.
Interpretation and limitations
Record location, dimensions, depth, epithelial defect and anterior chamber findings so that the next examination can identify progression or improvement.
02
Corneal scraping and microbiology when indicated
Why
Identify pathogens and support organism-directed antimicrobial treatment.
Interpretation and limitations
Ophthalmology selects sampling, particularly for significant, atypical or non-responding ulcers; obtaining samples should be coordinated promptly without an avoidable delay in necessary treatment.
03
Contact-lens and case assessment
Why
Preserve useful exposure and microbiological information for specialists.
Interpretation and limitations
Ask the patient to retain lenses, their case and relevant solution for the assessing service if requested, while avoiding further wear or contamination.
04
Targeted viral, fungal or amoebic testing
Why
Investigate a specific alternative suggested by exposure or examination.
Interpretation and limitations
Specialist testing may be needed when routine culture is insufficient; a negative routine bacterial result does not exclude every infectious cause.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Corneal abrasion

An abrasion causes an epithelial defect and pain without an established stromal infiltrate. Contact-lens association, a developing opacity or a worsening course increases concern for secondary infection.

Anterior uveitis

Intraocular inflammation causes photophobia, pain and redness, but chamber findings predominate. Corneal infection may itself produce an anterior chamber reaction, so the cornea must be examined.

Sterile contact-lens infiltrate

A non-infectious inflammatory infiltrate can follow lens wear and resemble early infection. Clinical overlap means the distinction should not be made from symptom severity alone.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First assessmentRecognise the corneal emergency and referFirst stepSymptoms or examination suggest a microbial ulcer, significant epithelial lesion or rapidly worsening keratitis.

1Record visual function and relevant lens, water, trauma and medication exposure, and contact the same-day emergency ophthalmic service.
2Remove contact lenses and avoid patching, empirical steroid preparations or unsupervised take-home topical anaesthetic drops.
3Provide a clear transfer plan and communicate any suspected thinning, hypopyon or rapid deterioration directly to the receiving team.

02Specialist treatmentSample appropriately and begin intensive therapyOphthalmic examination confirms an ulcer requiring antimicrobial treatment.

1Obtain indicated samples promptly and choose topical therapy according to severity, likely organism and the local corneal infection protocol.
2Explain the exact schedule, including overnight doses when prescribed, and assess whether the patient can deliver it reliably at home.
3Review closely and adjust therapy to culture results and clinical response; arrange admission when disease severity or practical barriers make outpatient care unsafe.

03Unexpected courseReassess a non-responding or atypical ulcerThe lesion enlarges, visual function worsens or expected improvement is absent despite treatment.

1Check drop delivery, adherence, drug availability and whether the prescribed overnight schedule has actually been followed.
2Reconsider antimicrobial resistance, a non-bacterial organism, toxicity, a retained foreign body or a non-infectious ulcerative process.
3EscalationEscalate microbiological investigation and corneal specialist care, including structural rescue treatment when progressive thinning or perforation threatens the globe.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Provides an intensive topical antibacterial option for an ophthalmologist-selected corneal-ulcer regimen.

Ciprofloxacin 0.3% eye drops, Ciloxan

When selected for a corneal ulcer, the licensed regimen is two drops into the affected eye every 15 minutes for the first six hours of day one, then every 30 minutes for the rest of that day; on day two give two drops hourly, and on days three to fourteen give two drops every four hours. These schedules include the night. Continuing beyond day fourteen requires physician direction; the SmPC gives a maximum recommended duration of 21 days.

Check ciprofloxacin, other quinolone and excipient allergy. Stop and seek advice for a hypersensitivity reaction. It does not treat every cause of keratitis, and contact lenses must not be worn during infection; response and lesion depth require specialist review.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Permanent visual impairment

A corneal scar, irregular astigmatism or central opacity can reduce vision despite successful antimicrobial treatment. The lesion's position influences the eventual functional outcome.

Perforation and intraocular spread

Progressive tissue destruction can breach the cornea and allow severe structural or intraocular complications. Thinning and rapid deterioration require immediate corneal specialist escalation.

Prolonged treatment burden

Atypical infection or severe ulceration may require extended therapy, repeated visits and additional procedures. Practical support for treatment delivery becomes part of protecting the eye.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Follow the review interval specified by the corneal team, often very frequent initially, with documented acuity, epithelial defect and infiltrate measurements.
Assess pain and adherence alongside objective findings; symptomatic relief alone does not prove that stromal infection has resolved.
Check that sufficient drops are available and that the patient or carer can manage the prescribed frequency, including overnight treatment when required.
A white deposit during ciprofloxacin treatment can be drug precipitation, but the clinician must distinguish this from worsening infiltrate through examination.
Maintain a clear emergency contact route for worsening vision, increasing pain, an enlarging white lesion or inability to administer treatment.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Corneal location matters

A central scar can impair vision after infection is controlled, while progressive thinning anywhere can threaten globe integrity. Both visual-axis involvement and structural damage shape management.

Herpetic disease has different layers

Epithelial herpes simplex and immune-mediated stromal inflammation require different specialist strategies. Selected deeper herpetic disease may receive steroids with antiviral treatment, which does not justify empirical steroids for an undiagnosed ulcer.

Anaesthesia can hide deterioration

A topical anaesthetic may help examination when used by a clinician, but unsupervised repeated use can damage healing epithelium and mask clinically important worsening.

Microbiology supports repeated clinical assessment

Culture results refine treatment but cannot replace serial examination. A negative sample, prior antibiotic exposure or an unusual organism must be interpreted alongside the actual trajectory.

11Common pitfallsFrequent interpretation and management errors.

01
Treating a contact-lens wearer with a painful red eye as ordinary conjunctivitis without inspecting the cornea and measuring acuity.
02
Waiting for routine microbiology results before arranging urgent assessment of a central or rapidly progressive ulcer.
03
Adding a steroid or combination drop to reduce redness before the organism and corneal integrity have been assessed.
04
Assuming a home treatment plan is safe without checking access to drops, night-time dosing and the patient's ability to attend early review.