Shingle ophthalmicus caused by Varicella zoster can occur by two mechanisms. Commonly, reactivation of a latent trigeminal nucleus infection occurs following a previous episode of chicken pox or Shingle ophthalmicus. Ocular infection may also occur via direct inoculation of exogenous virus by contact with a patient having Varicella or Shingle.
Varicella zoster vesicular lesions are distributed in a dermatomal pattern, respecting the facial midline. Ocular involvement occurs in one-third of cases of Shingle symptoms. Hutchinson ‘s sign (vesicular lesions on the tip of the nose) is associated with ocular shingle involvement in 50 to 85% of cases. Keratoconjunctivitis can occur within a few days of dermal involvement. Recurrent Herpes zoster ophthalmicus occurs in 20% of cases.
Symptoms of Shingle ophthalmicus include a sensation of flushing, hypesthesia, and edema of the skin. Photophobia and blurred vision may indicate ocular involvement. Pain, particularly if chronic, can cause severe morbidity in some patients. Ten percent of patients will have severe post-therapeutic pain for 1 month; 5% will have pain for 3 months; 2 to 3% will have pain for 1 year. Post-therapeutic neuralgia is more common in patients older than 60 years of age, with 50% experiencing severe pain for more than 12 months. Famciclovir (500 mg pro rid) but not Acyclovir significantly speeds resolution of skin lesions and post-therapeutic neuralgia. Oral corticosteroids are also used to reduce the incidence of post-therapeutic pain.
Shingle ophthalmicus with ocular involvement may present with signs affecting both the eye and the ocular adnexa. Conjunctivitis, cannuliculitis,ptosis, ectropion, and entropion may occur. Comeal involvement may occur at any layer. Pseudodendites affect the epithelium and are elevated, branching lesions that differ from dendritic lesions of herpes simplex. A chronic form of epithelial keratins with mucous plaques may occur 3 to 4 months after the onset of skin rash, but may appear as early as 1 week or as late as 2 years later. These are whitish-gray plaques, sharply demarcated, that lie on the epithelial surface in a branching or linear pattern whose shape and appearance changes from day to day.
Stromal Shingle involvement includes a number of different presentations, some of which may lead to substantial visual dysfunction. Nummular keratitis with anterior stromal coin-shaped lesions may resolve spontaneously. Disciform keratitis, and interstitial keratitis can also occur. Neurotrophic keratitis has been reported in 10 to 25% of patients suffeing Herpes zoster ophthalmicus.
Scleitis and episcleitis are rare complications of Shingle ophthalmicus. Optic neuitis, etinitis, and extra ocular muscle palsies from cranial nerve involvement are also associated with Herpes zoster infection of the eye. Shingle can also affect the seventh and eight cranial nerves (Ramsey Hunt syndrome), presenting initially with a viral prodrome followed by severe periauricular pain.
Subsequently, vesicles involving the external auditory canal and the pinna can be found as shingles in children. Vesicles may also be present along portions of the face, neck, tongue, larynx, or mouth and their distribution depends on which portions of the tigeminal nerve ae infected. Other cranial nerves in communication with the trigeminal nerve, such as the VII, VIII, IX, or X nerves and cervical nerves II to IV, may also be involved. Sensory-neural hearing loss may occur. The recovery from Herpes zoster cephalicus associated facial palsy (60%) is reportedly worse than that associated with Bell’s palsy (84%).
The development of lagophthalmus and paralytic ectropion requires lubrication and possibly tarsorrhaphy or other eyelid procedures to prevent corneal scarring or perforation.