Herpes Zoster Ophthalmicus

This is caused by the varicella-zoster virus, the same virus that causes chickenpox. It is thought that the initial infection with the virus occurs with an attack of childhood chickenpox and that the virus remains in the body in a latent form, subsequently to manifest itself as herpes zoster in some individuals. The virus appears to lodge in the Gasserian ganglion. The onset of the condition is heralded by headache and the appearance of one or two vesicles on the forehead. Over the next three or four days the vesicles multiply and appear on the distribution of one or all of the branches of the fifth cranial nerve. The patient can develop a raised temperature and usually experiences malaise and considerable pain. Sometimes a chickenpox-like rash appears over the rest of the body. The eye itself is most at risk when the upper division of the fifth nerve is involved. There might be vesicles on the lids and conjunctiva and, when the cornea is affected,punctate-staining areas are seen, which become minute subepithelial opacities. After four days to a week, the infection reaches its peak; the eyelids on the affected side might be closed by swelling, and oedema of the lids might spread across to the other eye (Figure 6.15). The vesicles become pustular and form crusts, which are then shed over a period of two or three weeks. In most cases, complete resolution

Figure 6.15. Herpes zoster ophthalmicus.03

occurs with remarkably little scarring of the skin considering the appearance in the acute stage. However, the cornea can be rendered permanently anaesthetic and the affected area of skin produces annoying paresthesiae, amounting quite often to persistent rather severe neu-ralgia,which can dog the patient for many years. Other complications include extraocular muscle palsies or rarely, encephalitis. Iridocyclitis is fairly common and glaucoma can develop and lead to blindness if untreated. At present, there is no known effective treatment other than the use of local steroids and acyclovir for the uveitis, and acetazolamide or topical beta-blockers for the glaucoma. Administration of systemic acyclovir or famciclovir early in the disease is known to reduce the severity of the neuralgia, but these medications need to be administered as soon as possible after the onset of symptoms for best effect. The disease has to run its course and the patient, who is usually elderly, could require much support and advice, especially when post-herpetic neuralgia is severe. It is accepted practice to treat the eye at risk with antibiotic drops and a weak mydriatic. Analgesics are, of course, also usually needed, often on a long-term basis.

Other causes of corneal anaesthesia include surgical division of the fifth cranial nerve for trigeminal neuralgia or any space-occupying lesion along the nerve pathway. The possibility of exposure and drying of the cornea must always be borne in mind in the unconscious or the anaesthetized patient because corneal ulceration and infection will soon result if this is neglected.

Corneal anaesthesia caused by nerve damage is nearly always permanent and,if it is complete, it can often be necessary to protect the eye by means of a tarsorrhaphy or botulinum toxin.

Lesser degrees of corneal anaesthesia can be treated by instilling an antibiotic ointment at night and, if a more severe punctate keratitis develops, by padding the eye.

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