Topical corticosteroids are effective in suppressing the inflammatory response of herpetic keratitis. However, their inappropriate use may result in severe epithelial disease or stromal necrosis, corneal perforation, increased tendency toward recurrence, secondary microbial infections, elevation of the intraocular pressure, and lenticular changes.
Patients requiring topical corticosteroids for suppression of the inflammatory response usually require the drug for a period of months, and withdrawal often is complicated by a recurrence of inflammation. The immunosuppressive complications of steroid administration (eg, recurrent epithelial disease) largely can be avoided by the concurrent administration of antiviral therapy.
Patient cooperation is a prerequisite for the safe administration of corticosteroids in herpetic keratitis. An extremely slow corticosteroid taper typically is required.
Antiviral agents, topical or oral, are prescribed to inhibit viral replication in infected cells. All topical antiviral medications available for clinical use in the United States are toxic, with signs of toxicity being similar for all such drugs. Punctate epithelial keratopathy, limbal follicles, a follicular conjunctival response, ptosis, punctal stenosis, and contact dermatitis can occur at any time after 10-14 days of therapy.
In mild cases of antiviral toxicity, epithelial changes may be the only manifestation. The toxic potential of antiviral agents always should be considered in patients who heal poorly, because these agents are inhibitors of cell division. 
These agents inhibit herpes simplex virus (HSV) replication. Treatment of viral infections begins with mechanical debridement of the involved rim along with a rim of normal epithelium. This is followed by the topical instillation of antiviral medications (eg, trifluridine, ganciclovir). 
A structural analogue of thymidine, this agent inhibits viral DNA polymerase. Viroptic has better penetration through the cornea and greater efficacy (95% heal rate) than other topical agents. If no response occurs in 7-14 days, consider other treatments.
Valacyclovir is a prodrug that is rapidly converted to the active drug acyclovir. It produces a greater serum concentration of acyclovir with smaller oral dosing. Valacyclovir is more expensive than acyclovir but can be as effective with a more convenient dosing regimen.  The optimal dose for ocular disease has not been determined.
This agent is a prodrug that, when biotransformed into its active metabolite, penciclovir, may inhibit viral DNA synthesis/replication. It has been used successfully in the suppression of genital herpes. Its efficacy in HSV keratitis currently is under study.
Acyclovir is a synthetic guanosine analogue that requires activation by viral thymidine kinase. The activated acyclovir triphosphate, concentrated 50-100 times in HSV-infected cells, suppresses viral replication by preferentially inhibiting viral DNA polymerase, serving as a DNA chain terminator and inducing irreversible binding between polymerase enzyme and the interrupted DNA chain.
Acyclovir is a potent inhibitor of viral growth with minimal toxicity to uninfected epithelial cells. Oral acyclovir at a dose of 2 g/day for 10 days has been reported to be as effective as topical agents for epithelial keratitis, with the advantage of no ocular toxicity.
This agent is an acyclic nucleoside analogue of 2'deoxyguanasine. It phosphorylates first to monophosphate form by a viral-encoded protein kinase homologue, and then to diphosphate and triphosphate forms by cellular kinases. This allows for greater concentration of ganciclovir in virus-infected cells, possibly because of preferential phosphorylation of this agent in infected cells.
Ganciclovir is thought to inhibit HSV replication by competitive inhibition of viral DNA polymerases and by incorporating itself into viral DNA, causing termination of viral DNA elongation. Like acyclovir, ganciclovir is virostatic and exerts its effect only on replicating virus.
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