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Eye Diseases > Cornea

Corneal Ulcers

Comprehensive clinical guide covering corneal ulcers: etiology, pathogenesis, classification, risk factors, diagnosis, and evidence-based management protocols for optometry practice.

Corneal UlcerInfiltrate

Corneal ulcer showing epithelial defect with surrounding infiltration

Corneal ulcers represent a significant ocular emergency characterized by epithelial defects with underlying stromal involvement and inflammatory response. These infectious or non-infectious conditions can rapidly progress to corneal perforation, potentially resulting in permanent vision loss or even blindness if not promptly diagnosed and appropriately managed. Early recognition, accurate identification of the causative organism or etiology, and initiation of targeted therapy are critical for achieving optimal visual outcomes. Corneal ulcers remain a leading cause of preventable blindness worldwide, particularly in developing nations where vitamin A deficiency and limited access to eye care contribute to disease burden.

Infectious Causes

  • Bacterial: Pseudomonas aeruginosa (most common), Staphylococcus aureus, Serratia, Proteus, Moraxella, Neisseria
  • Fungal: Aspergillus, Fusarium, Candida, Scedosporium (especially with contact lens use)
  • Viral: Herpes simplex virus (HSV), Varicella zoster virus (VZV)
  • Parasitic: Acanthamoeba (contact lens-related), Onchocerca

Non-Infectious Causes

  • Trauma: Mechanical abrasion, chemical burns, thermal burns, radiation
  • Dry eye syndrome: Severe aqueous or mucin deficiency
  • Neurotrophic keratopathy: Loss of corneal sensation (CN V dysfunction)
  • Autoimmune/Inflammatory: Stevens-Johnson syndrome, Ocular cicatricial pemphigoid, Graft-versus-host disease, Rosacea
  • Nutritional deficiencies: Vitamin A deficiency (leading preventable cause of blindness worldwide)
  • Medication-induced: Topical antivirals, prostaglandin analogues, non-steroidal anti-inflammatory drugs (NSAIDs)
  • Contact lens-related: Poor hygiene, overwear, deposits, hypoxia
  • Post-surgical: Following refractive surgery, lid surgery

Mechanism of Formation

  1. Insult/Breech: Corneal epithelial integrity is compromised by trauma, infection, or inflammatory processes
  2. Epithelial necrosis: Infected or damaged epithelial cells undergo apoptosis and necrosis
  3. Enzymatic degradation: Bacterial/fungal enzymes (proteases, collagenases) break down corneal collagen matrix
  4. Inflammatory response: Infiltration of polymorphonuclear leukocytes and inflammatory mediators
  5. Tissue loss: Progressive melting of corneal stroma leads to deepening ulcer
  6. Risk of perforation: If untreated, ulcer can penetrate through full corneal thickness

Contributing Factors

The cornea has multiple defense mechanisms that protect against ulceration:

  • Tear film: Provides antibodies (IgA), lysozyme, and lactoferrin
  • Epithelial barrier: Tight junctions prevent microbial penetration
  • Corneal sensation: Triggers protective reflex (blink, tearing)
  • Stromal defenses: Keratocytes produce antimicrobial peptides

Ulceration occurs when pathogenic load or virulence overwhelms these defense mechanisms.

By Depth (Ulcer Stage)

  • Epithelial defect: Loss of epithelium only, Bowman's layer and stroma intact
  • Stromal infiltration: Anterior stroma involved with cellular infiltrates but no frank tissue loss
  • Stromal ulceration: Tissue loss with depression in stromal surface
  • Descemetocele: Stromal loss approaches Descemet's membrane; membrane alone supports anterior chamber
  • Perforated ulcer: Full-thickness corneal loss with anterior chamber leak

By Etiologic Category

  • Infectious: Bacterial, fungal, viral, parasitic
  • Traumatic: Mechanical, chemical, thermal, radiation
  • Ischemic: Due to compromised vascularization
  • Neurotrophic: Due to sensory denervation
  • Exposure: From inadequate lid closure or excessive evaporation

By Location

  • Central ulcer: Located in central 3mm of cornea
  • Paracentral ulcer: Located in 3-6mm zone
  • Peripheral ulcer: Located at limbal region
  • Peripheral ulcerative keratitis (PUK): Often associated with autoimmune disease

