Herpes Zoster Ophthalmicus (HZO) Keratitis

Abstract

Herpes Zoster Ophthalmicus (HZO) is caused by reactivation of latent Varicella zoster virus in the ophthalmic branch of the trigeminal ganglion. Typically, this occurs in the elderly but is increasingly occurring in younger individuals. It starts with pain in the distribution of the nerve followed by dermatitis. The vesicular rash becomes pustular and then crusts forming a black eschar before being shed off. If the associated pain persists beyond 2–4 weeks, it is called postherpetic neuralgia (PHN) and can be very debilitating.

HZO usually causes follicular conjunctivitis, keratitis, or uveitis, but may also cause other complications such as retinitis, optic neuritis, and extraocular muscle palsies. Early epithelial keratitis manifests as pseudodendrites or superficial punctate keratopathy; the late stage is characterized by mucus plaques. Classic stromal lesions are called nummular keratitis; untreated, they can lead to vascularization and lipid keratopathy. Endotheliitis is characterized by granulomatous keratic precipitates with overlying stromal edema. HZO uveitis is severe and can cause iris atrophy and hyphema. HZO also causes severe hypoesthesia of the cornea which can result in recalcitrant neurotrophic ulcers.

A recombinant vaccine (Shingrix^®, GlaxoSmithKline) is very effective at preventing HZO and is approved for adults ≥50 years. Once HZO occurs, however, the treatment options are limited. Antivirals in the acute stage may decrease the risk of developing PHN. Keratouveitis is treated with steroids but care must be taken to taper them very slowly to prevent recurrences. Unfortunately, HZO manifestations repeatedly recur and can cause significant vision loss.