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Corneal Ulcer and Hypopyon
Cornea
1. Overview
The Clinical Analogy - The Flooded Basement
Imagine the anterior chamber of the eye as a sealed basement with a drainage system (trabecular meshwork). The cornea is the front wall. When bacteria or fungi breach this wall (corneal ulcer), the body mounts an inflammatory response - neutrophils flood the anterior chamber like water rushing into a broken basement. These neutrophils, being heavier than aqueous, sink to the bottom by gravity - forming the hypopyon: a white-yellow, sterile-looking but inflammation-driven sediment. The ulcer is the breach; the hypopyon is the flood response. Understanding this gravity-dependent layering immediately tells you why hypopyon is mobile with change of posture and why it is not pus in the AC per se but a sterile exudate of dead neutrophils (unless there is endophthalmitis).
Exam pearl
- Hypopyon = gravity-dependent inferior layering of inflammatory cells, predominantly neutrophils, in the anterior chamber.
- It is usually sterile in bacterial corneal ulcers, reflecting anterior-chamber inflammation rather than established microbial endophthalmitis.
- Extension of infection from the cornea into the eye can cause microbial endophthalmitis - an intraocular infection involving the aqueous and/or vitreous - with potentially poor visual outcomes.
Definitions & Terminology
Corneal Ulcer
- A corneal ulcer is an epithelial defect with an underlying inflammatory stromal infiltrate. Suppuration and stromal necrosis may subsequently produce excavation.
- It differs from a superficial erosion (epithelial defect only, without stromal involvement). A corneal infiltrate may occur with or without an epithelial defect; an infiltrate with an overlying epithelial defect is a corneal ulcer.
| Term | Definition | Epithelium | Stroma | Fluorescein |
|---|---|---|---|---|
| Corneal erosion | • Superficial epithelial defect | • Absent | • Intact | • Positive |
| Corneal infiltrate/abscess | • Focal stromal inflammation • May occur with or without an epithelial defect | • Intact when no epithelial defect is present • Defective when ulceration is present | • Infiltrated | • Negative when epithelium is intact • Positive over an epithelial defect |
| Corneal ulcer | • Epithelial defect with stromal opacification and breakdown • Stromal thinning or excavation may occur | • Absent over the defect | • Opacified and breaking down • May be thinned or excavated | • Positive over the epithelial defect |
| Descemetocele | • Deep corneal ulcer reaching Descemet's membrane • Overlying epithelium and stroma are absent or markedly deficient • Intact Descemet's membrane is exposed and may bulge forward | • Absent or markedly deficient | • Absent or markedly deficient | • Positive over the epithelial defect • A ring pattern is not definitional |
| Perforation | • Full-thickness corneal breach • Loss of corneal tissue | • Absent at the breach | • Perforated | • Seidel test positive when aqueous leakage is present |
| Term | Definition | Epithelium | Stroma | Fluorescein |
|---|---|---|---|---|
| Corneal erosion | • Superficial epithelial defect | • Absent | • Intact | • Positive |
| Corneal infiltrate/abscess | • Focal stromal inflammation • May occur with or without an epithelial defect | • Intact when no epithelial defect is present • Defective when ulceration is present | • Infiltrated | • Negative when epithelium is intact • Positive over an epithelial defect |
| Corneal ulcer | • Epithelial defect with stromal opacification and breakdown • Stromal thinning or excavation may occur | • Absent over the defect | • Opacified and breaking down • May be thinned or excavated | • Positive over the epithelial defect |
| Descemetocele | • Deep corneal ulcer reaching Descemet's membrane • Overlying epithelium and stroma are absent or markedly deficient • Intact Descemet's membrane is exposed and may bulge forward | • Absent or markedly deficient | • Absent or markedly deficient | • Positive over the epithelial defect • A ring pattern is not definitional |
| Perforation | • Full-thickness corneal breach • Loss of corneal tissue | • Absent at the breach | • Perforated | • Seidel test positive when aqueous leakage is present |
Hypopyon
- Hypopyon (Greek: hypo = under, pyon = pus).
- It refers to a collection of inflammatory cells (predominantly neutrophils).