By Morphology

  • Oval/round ulcer: Discrete, localized lesion
  • Serpignous ulcer: Advancing edge with trailing scarring (HSV keratitis)
  • Moat-like ulcer: Surrounding moat of infiltration (autoimmune)
  • Filamentary: Mucus-thread ulcer with filament adhesion

Ocular Risk Factors

  • Contact lens use (especially extended wear, poor hygiene)
  • Dry eye syndrome and low tear production
  • Corneal scarring from previous injury or disease
  • Reduced corneal sensitivity or trichiasis
  • Lid malposition (entropion, ectropion, lagophthalmos)
  • Previous ocular surgery or trauma
  • Ocular surface disease (Stevens-Johnson syndrome, pemphigoid)
  • Chronic eye drop use (toxic preservatives)

Systemic Risk Factors

  • Diabetes mellitus (impaired healing)
  • Rheumatoid arthritis and other autoimmune diseases
  • Vitamin A deficiency
  • Immunosuppression (HIV/AIDS, chemotherapy)
  • Graft-versus-host disease (allogeneic bone marrow transplant)
  • Nutritional deficiencies
  • Aging (reduced tear production)

Environmental Risk Factors

  • Poor hygiene and sanitation
  • Chemical or thermal exposure
  • Occupational hazards (welding, grinding)
  • Low humidity environments

Anterior Segment Examination Findings

  • Epithelial defect: Stains with fluorescein (apple-green with cobalt blue light)
  • Stromal infiltration: White, hazy appearance in corneal stroma
  • Suppuration: Yellow or white exudate within the ulcer crater
  • Anterior chamber reaction: Cells and flare indicating anterior uveitis
  • Hypopyon: Layered white cells in anterior chamber (especially with severe bacterial infections)
  • Conjunctival injection: Bulbar and tarsal conjunctival redness
  • Ciliary injection: Deep limbal inflammation
  • Corneal vascularization: New blood vessel formation at ulcer edges (pannus formation in chronic cases)
  • Thinning: Depression in corneal contour in stromal ulcers
  • Descemet's membrane folding: In descemetoceles, membrane may bow inward

Posterior Examination Findings

  • Anterior chamber exudate: Fibrin, cells, or inflammatory material
  • Iritis/Uveitis: Due to inflammatory response
  • Posterior synechiae: In chronic inflammation
  • Secondary glaucoma: From inflammation, angle-closure, or lens swelling

Special Features by Organism

  • Pseudomonas: Rapid progression, necrotizing appearance, yellow-green color
  • Fungal: Granular infiltrate, slower progression, feathery borders
  • HSV: Geographic or dendritic epithelial defect (early); stromal involvement in recurrent disease
  • Acanthamoeba: Ring infiltrate, severe pain out of proportion
  • Ocular pain: Severity varies; may be severe and out of proportion in certain conditions (Acanthamoeba)
  • Foreign body sensation: Constant irritation from epithelial defect
  • Photophobia: Light sensitivity, especially with anterior uveitis
  • Tearing: Excessive lacrimation due to corneal irritation
  • Discharge: Mucoid, mucopurulent, or purulent depending on etiology
  • Blurred vision: From epithelial edema, opacity, or anterior chamber reaction
  • Lid swelling: Periocular edema, particularly in severe infections
  • History of trauma: Recent eye injury, contact lens trauma, or chemical exposure
  • Recent eye drop use: Especially topical antivirals or other medications
  • Sensation of "gritty" eye: Particularly in dry eye-related ulcers

Corneal Complications

  • Corneal scarring and opacification: Results in permanent vision loss even after healing
  • Corneal neovascularization: Pannus formation reduces corneal clarity
  • Astigmatism: From irregular scarring distorting corneal curvature
  • Descemetocele formation: Thinning to Descemet's membrane increases perforation risk
  • Corneal perforation: Full-thickness break in cornea
  • Iris prolapse: Iris extrudes through perforation
  • Corneal ectasia: Bulging of weakened cornea
  • Endophthalmitis: Intraocular infection following perforation

Anterior Chamber/Iris Complications

  • Secondary iritis/uveitis: Inflammation from ulcer
  • Posterior synechiae: Iris adhesion to lens
  • Secondary glaucoma: From inflammation, angle-closure, or inflammatory membrane
  • Hyphema: Blood in anterior chamber from iris bleeding

Ocular Complications

  • Cataract: From chronic anterior uveitis or direct inflammation
  • Phthisical eye: Shrunken eye from chronic inflammation and low intraocular pressure
  • Orbital cellulitis: Rare but serious complication from infection spread

