Dormant from childhood, the varicella-zoster virus (VZV) can cause a great deal of pain and can affect the ocular adnexa and eye. We often think of the associated vesicular cutaneous rash and corneal pseudodendrites; however, the virus can cause uveitis, trabeculitis, scleritis, choroiditis, and acute retinal necrosis as well as affect the optic nerve. Triggers for activation are not clearly known. Prevalence is increased in patients over the age of 60 and in those who are immunocompromised, though the disease can occur at any age. Because of the increased prevalence in older patients, a shingles vaccination is now recommended by the Centers for Disease Control and Prevention (CDC) for patients over age 50 (www.CDC.gov ).
Of the patients who develop herpes zoster, nearly 25% have herpes zoster ophthalmicus (HZO). Prodromal symptoms are similar to the flu. These are followed by skin lesions (Figure 1) and paresthesia/hyperesthesia described as burning and/or tingling along the affected dermatome. Hutchinson sign (nasociliary nerve involvement producing cutaneous vesicles on the tip of the nose) is correlated with ocular involvement, although its absence does not indicate a lack of ocular involvement (Zaal et al, 2003).
Acute corneal signs can be delayed for a month following the onset of vesicular pustules. These signs include pseudodendrites (no terminal end bulbs, minimal rose bengal and fluorescein staining), punctate keratitis (periphery with adherent epithelial cells), nummular stromal lesions (immune reaction), keratouveitis, and endotheliitis. Recalcitrant episodes of mucous plaques may present in some patients, sometimes several months after the initial HZO episode, resulting in corneal scarring (Liesegang, 1985). They are easily removed, revealing a poorly adherent epithelium beneath, much like filamentary keratitis. Long-term damage can result in neurotrophic keratopathy, with a high risk for ulcer perforation. Up to 20% of HZO patients have hypoesthesia after one year (Cobo, 1987).
Though VZV has been detected in the cornea and mucous plaques of HZO patients, topical antiviral therapy is ineffective. Oral antivirals are the focused option and are especially helpful in reducing disease severity and long-term complications if initiated within 72 hours of the onset of symptoms in immunocompetent patients. Although effective in the acute phase, the benefit toward reducing post-herpetic neuralgia (PHN) is less clear (Marsh and Cooper, 1991).
Therapy once consisted of acyclovir 800mg given five times per day, but compliance and improvement of PHN favor prescribing famciclovir (500mg, three times per day) or valacyclovir (1,000mg, three times per day) (Decroix et al, 2000). Both are as effective as acyclovir (Pavan-Langston, 2008). Antiviral treatments should be continued for seven to 10 days.
Oral and topical steroids can be prescribed, but only in healthy patients who have no contraindications. They, like antivirals, are not helpful with PHN. Medications that have been useful for managing pain and PHN include ibuprofen (800mg t.i.d.), tricyclic antidepressants, gabapentin (30mg to 600mg t.i.d.) and oxycodone HCl (10mg to 20mg b.i.d.); however, oxycodone should be used with extreme care and as a last resort given the increased risk for addiction.
Another common drug for PHN is pregabalin (150mg to 300mg/day b.i.d. or t.i.d., not to exceed 600mg). This can be increased for pain management after the first week to 600mg/day for another two to four weeks, then taper the dose. Skin lesions can be managed topically with capsaicin ointment. CLS
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