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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.
Corneal ulcers have many causes (see Causes of Corneal Ulcers). Bacterial ulcers (most commonly due to contact lens wear) may occasionally complicate herpes simplex keratitis and, depending on the bacterial species, may be particularly refractory to treatment. The time course for ulcers varies. Ulcers caused by Acanthamoeba (also most commonly due to exposure to contaminated water while wearing contact lenses) and fungi (most commonly due to trauma with vegetable material) are indolent but progressive, whereas 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 Contact Lenses : Care and Complications).
Causes of Corneal Ulcers
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 (see Overview of Uveitis ), corneal perforation with iris prolapse, pus in the anterior chamber (hypopyon), panophthalmitis, and destruction of the eye may occur without treatment and, on occasion, even with the best available treatment, particularly if treatment is delayed. More severe symptoms and complications tend to occur with deeper ulcers.
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 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 disposable #15 blade, sterile platinum spatula, or jeweler's forceps (typically by an ophthalmologist). Microscopic examination of scrapings can identify Acanthamoeba.
Treatment for corneal ulcers, regardless of cause, begins with moxifloxacin 0.5% or gatifloxacin 0.3 to 0.5% 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 Herpes Simplex Keratitis ) is treated with trifluridine 1% drops q 2 h while the patient is awake to a total of 9 times/day, ganciclovir 0.15% gel 5 times/day, valacyclovir 1000 mg po bid, or acyclovir 400 mg po 5 times/day (or tid for recurrent herpes simplex keratitis) for about 14 days.
Fungal infections are treated with one of many topical antifungal drops (eg, voriconazole 1%, 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 voriconazole 200 mg bid, ketoconazole 400 mg once/day, fluconazole 400 mg once then 200 mg once/day, or itraconazole 400 mg once then 200 mg once/day.
If Acanthamoeba is identified, therapy can include topical propamidine 0.1%, neomycin 0.175%, and polyhexamethylene biguanide 0.02% or chlorhexidine 0.02% supplemented with miconazole 1%, clotrimazole 1%, or oral ketoconazole 400 mg once/day or itraconazole 400 mg once then 200 mg once/day. The drops are used 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.
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.
Causes of corneal ulcers include infection of the cornea (including overwearing of contact lenses), eye trauma, abnormalities of the eyelid, and nutritional deficiencies.
Ulcers may be accompanied by circumcorneal hyperemia and WBC layering in the anterior chamber (hypopyon).
All but the smallest ulcers are cultured, usually by an ophthalmologist.
Treatment usually involves frequent (eg, every 1 to 2 h around the clock) application of topical antimicrobials.
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