Herpes Simplex Keratitis
(Herpes Simplex Keratoconjunctivitis)
Herpes simplex keratitis usually affects the corneal surface but sometimes involves the corneal stroma (the deeper layers of the cornea) or the inner corneal surface (endothelium), anterior chamber, and iris. Stromal involvement is probably an immunologic response to the virus.
As with all herpes simplex virus infections, there is a primary infection, followed by a latent phase, in which the virus goes into the nerve roots. Latent virus may reactivate, causing recurrent symptoms.
Herpes simplex keratitis is a major cause of blindness worldwide.
(See also Introduction to Corneal Disorders.)
The initial (primary) infection is usually nonspecific self-limiting conjunctivitis, often in early childhood and usually without corneal involvement. If the cornea is involved, symptoms include foreign body sensation, lacrimation, photophobia, and conjunctival hyperemia. Sometimes vesicular blepharitis (blisters on the eyelid) follows, symptoms worsen, vision blurs, and blisters break down and ulcerate, then resolve without scarring in about a week.
Recurrent ocular herpes affects the cornea. Three main types of herpes simplex keratitis are
Recurrences usually take the form of epithelial keratitis (also called dendritic keratitis) with tearing, foreign body sensation, and a characteristic branching (dendritic or serpentine) lesion of the corneal epithelium with bulb-like terminals that stain with fluorescein. Multiple recurrences may result in corneal hypoesthesia or anesthesia, ulceration, permanent scarring, and decreased vision.
Most patients with disciform keratitis, which involves the corneal endothelium primarily, have a history of epithelial keratitis. Disciform keratitis is a deeper, disc-shaped, localized area of secondary corneal edema and haze accompanied by anterior uveitis. This form may cause pain and reversible vision loss.
Stromal keratitis can cause necrosis of the stroma and severe ache, photophobia, foreign body sensation, and irreversible decreased vision.
Slit-lamp examination is mandatory. Finding a dendrite is enough to confirm the diagnosis in most cases. When the appearance is not conclusive, viral culture of the lesion can confirm the diagnosis.
Most patients are managed by an ophthalmologist. If stromal or uveal involvement occurs, treatment is more involved and referral to an ophthalmologist is mandatory.
Topical therapy (eg, ganciclovir 0.15% gel applied every 3 hours while awake [5 times/day] or trifluridine 1% drops every 2 hours while awake [9 times/day]) is usually effective and is tapered off over 2 to 3 weeks.
Alternatively, oral therapy (eg, acyclovir 400 mg orally 3 to 5 times/day or valacyclovir 1000 mg orally twice/day) is effective and—at reduced doses—may be used indefinitely to prevent frequent recurrences in patients whose vision has been threatened.
Immunocompromised patients may require IV antivirals (eg, acyclovir 5 mg/kg IV every 8 hours for 7 days).
Topical corticosteroids are contraindicated in epithelial keratitis, but they may be effective when used with an antiviral to manage later-stage stromal involvement (disciform or stromal keratitis) or uveitis. In such cases, patients may be given prednisolone acetate 1% instilled every 2 hours initially, lengthening the interval to every 4 to 8 hours as symptoms improve.
If the epithelium surrounding the dendrite is loose and edematous, debridement by gentle swabbing with a cotton-tipped applicator before beginning drug therapy may speed healing. Topical drugs to relieve photophobia include atropine 1% or scopolamine 0.25% three times a day.
Herpes simplex keratitis typically is a recurrence of primary herpes simplex eye infection that was typically a nonspecific, self-limiting conjunctivitis.
Characteristic findings include a branching dendritic or serpentine corneal lesion (indicating dendritic keratitis), disc-shaped, localized corneal edema and haze plus anterior uveitis (indicating disciform keratitis), or stromal scarring (indicating stromal keratitis).
Diagnosis is confirmed by finding a dendritic ulcer or by viral culture.
Treatment requires antivirals, usually topical ganciclovir or trifluridine or oral acyclovir or valacyclovir.
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