- These cells settle by gravity in the inferior part of the anterior chamber, forming a visible white/yellow horizontal level.
- It signals severe anterior segment inflammation.
Epidemiology & Predisposing Risk Factors
- Corneal ulcers with hypopyon represent a vision-threatening ocular emergency.
- The burden of infective corneal ulceration varies by geography and occupational exposure; agricultural trauma is an important risk factor in affected regions.
- In India, it is a leading cause of corneal blindness .
- Hypopyon may occur in infective corneal ulcers; its frequency varies by clinical setting and disease severity.
| Risk Factor | Mechanism | Organism Predisposed |
|---|---|---|
| • Contact lens wear | • Hypoxia • Epithelial trauma | • Pseudomonas • Acanthamoeba |
| • Ocular surface disease (dry eye, trichiasis) | • Epithelial barrier disruption | • Bacteria • Fungi |
| • Corneal trauma (vegetative) | • Direct inoculation | • Fungi (Fusarium, Aspergillus) |
| • Previous corneal surgery / graft | • Epithelial vulnerability • Immunosuppression | • Bacteria • Fungi |
| • Topical steroid use | • Local immunosuppression • Impaired infection control | • Fungi • Acanthamoeba • Herpetic keratitis requires antiviral context |
| • Neurotrophic keratopathy | • Loss of corneal sensation and trophic support • Epithelial breakdown • Impaired healing | • Increased susceptibility to microbial keratitis • Including secondary bacterial infection |
| • Immunocompromised state (diabetes mellitus (DM), human immunodeficiency virus (HIV)) | • Impaired host defense • Altered ocular-surface homeostasis • Reduced corneal sensation • Impaired epithelial healing | • Bacterial and fungal keratitis • Human immunodeficiency virus (HIV) may be associated with opportunistic ocular infections |
| • Ocular surface tumour / pterygium | • Epithelial disruption | • Bacteria |
| • Epidemic keratoconjunctivitis | • Adenoviral infection with corneal involvement • Subepithelial infiltrates may occur | • Adenovirus • Bacterial superinfection can occur |
| Risk Factor | Mechanism | Organism Predisposed |
|---|---|---|
| • Contact lens wear | • Hypoxia • Epithelial trauma | • Pseudomonas • Acanthamoeba |
| • Ocular surface disease (dry eye, trichiasis) | • Epithelial barrier disruption | • Bacteria • Fungi |
| • Corneal trauma (vegetative) | • Direct inoculation | • Fungi (Fusarium, Aspergillus) |
| • Previous corneal surgery / graft | • Epithelial vulnerability • Immunosuppression | • Bacteria • Fungi |
| • Topical steroid use | • Local immunosuppression • Impaired infection control | • Fungi • Acanthamoeba • Herpetic keratitis requires antiviral context |
| • Neurotrophic keratopathy | • Loss of corneal sensation and trophic support • Epithelial breakdown • Impaired healing | • Increased susceptibility to microbial keratitis • Including secondary bacterial infection |
| • Immunocompromised state (diabetes mellitus (DM), human immunodeficiency virus (HIV)) | • Impaired host defense • Altered ocular-surface homeostasis • Reduced corneal sensation • Impaired epithelial healing | • Bacterial and fungal keratitis • Human immunodeficiency virus (HIV) may be associated with opportunistic ocular infections |
| • Ocular surface tumour / pterygium | • Epithelial disruption | • Bacteria |
| • Epidemic keratoconjunctivitis | • Adenoviral infection with corneal involvement • Subepithelial infiltrates may occur | • Adenovirus • Bacterial superinfection can occur |
| Risk Factor | Mechanism | Organism Predisposed |
|---|---|---|
| • Contact lens wear | • Hypoxia • Micro-trauma • Biofilm formation | • Pseudomonas • Acanthamoeba |
| • Ocular surface disease (dry eye, trichiasis) | • Epithelial barrier disruption | • Bacteria • Fungi |
| • Corneal trauma (vegetative) | • Direct inoculation | • Fungi (Fusarium, Aspergillus) |
