This patient has herpes zoster ophthalmicus. Particular attention must be paid to evaluating his eye, and the patient must be referred to an ophthalmologist.
Herpes zoster infection (more commonly referred to as shingles) is a reactivation of the varicella-zoster virus (VZV). Varicella-zoster is a member of the Herpesviridae family like herpes simplex virus, cytomegalovirus, and Epstein-Barr virus. Primary infection with VZV results in chicken pox. During recovery from the initial infection, the VZV gains entry into the sensory dorsal root ganglia where it remains latent. Reactivation is thought to occur secondarily to a decrease in virusspecific cell mediated immunity.
The virus travels down the sensory nerve, producing pain and skin lesions in a dermatomal distribution which does not cross the midline. There may be a prodromal phase of influenza-like symptoms followed by the development of pain in a dermatomal distribution. The sensory complaints often precede the development of rash by a few days but may be as long as one week.
The patient may report hyperesthesias, paresthesias, pruritus, and burning pain. The rash begins as a maculopapular rash which becomes vesicular. Initially the vesicles contain clear fluid which then progress to pustules. The rash then begins to crust over and heal. The entire outbreak and clearing takes approximately two weeks. Disseminated disease is present if the rash crosses the midline or if there are more than 20 lesions outside the affected dermatome. While shingles is not as contagious as chicken pox, it can be transmitted to non-immune persons via contact with secretions from the vesicles.
While herpes zoster reactivation can occur in anyone, it is more common in those over 50. Other factors contributing to the development of shingles are immunodeficiency, chronic steroid use, chemotherapy/radiation therapy, and malignancy.
Herpes zoster ophthalmicus (HZO) deserves special mention because the sequela may be permanent vision loss. HZO refers to reactivation of the VZV in the ophthalmic division of the trigeminal nerve. The rash may be observed unilaterally on the forehead, upper eyelid, or nose. Lesions on the tip of the nose are referred to as Hutchinson's sign. Its significance is that it represents an increase likelihood of ocular involvement. While often times there are skin lesions associated with HZO, it is possible to have ocular findings alone.
The ocular findings are broad. The classic finding is that of a dendritic lesion on the cornea, identified by fluorescein staining. This usually presents several days after the outbreak of the rash. The earliest ocular finding one may observe is a blepharoconjunctivitis or punctuate epithelial keratitis. An episcleritis, scleritis, or anterior stromal keratitis may develop over the next week. Deeper structures may become involved resulting in uveitis, optic neuritis, and retinal necrosis. Timely consultation with an ophthalmologist is necessary to help prevent permanent vision loss. Cranial nerve palsies also may occur. Patients should have documentation of extraocular muscle function.
Ramsey-Hunt syndrome refers to VZV reactivation involving cranial nerve seven. Patients present with a peripheral seven nerve facial palsy. They may report decreased taste sensation of the anterior two-thirds of the tongue. Careful inspection of the auricle, external auditory canal, and tympanic membrane may reveal the presence of vesicles. Follow-up evaluation by an ENT physician is necessary.
Treatment is acyclovir. In the non-immunocompromised patient, oral acyclovir is started if he presents within 72 hours of the development of rash. Famciclovir or valacyclovir also may be used. If a patient presents later than 72 hours after onset, oral acyclovir may be considered if new lesions are still being formed. The goal of treatment is to help reduce the risk of post-herpetic neuralgia. It also may decrease the time to lesion crusting over.
Patients who present with disseminated disease should be admitted for IV acyclovir and followed for the possible development of pneumonitis, hepatitis, or meningoencephalitis. Patients who are immunocompromised do not necessarily need to be admitted. If they present with a localized outbreak with no signs of dissemination, they may be treated with oral acyclovir. Patients with Ramsey-Hunt syndrome or herpes zoster ophthalmicus are treated with oral acyclovir but also require appropriate specialty follow-up.
The use of steroids is controversial. While evidence is lacking, they may help decrease the long-term pain experienced by patients after herpes zoster infection. This may be particularly true in the elderly who are at greatest risk of chronic pain. It should be mentioned, however, that side effects such as glucose intolerance and hypertension should be considered in the risk-benefit analysis of their use.
Post-herpetic neuralgia is the most common complication of herpes zoster infection. Pain in the dermatomal distribution of the rash may persist for weeks to months after rash resolution. While the initial management of the pain associated with zoster is NSAIDs and narcotic medications, various topical medications such as lidocaine patches or capsaicin cream may be used. Other medications used in the treatment of post-herpetic neuralgia include tricyclic antidepressants and anticonvulsants.