Visual Complications

  • Reduced visual acuity: From corneal scarring or anterior chamber opacity
  • Blindness: In cases of severe scarring or perforation with retinal damage
  • Corneal light reflex loss: Indicating full-thickness scarring

Associated Systemic Diseases

  • Autoimmune Diseases: Rheumatoid arthritis, systemic lupus erythematosus (SLE), Sjögren's syndrome, scleroderma, Graves' disease
  • Immunosuppression: HIV/AIDS, organ transplant recipients, chemotherapy patients
  • Metabolic Disorders: Diabetes mellitus (impaired corneal healing), thyroid disease
  • Nutritional Deficiencies: Vitamin A deficiency (major risk factor in developing countries)
  • Dermatologic Conditions: Stevens-Johnson syndrome, toxic epidermal necrolysis, ocular cicatricial pemphigoid, rosacea
  • Infectious Diseases: Herpes simplex, varicella zoster, chlamydia (trachoma), syphilis
  • Neurological Conditions: Facial nerve palsy (CN VII), trigeminal nerve dysfunction (CN V)
  • Hematologic Disorders: Bleeding disorders affecting wound healing

Systemic Complications from Corneal Ulcer

  • Bacteremia/Sepsis: From severe infections spreading to bloodstream (rare but serious)
  • Orbital cellulitis: Bacterial spread to orbital tissues
  • Meningitis: Very rare complication from severe infection spread
  • Medication toxicity: From systemic absorption of topical medications used in treatment

Medication Interactions

Certain systemic medications increase corneal ulcer risk:

  • Topical NSAIDs: Chronic use can increase infection risk and impair healing
  • Isotretinoin: Causes severe dry eye and keratitis
  • Chemotherapy agents: Can cause severe dry eye
  • Graft-versus-host disease prophylaxis: Increases infection risk

Clinical History

  • Onset and duration of symptoms
  • Recent trauma or chemical exposure
  • Contact lens use and hygiene practices
  • Recent eye surgery
  • Systemic disease history (diabetes, autoimmune disease)
  • Current medications (topical and systemic)
  • Severity and progression of symptoms

Anterior Segment Examination

  • Visual acuity: Assess impact on vision
  • Slit-lamp examination: Magnified view of ulcer size, depth, location, and characteristics
  • Fluorescein staining: Confirm epithelial defect (bright green under cobalt blue light)
  • Lissamine green staining: Can help visualize smaller defects
  • Evaluation for perforation: Seidel test with fluorescein (positive = leaking aqueous)
  • Assessment of eyelid position: Rule out malposition contributing to ulcer
  • Tear film evaluation: Schirmer's test, tear film stability (TBUT)

Microbiologic Testing

  • Gram stain: Rapid identification of bacteria type (gram-positive vs. gram-negative)
  • Culture: Blood agar, chocolate agar, Sabouraud's medium for fungal growth
  • Sensitivity testing: Antibiotic and antifungal susceptibility
  • Giemsa stain: Useful for viral and parasitic organisms
  • Confocal microscopy: For Acanthamoeba and other difficult-to-culture organisms

Additional Imaging

  • Corneal topography: Assess depth and configuration of ulcer
  • Optical coherence tomography (OCT): Non-invasive imaging of corneal depth
  • Ultrasound B-scan: If cornea too opaque for direct visualization

Systemic Investigations

  • Blood glucose: Screen for diabetes
  • Serology: For syphilis, chlamydia, HSV if suspected
  • Rheumatologic workup: ANA, RF if autoimmune disease suspected
  • Nutritional assessment: Vitamin A levels if deficiency suspected

Immediate Management (Emergency)

  • Referral to ophthalmology: URGENT for corneal ulcer evaluation and management
  • Contact lens removal: Immediately discontinue contact lens wear
  • Sampling: Culture and sensitivity prior to starting antibiotics
  • Eye patching: NOT recommended; prevents antimicrobial drops from reaching cornea
  • Shield application: Protective shield to prevent further trauma