| • Previous corneal surgery / graft | • Epithelial vulnerability • Immunosuppression | • Bacteria • Fungi • Herpes simplex virus |
| • Topical steroid use | • Immunosuppression • Delayed epithelial healing | • Fungi • Acanthamoeba • Herpes simplex virus epithelial disease may worsen without appropriate antiviral therapy |
| • Neurotrophic keratopathy | • Loss of trophic support | • Persistent epithelial defect • Sterile ulceration • Secondary infection may occur |
| • Immunocompromised state (diabetes mellitus (DM), human immunodeficiency virus (HIV)) | • Impaired host defenses • Ocular-surface compromise | • Opportunistic fungi • Bacteria |
| • Ocular surface squamous neoplasia | • Corneal component or noduloulcerative morphology | • Bacteria • Fungi |
| • Epidemic keratoconjunctivitis | • Adenoviral keratitis with subepithelial infiltrates | • Adenovirus |
| Risk Factor | Mechanism | Organism Predisposed |
|---|---|---|
| • Contact lens wear | • Hypoxia • Micro-trauma • Biofilm formation | • Pseudomonas • Acanthamoeba |
| • Ocular surface disease (dry eye, trichiasis) | • Epithelial barrier disruption | • Bacteria • Fungi |
| • Corneal trauma (vegetative) | • Direct inoculation | • Fungi (Fusarium, Aspergillus) |
| • Previous corneal surgery / graft | • Epithelial vulnerability • Immunosuppression | • Bacteria • Fungi • Herpes simplex virus |
| • Topical steroid use | • Immunosuppression • Delayed epithelial healing | • Fungi • Acanthamoeba • Herpes simplex virus epithelial disease may worsen without appropriate antiviral therapy |
| • Neurotrophic keratopathy | • Loss of trophic support | • Persistent epithelial defect • Sterile ulceration • Secondary infection may occur |
| • Immunocompromised state (diabetes mellitus (DM), human immunodeficiency virus (HIV)) | • Impaired host defenses • Ocular-surface compromise | • Opportunistic fungi • Bacteria |
| • Ocular surface squamous neoplasia | • Corneal component or noduloulcerative morphology | • Bacteria • Fungi |
| • Epidemic keratoconjunctivitis | • Adenoviral keratitis with subepithelial infiltrates | • Adenovirus |
2. Etiology & Microbial Classification
Bacterial Ulcers (Most Common)
Bacterial keratitis is the most common type of infectious keratitis, but its reported proportion varies substantially by region.
| Organism | Characteristic Feature | Clinical Clue |
|---|---|---|
| Pseudomonas aeruginosa | • Highly virulent • Rapid progression | • Contact lens • Blue-green pigment • Ring ulcer |
| Staphylococcus aureus | • Common • Oval grey-white ulcer | • Blepharitis associated • Methicillin-resistant Staphylococcus aureus (MRSA) occurs |
| Streptococcus pneumoniae | • Serpinginous/creeping ulcer | • Hypopyon • Dacryocystitis (Mooren-like) |
| Moraxella spp. | • Indolent • Peripheral anterior stromal infiltrate | • Alcoholism • Local ocular predisposing factors |
| Neisseria gonorrhoeae | • Rapid progression • May cause corneal ulceration, thinning, and perforation | • Purulent discharge • Neonatal infection (ophthalmia neonatorum) |
| Corynebacterium diphtheriae | • No distinctive clinical findings | • History of diphtheria |
| Organism | Characteristic Feature | Clinical Clue |
|---|---|---|
| Pseudomonas aeruginosa | • Highly virulent • Rapid progression | • Contact lens • Blue-green pigment • Ring ulcer |
| Staphylococcus aureus | • Common • Oval grey-white ulcer | • Blepharitis associated • Methicillin-resistant Staphylococcus aureus (MRSA) occurs |
| Streptococcus pneumoniae | • Serpinginous/creeping ulcer | • Hypopyon • Dacryocystitis (Mooren-like) |
| Moraxella spp. | • Indolent • Peripheral anterior stromal infiltrate | • Alcoholism • Local ocular predisposing factors |
| Neisseria gonorrhoeae | • Rapid progression • May cause corneal ulceration, thinning, and perforation | • Purulent discharge • Neonatal infection (ophthalmia neonatorum) |
