This 5-year-old girl developed redness and pain on the right side of her forehead. Later a vesicular rash developed (Figure 110-1). She was diagnosed with herpes zoster involving the first (ophthalmic) branch of the trigeminal nerve. Note the vesicles and bullae on the forehead and eyelid and the crust on the nasal tip (Hutchinson sign). Fortunately, she did not have ocular complications and her case of zoster fully healed with systemic acyclovir and acyclovir eye ointment.
FIGURE 110-1
A 5-year-old girl with herpes zoster involving the ophthalmic branch of the trigeminal nerve. Note the vesicles and bullae on the forehead and eyelid and the crust on the nasal tip (Hutchinson sign). Fortunately, she did not have ocular complications and her case of zoster fully healed with oral acyclovir and acyclovir eye ointment. (Used with permission from Amor Khachemoune, MD.)
Herpes zoster is a common infection caused by varicella-zoster virus, the same virus that causes chickenpox. Reactivation of the latent virus in neurosensory ganglia produces the characteristic manifestations of herpes zoster (shingles). Herpes zoster outbreaks may be precipitated by aging, poor nutrition, immunocompromised status (Figures 110-2 to 110-4), physical or emotional stress, and excessive fatigue. Although zoster most commonly involves the thoracic and lumbar dermatomes, reactivation of the latent virus in the trigeminal ganglia may result in herpes zoster ophthalmicus (HZO) (Figures 110-1 to 110-5).
FIGURE 110-3
Acute zoster ophthalmicus of the patient in Figure 110-2. Note the conjunctival injection, corneal punctation (keratitis), and a small layer of blood in the anterior chamber (hyphema). A diagnosis of anterior uveitis was suspected based on the irregularly shaped pupil, the hyphema, and ciliary flush. A slit-lamp examination confirmed the anterior uveitis (iritis). (Used with permission from Paul Comeau.)
FIGURE 110-4
Corneal scarring and conjunctival injection of the same patient in Figure 110-2 6 months later after being lost to follow-up. (Used with permission from Paul Comeau.)
Incidence rates of HZO complicating herpes zoster range from 8 to 56 percent.1
Ocular involvement is not correlated with age, gender, or severity of disease.
Serious sequelae may occur including chronic ocular inflammation, vision loss (Figures 110-2 to 110-4), and disabling pain. Early diagnosis is important to prevent progressive corneal involvement and potential loss of vision.2
Because the nasociliary branch of the first (ophthalmic) division of the trigeminal (fifth cranial) nerve innervates the globe (Figure 110-6), the most serious ocular involvement develops if this branch is involved.
Classically, involvement of the side of the tip of the nose (Hutchinson sign) has been thought to be a clinical predictor of ocular involvement via the external nasal nerve (Figures 110-1 and 110-5). The Hutchinson sign is a powerful predictor of ocular inflammation and corneal denervation with relative risks of 3.35 and 4.02, respectively. In one study, the manifestation of herpes zoster skin lesions at the dermatomes of both nasociliary branches (at the tip, the side, and the root of the nose) was invariably associated with the development of ocular inflammation.3
Epithelial keratitis is the earliest potential corneal finding (Figure 110-3). On slit-lamp examination, it appears as multiple, focal, swollen spots on the cornea that stain with fluorescein dye. They may either resolve or progress to dendrite formation. Herpes zoster virus dendrites form branching or frond-like patterns that have tapered ends and stain with fluorescein dye. These lesions can lead to anterior stromal corneal infiltrates.
Stromal keratitis occurs in 25 to 30 percent of patients with HZO, and is characterized by multiple fine granular infiltrates in the anterior corneal stroma. The infiltrates probably arise from antigen–antibody reaction and may be prolonged and recurrent.4
Anterior uveitis evolves to inflammation of the iris and ciliary body and occurs frequently with HZO (Figure 110-3). The inflammation is usually mild, but may cause a mild intraocular pressure elevation. The course of disease may be prolonged, especially without timely treatment, and may lead to glaucoma and cataract formation.
Herpes zoster virus is the most common cause of acute retinal necrosis. Symptoms include blurred vision and/or pain in one or both eyes and signs include peripheral patches of retinal necrosis that rapidly coalesce, occlusive vasculitis, and vitreous inflammation. It commonly causes retinal detachment. Bilateral involvement is observed in 1/3 of patients, but may be as high as 70 percent in patients with untreated disease. Treatment includes long courses of oral and intravenous acyclovir, and corticosteroids.5
Varicella-zoster virus is a member of the same family (Herpesviridae) as herpes simplex virus, Epstein-Barr virus, and cytomegalovirus.
The virus damages the eye and surrounding structures by neural and secondary perineural inflammation of the sensory nerves. This often results in corneal anesthesia.
Conjunctivitis, usually with Staphylococcus aureus, is a common complication of HZO.
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