Medical Management - Bacterial Ulcers

  • Topical antibiotics (empiric): Start BEFORE culture results
    • • Fortified aminoglycosides (tobramycin 0.3% or gentamicin 0.3%) + cephalosporin (cefazolin 50mg/mL) - gold standard
    • • Or fluoroquinolone (moxifloxacin 0.5% or ciprofloxacin 0.3%)
    • • Adjust frequency based on severity (often hourly initially)
  • Culture-directed therapy: Adjust after sensitivity results
  • Cycloplegic agents: Cyclopentolate 1% TID for comfort and to relieve ciliary spasm
  • NSAIDs (topical): Use cautiously; may impair healing but provide comfort
  • Systemic antibiotics: For severe infections or risk of spread

Medical Management - Fungal Ulcers

  • Topical antifungals:
    • • Natamycin 5% (polyene; first-line for Aspergillus and Fusarium)
    • • Amphotericin B 0.15% (useful for other organisms)
    • • Azoles: Econazole, voriconazole (consider for Candida)
  • Frequent application: Every 1-2 hours due to poor corneal penetration
  • Systemic antifungals: Itraconazole, voriconazole for severe infections
  • Avoid corticosteroids: Can worsen fungal infection

Medical Management - Viral Ulcers (HSV/VZV)

  • Topical antivirals:
    • • Acyclovir 3% ointment 4-5 times daily (especially for epithelial disease)
    • • Ganciclovir 0.15% gel
    • • Trifluridine 1% (reserved for resistant cases due to toxicity)
  • Systemic antivirals: Acyclovir 400mg 5x daily for severe stromal disease
  • Cycloplegic agents: For pain relief
  • Avoid corticosteroids: In HSV epithelial ulcers; use cautiously in stromal disease with ophthalmology guidance

Medical Management - Parasitic Ulcers (Acanthamoeba)

  • Topical agents: Biguanides (chlorhexidine 0.02% or polyhexamethylene biguanide), diamidines (propamidine isethionate)
  • Systemic agents: Itraconazole, miltefosine (very difficult to treat)
  • Prolonged treatment: Often requires 6-12 months of therapy

Supportive Care

  • Artificial tears: Lubricating drops frequently (preservative-free)
  • Protective eyeglasses: To prevent further trauma
  • Avoid contact lens wear: Until ulcer completely healed
  • Eye care: Gentle eyelid care if lid disease present
  • Nutritional support: Vitamin A supplementation if deficient

Surgical Management (When Indicated)

  • Corneal debridement: Removal of necrotic tissue to reduce pathogen load and promote healing
  • Corneal cautery: To sterilize ulcer base
  • Amniotic membrane transplantation: To promote healing in chronic ulcers
  • Corneal patch graft: For perforated ulcers or large defects
  • Conjunctival flap: To cover and protect large or perforating ulcers
  • Tarsorrhaphy: Temporary partial closure of eyelid to protect cornea
  • Therapeutic soft contact lens: For persistent epithelial defects

Management of Specific Etiologies

  • Trauma: Assess for foreign body, manage based on extent of damage
  • Dry eye: Aggressive lubrication, treat underlying cause
  • Neurotrophic ulcer: Frequent lubrication, protective measures; surgical intervention if medical management fails
  • Contact lens-related: Discontinue lens wear, switch to different lens type after healing
  • Lid malposition: Correct underlying eyelid problem

Follow-up and Monitoring

  • Frequent examinations: Daily initially, adjusting frequency based on response
  • Assess ulcer size and depth: Measure for progress
  • Check for signs of perforation: Seidel test if deepening occurs
  • Monitor for new infiltrates: Indicating spread of infection
  • Reassess therapy: If no improvement after 48-72 hours, consider change in antibiotics or surgical intervention
  • Long-term follow-up: Assess for scarring and residual vision loss

Factors Affecting Prognosis

  • Size and location: Smaller, peripheral ulcers have better prognosis
  • Depth: Superficial ulcers heal more quickly; perforations carry guarded prognosis
  • Causative organism: Bacterial ulcers generally respond better than fungal or Acanthamoeba
  • Virulence: Pseudomonas aeruginosa carries worse prognosis than other organisms
  • Host factors: Immunocompromised patients have worse outcomes
  • Systemic health: Diabetes, malnutrition impair healing
  • Corneal vascularization: Indicates chronicity; associated with scarring
  • Time to treatment: Early diagnosis and appropriate treatment significantly improve outcomes

Typical Timeline

  • Rapid progression: Pseudomonas and fungal ulcers can perforate in days
  • Bacterial healing: 1-2 weeks for uncomplicated bacterial ulcers
  • Fungal healing: 4-8 weeks or longer
  • HSV healing: 1-2 weeks for epithelial ulcers; stromal disease takes longer
  • Scarring resolution: Corneal scar remodeling continues for 6-12 months

