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A corneal ulcer is a corneal epithelial defect with underlying inflammation (which soon results in necrosis of corneal tissue) due to invasion by bacteria, fungi, viruses, or Acanthamoeba. It can be initiated by mechanical trauma or nutritional deficiencies. Symptoms are progressive redness, foreign body sensation, ache, photophobia, and lacrimation. Diagnosis is by slit-lamp examination, fluorescein staining, and microbial studies. Treatment with topical antimicrobials and often dilating drops is urgent and requires an ophthalmologist.
Etiology
Corneal ulcers have many causes (see Table 1: Corneal Disorders: Causes of Corneal Ulcers ). Bacterial ulcers (most commonly due to contact lens wear) may complicate herpes simplex keratitis and be particularly refractory to treatment. Ulcers caused by Acanthamoeba (also most commonly due to contact lens wear) and fungi (most commonly due to trauma with vegetable material) are indolent but progressive; those caused by Pseudomonas aeruginosa (seen almost exclusively in contact lens wearers) develop rapidly, causing deep and extensive corneal necrosis. Wearing contact lenses while sleeping or wearing inadequately disinfected contact lenses can cause corneal ulcers (see Refractive Error: Care and Complications).
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Table 1
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| Causes of Corneal Ulcers |
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Category
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Examples
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Nontraumatic corneal abnormalities
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Bullous keratopathy (ie, ruptured bullae)
Cicatricial pemphigoid
Herpes simplex keratitis with secondary bacterial superinfection
Dry eyes (primary dry eyes or secondary dry eyes, eg, neurotrophic keratitis)
Trachoma
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Corneal injury (typically followed by bacterial infection)
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Corneal abrasion
Penetrating corneal trauma
Corneal foreign body (rare)
Contact lenses (most commonly when worn during sleep)
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Eyelid abnormalities
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Chronic blepharitis
Entropion
Incomplete eye closure (eg, due to lagophthalmos, Bell's palsy, eyelid defects after trauma, or exophthalmos)
Trichiasis
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Nutritional deficiencies
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Protein undernutrition
Vitamin A deficiency
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Pathophysiology
Ulcers are characterized by corneal epithelial defects with underlying inflammation, and soon necrosis of the corneal stroma develops. Corneal ulcers tend to heal with scar tissue, resulting in opacification of the cornea and decreased visual acuity. Uveitis, corneal perforation with iris prolapse, pus in the anterior chamber (hypopyon), panophthalmitis, and destruction of the eye may occur with or without treatment. More severe symptoms and complications tend to occur with deeper ulcers.
Symptoms and Signs
Conjunctival redness, eye ache, foreign body sensation, photophobia, and lacrimation may be minimal initially.
A corneal ulcer begins as a corneal epithelial defect that stains with fluorescein and an underlying dull, grayish, circumscribed superficial opacity. Subsequently, the ulcer suppurates and necroses to form an excavated ulcer. Considerable circumcorneal conjunctival hyperemia is usual. In long-standing cases, blood vessels may grow in from the limbus (corneal neovascularization). The ulcer may spread to involve the width of the cornea, may penetrate deeply, or both. Hypopyon (layered WBCs in the anterior chamber) may occur.
Corneal ulcers due to Acanthamoeba are often intensely painful and may show transient corneal epithelial defects, multiple corneal stromal infiltrates, and, later, a large ring-shaped infiltrate. Fungal ulcers, which are more chronic than bacterial ulcers, are densely infiltrated and show occasional discrete islands of infiltrate (satellite lesions) at the periphery.
Diagnosis
Diagnosis is made by slit-lamp examination; a corneal infiltrate with an epithelial defect that stains with fluorescein is diagnostic. All but small ulcers should be cultured by scraping with a sterile platinum spatula (typically by an ophthalmologist). Microscopic examination of scrapings can identify Acanthamoeba.
Treatment
Treatment for corneal ulcers, regardless of cause, begins with moxifloxacin 0.5% or gatifloxacin 0.3% for small ulcers and fortified (higher than stock concentration) antibiotic drops, such as tobramycin 15 mg/mL and cefazolin 50 mg/mL, for more significant ulcers, particularly those that are near the center of the cornea. Frequent dosing (eg, q 15 min for 4 doses, followed by q 1 h around the clock) is necessary initially. Patching is contraindicated because it creates a stagnant, warm environment that favors bacterial growth and prevents the administration of topical drugs.
Herpes simplex (see Corneal Disorders: Herpes Simplex Keratitis) is treated with trifluridine 1% drops q 2 h while the patient is awake or acyclovir 400 mg po 5 times/day for about 14 days.
Fungal infections are treated with one of many topical antifungal drops (eg, natamycin 5%, amphotericin B 0.15%), initially q 1 h during the day and q 2 h overnight. Deep infections may require addition of oral ketoconazole, fluconazole, or itraconazole.
If Acanthamoeba is identified, traditional therapy is propamidine and neomycin supplemented with miconazole, clotrimazole, or oral ketoconazole. Additional treatments include polyhexamethylene biguanide 0.02% or chlorhexidine 0.02% q 1 to 2 h until clinical improvement is evident, then gradually reduced to 4 times/day and continued for a number of months until all inflammation has resolved. Polyhexamethylene biguanide and chlorhexidine are not commercially available as ocular agents but can be prepared by a compounding pharmacy. Topical propamidine 0.1% q 1 to 2 h is often added for 3 days.
For all ulcers, treatment may also include a cycloplegic, such as atropine 1% or scopolamine 0.25% 1 drop tid, to decrease the ache of a corneal ulcer and to reduce the formation of posterior synechiae. In severe cases, debridement of the infected epithelium or even penetrating keratoplasty may be required. Patients who are poorly compliant or who have large, central, or refractory ulcers may need to be hospitalized.
Last full review/revision October 2008 by Melvin I. Roat, MD. FACS
Content last modified October 2008
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