HERPES-ZOSTER OPHTHALMICUS

Herpes zoster ophthalmicus occurs worldwide, usually in healthy adults, but, increasingly in patients who are immunocompromised. After primary varicella infection (chickenpox), the virus lies dormant in the sensory ganglion until it becomes reactivated as zoster. Involvement of the ophthalmic branch of the trigeminal nerve is characterized early by corneal dysesthesia and dendritiform keratopathy, and these are self-limited. However, smoldering disease may cause pathological changes in the ocular structures through direct invasion of virus, secondary inflammation, and alterations of autoimmune mechanisms. Antiviral agents have demonstrated some success in resolving early signs and symptoms, but their role in preventing and treating late complications remains to be fully studied. Until a definitive antiviral agent is established, the benefits of steroid use in certain acute inflammatory processes outweigh its risk of reducing host immunity. Corneal complications of herpes zoster ophthalmicus sometimes require surgical intervention.