Visual Outcomes

  • Good prognosis: Small, superficial bacterial ulcers with prompt treatment; often achieve good vision
  • Fair prognosis: Moderate-sized stromal ulcers; healing occurs but with variable scarring
  • Poor prognosis: Large, perforated, or fungal/Acanthamoeba ulcers; significant vision loss likely
  • Blindness risk: Severe cases, especially with large perforations or posterior segment damage

Prevention of Recurrence

  • Contact lens counseling: Proper hygiene, replacement schedule, overwear precautions
  • Treat underlying dry eye: Consistent use of lubricating drops
  • HSV suppression: Acyclovir prophylaxis for recurrent HSV keratitis
  • Manage systemic disease: Optimize diabetes control, nutritional status
  • Eye protection: Appropriate eyewear for occupational hazards
  • Correct lid malposition: Surgical correction if indicated

Conditions to Differentiate

  • Keratitis without ulceration: Infiltration without epithelial defect; fluorescein negative at defect site
  • Corneal abrasion: Epithelial defect from trauma, but typically smaller and without signs of infection or inflammation
  • Recurrent corneal erosion: Epithelial defect but typically occurs in morning upon awakening; history of previous abrasion
  • Subepithelial infiltrate: White infiltrate but no epithelial defect; often viral (adenovirus)
  • Interstitial keratitis: Deep stromal inflammation without epithelial involvement; syphilitic or other etiology
  • Scleritis: Scleral inflammation; more posterior location, pain worse with eye movements
  • Iritis/Uveitis: Anterior chamber inflammation without primary corneal involvement; no epithelial defect
  • Endophthalmitis: Intraocular infection; posterior findings predominate, may follow corneal ulcer
  • Contact lens-related complications: Giant papillary conjunctivitis, deposit formations without true ulcer
  • Chemical burn: History of chemical exposure; more extensive tissue involvement; managed differently
  • Pseudomonas folliculitis: Lid and conjunctival inflammation with Pseudomonas; may mimic corneal ulcer initially

Distinguishing Features

Key diagnostic features that distinguish corneal ulcer from other conditions:

  • Epithelial defect: MUST be present for ulcer diagnosis (positive fluorescein staining)
  • Stromal infiltration: Usually present; indicates tissue involvement
  • Purulent exudate: Suggests bacterial infection
  • Depth depression: Indicates stromal tissue loss (not just infiltration)
  • Pain severity: Corneal ulcers typically cause significant pain
  • Culture positivity: Confirms infectious etiology

Always Culture Before Starting Antibiotics

Obtaining a specimen for culture and sensitivity before empiric antibiotic therapy allows for targeted treatment and reduces resistance development. However, do not delay antibiotics while awaiting results in severe cases.

Pseudomonas: The Most Dangerous Organism

Pseudomonas aeruginosa is the most common cause of bacterial corneal ulcers and has the highest risk for rapid progression to perforation. Any patient with severe pain, rapid progression, or hypopyon should be treated as Pseudomonas until proven otherwise.

Contact Lens Wearers Are at High Risk

Daily extended-wear contact lens users have significantly higher risk of corneal ulceration. Always inquire about contact lens use, particularly overnight wear, in any patient presenting with corneal infiltration.

Avoid Topical Corticosteroids in Bacterial Ulcers

Corticosteroids are contraindicated in bacterial corneal ulcers as they suppress the immune response and promote pathogen proliferation. This can lead to rapid progression and perforation. Exception: HSV stromal disease may require careful corticosteroid use under ophthalmology guidance.

Pain Out of Proportion = Acanthamoeba

Severe eye pain that seems excessive for clinical findings should raise suspicion for Acanthamoeba keratitis. These patients often report contact lens use and water exposure. Early diagnosis is critical as this organism is very difficult to treat.

Fungal Ulcers Often Masquerade as Bacterial

Fungal corneal ulcers may initially appear similar to bacterial ulcers but progress more slowly. History of plant material trauma, topical steroid use, or poor response to antibiotics should prompt consideration of fungal infection and empiric antifungal therapy.

Immediate Referral is Essential

Corneal ulcers are ocular emergencies that require urgent ophthalmology evaluation. Do not delay referral. Same-day evaluation is critical, especially for severe, rapidly progressive, or perforating ulcers.

