Varicella-zoster virus causes two distinct syndromes. Primary infection presents as varicella (or chickenpox), a contagious and usually benign childhood illness that occurs in epidemics among susceptible children. The reactivation of the virus, usually associated with decline in cell-mediated immunity, occurs as herpes zoster (HZ) (shingles). Varicella is spread through droplet infection with an initial viremia, and subsequent viral spread to the skin and the eye. It is easily disseminated to susceptible individuals. Ninety-five percent of the population has serological evidence of prior VZV infection with or without symptomatic varicella. The incidence of varicella has diminished 70% after implementation of the varicella vaccine in 1995.Herpes zoster ophthalmicus (HZO) is defined as HZ involvement of the ophthalmic division of the fifth cranial nerve. The ophthalmic division further divides into the nasociliary, frontal, and lacrimal branches, of which the frontal nerve is most commonly involved with HZO.1 Without the use of antiviral therapy, approximately 50% of HZ patients develop ocular involvement. 2,3 There is a long list of complications from HZ, including those that involve the optic nerve and retina in HZO, but the most frequent and debilitating complication of HZ regardless of dermatomal distribution is post-herpetic neuralgia (PHN), a neuropathic pain syndrome that persists or develops after the zoster rash has resolved.
Herpes Zoster Ophthalmicus and GlaucomaHerpes zoster presents as an acute, painful, vesicular eruption distributed along a single dermatome. Most cases of HZO have a prodromal period before skin eruptions that may include fever, malaise, headache, and pain in the eye. Hutchinson's sign is defined as skin lesions at the tip, side, or root of the nose and is a strong predictor of ocular inflammation and corneal denervation in HZO, especially if both branches of the nasociliary nerve are involved. 5,6 A study by Thean et al. 7 identified the clinical features of uveitis secondary to HZO. Most patients were immunocompetent. The course of the uveitis was generally uniphasic in nature and of a relatively short duration. There was a high incidence of secondary glaucoma, with 15% of all patients requiring surgical intervention. The visual loss in several patients was not directly related to the uveitis and secondary glaucoma but to other complications associated with HZO. The authors report that the secondary glaucoma may be the result of several mechanisms: (1) plugging of the trabecular meshwork due to the presence of cellular debris and iris pigment; (2) trabeculitis; (3) pupillary-block glaucoma secondary to posterior synechiae, with resultant iris bombé; (4) peripheral anterior synechiae; or (5) chronic open-angle glaucoma presumably due to damage to the trabecular meshwork or as a result of the use of topical steroids (Figs. 45.1-45.3).Van der Lelij et al. 8 reported on a large cohort of patients who were initially seen with unilateral anterior uveitis in association with sectoral iri...