| Corynebacterium diphtheriae | • No distinctive clinical findings | • History of diphtheria |
Fungal Ulcers
| Organism | Type | Setting | Key Feature |
|---|---|---|---|
| Fusarium species | Filamentous | • Tropical settings • Vegetative trauma | • Feathery or serrated margins • Non-yellow infiltrate • Satellite lesions and immune rings are nonspecific |
| Aspergillus species | Filamentous | • Agricultural or vegetative-trauma exposure • Host factors vary by case | • Raised surface • Hypopyon • Deep stromal involvement may occur but is nonspecific |
| Candida albicans | Yeast | • Compromised ocular surface • Immunosuppression • Prior corneal surgery or grafting • Contact-lens wear may be a risk factor | • Cream-colored, discrete infiltrate • May resemble bacterial keratitis • Relatively slow progression |
| Curvularia, Alternaria | Dematiaceous | • Trauma • Soil or plant-material exposure | • Pigmented fungal elements • Brown or pigmented stromal infiltrate may occur |
| Organism | Type | Setting | Key Feature |
|---|---|---|---|
| Fusarium species | Filamentous | • Tropical settings • Vegetative trauma | • Feathery or serrated margins • Non-yellow infiltrate • Satellite lesions and immune rings are nonspecific |
| Aspergillus species | Filamentous | • Agricultural or vegetative-trauma exposure • Host factors vary by case | • Raised surface • Hypopyon • Deep stromal involvement may occur but is nonspecific |
| Candida albicans | Yeast | • Compromised ocular surface • Immunosuppression • Prior corneal surgery or grafting • Contact-lens wear may be a risk factor | • Cream-colored, discrete infiltrate • May resemble bacterial keratitis • Relatively slow progression |
| Curvularia, Alternaria | Dematiaceous | • Trauma • Soil or plant-material exposure | • Pigmented fungal elements • Brown or pigmented stromal infiltrate may occur |
Exam pearl
- Filamentous fungi (Fusarium, Aspergillus) can invade the corneal stroma.
- Fungal keratitis may show satellite lesions beyond the main ulcer margin.
- Repeated debridement of the ulcer can facilitate penetration of topical medication.
- Many topical antifungals have poor corneal penetration, especially when an intact epithelium overlies stromal infection.
Other Causes
| Cause | Organism/Type | Distinguishing Feature |
|---|---|---|
| Viral | Herpes simplex virus type 1 (HSV-1) • Dendrite → geographic | Dendritic staining • Reduced sensation • Recurrent |
| Acanthamoeba | Free-living amoeba (contact lens) • Also occurs in non-contact-lens users | Radial perineuritis • SEVERE pain disproportionate to signs • Ring infiltrate late |
| Sterile (non-infectious) | Mooren's • Peripheral ulcerative keratitis (PUK) • Neurotrophic | No growth • Systemic associations • Quiet anterior chamber (AC) (mostly) |
| Exposure keratopathy | Neuroparalytic / lagophthalmos | Inferior cornea • Minimal inflammation |
| Cause | Organism/Type | Distinguishing Feature |
|---|---|---|
| Viral | Herpes simplex virus type 1 (HSV-1) • Dendrite → geographic | Dendritic staining • Reduced sensation • Recurrent |
| Acanthamoeba | Free-living amoeba (contact lens) • Also occurs in non-contact-lens users | Radial perineuritis • SEVERE pain disproportionate to signs • Ring infiltrate late |
| Sterile (non-infectious) | Mooren's • Peripheral ulcerative keratitis (PUK) • Neurotrophic | No growth • Systemic associations • Quiet anterior chamber (AC) (mostly) |
| Exposure keratopathy | Neuroparalytic / lagophthalmos | Inferior cornea • Minimal inflammation |
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Keep reading Corneal Ulcer and Hypopyon
13 more sections are included with the Clinical plan.
- Clinical Features - Symptoms & Signs
- Grading Systems
- Investigations - Systematic Approach
- Pathophysiology - From Breach to Hypopyon
- Corneal Ulcer Presentation
- Antibiotic Therapy - Bacterial Ulcers