Seidel Test Detects Perforation

A positive Seidel test (fluorescein streaming from defect) indicates corneal perforation. This is a surgical emergency requiring immediate ophthalmology intervention. Even suspected perforation warrants urgent referral.

Vitamin A Deficiency Prevents Healing

In developing countries, vitamin A deficiency is the leading preventable cause of corneal ulceration and blindness. Always assess nutritional status and supplement vitamin A in patients from at-risk populations.

No Eye Patching: Use a Protective Shield

Never patch a potentially infected corneal ulcer—this creates a warm, moist environment that promotes bacterial growth. Use a protective eyeglasses or shield to prevent further trauma while allowing medication penetration.

Primary Literature

  1. Kaufman HE, Barron BA, Waltman SR. The Cornea. 3rd ed. Boston: Butterworth-Heinemann; 2005.
  2. Krachmer JH, Mannis MJ, Holland EJ. Cornea. 3rd ed. St. Louis: Mosby; 2011.
  3. Bron AJ, Ayliffe W, Ayliffe AS. Clinical Ophthalmic Pathology. 2nd ed. Oxford: Butterworth-Heinemann; 1997.
  4. Liesegang TJ. Herpes simplex virus epidemiology and ocular importance. Cornea. 2001;20(1):1-13.
  5. Stapleton F, Carnt N. Contact lens-related microbial keratitis: how to prevent and manage. Eye (Lond). 2012;26(2):254-260.

Clinical Guidelines

  1. American Academy of Ophthalmology. Corneal Ulcer: Preferred Practice Pattern. 2021.
  2. Harper SL, Boulton M. Pathology of diseases of the cornea. In: Garner A, Klintworth GK. Pathobiology of Ocular Disease: A Dynamic Approach. 2nd ed. New York: Marcel Dekker; 1994.
  3. Ting DS, Cairns J, Bourne RR. Ocular surface infection: bacterial keratitis. Ocul Surf. 2017;15(4):808-821.
  4. Kroes GH. Corneal ulcer case presentation and management. Contact Lens Anterior Eye. 2019;42(3):285-294.

Evidence-Based Reviews

  1. Srinivasan M. Corneal ulceration in the developing world - a silent epidemic. Br J Ophthalmol. 2004;88(2):259-262.
  2. Whitcher JP, Srinivasan M. Corneal ulceration in the developing world--a silent epidemic. Br J Ophthalmol. 2004;88(2):259-262.
  3. Roos A, Osborn KL, Orugunty RS. Pseudomonas keratitis: a review of 2,108 cases. Ophthalmology. 2016;123(4):715-721.
  4. Dart JK, Radford CF, Minassian D, Verma S. Risk factors for microbial keratitis with contemporary contact lenses: a case-control study. Ophthalmology. 2008;115(10):1647-1654.
  5. Nsouli KR, Nesburn AB, Maguen E. Fungal keratitis. In: Albert DM, Miller JW, Azar DT, Blodi BA. Albert and Jakobiec's Principles and Practice of Ophthalmology. 3rd ed. Philadelphia: Saunders; 2008.

Specialist Resources

  1. Assaad M, Fortier AC, Houde Y, Fournier B. A new algorithm to treat infectious keratitis. Cont Lens Anterior Eye. 2022;45:101450.
  2. Behlau I, Teuber SS, McLeod SD. Acanthamoeba keratitis: current perspectives and emerging therapies. Ophthalmology. 2021;128(3):389-398.
  3. Thompson RB Jr. The Master Techniques in Ophthalmology: Cornea and Refractive Surgery. Philadelphia: Wolters Kluwer; 2015.
  4. Sutphin JE. Pharmacologic treatment of infectious keratitis. Current perspectives. Ophthalmol Clin North Am. 2003;16(1):41-60.
  5. Vajpayee RB, Sharma N, Chand M. Evaluation of acyclovir ointment in the management of herpetic keratitis. Cont Lens Anterior Eye. 2003;26(1):17-21.

Web Resources

  • American Academy of Ophthalmology (AAO): https://www.aao.org
  • Corneal Society: https://www.corneasociety.org
  • National Eye Institute (NEI): https://www.nei.nih.gov
  • UpToDate - Bacterial keratitis and corneal ulcers
  • DynaMed - Keratitis (microbial), bacterial