The eyelids are commonly involved in herpes zoster ophthalmicus Figure 1 , part b. Patients may develop blepharitis and present with ptosis secondary to edema and inflammation. A vast majority of patients will have vesicular lesions on the eyelids that resolve with minimal scarring. Conjunctivitis is one of the most common complications of herpes zoster ophthalmicus. The conjunctiva appears injected and edematous, often with petechial hemorrhages. Unlike eyelid or conjunctival involvement, corneal involvement can result in significant vision loss.
The clinical features of corneal disease include direct viral infection, antigen-antibody reactions, delayed cell-mediated hypersensitivity reactions, and neurotrophic damage. Corneal complications occur in approximately 65 percent of cases of herpes zoster ophthalmicus. Epithelial Keratitis. The earliest corneal finding is punctate epithelial keratitis.
These lesions probably contain live virus and may either resolve or progress to dendrite formation. Punctate epithelial keratitis may present as early as one or two days after the initial skin rash, while dendrites often present at four to six days but can appear many weeks later.
Herpes zoster virus dendrites appear as elevated plaques and consist of swollen epithelial cells. Dendrites also stain with rose bengal and fluorescein dye Figure 2 , part b and can be viewed by Wood's lamp or slit lamp examination. Punctate and dendritic lesions can lead to anterior stromal corneal infiltrates. Slit lamp examination in a patient with herpes zoster ophthalmicus. Epithelial keratitis may have a dendritic appearance mimicking herpes simplex virus keratitis a and stains with fluorescein dye b.
Stromal Keratitis — Anterior Stromal Keratitis. The earliest finding of corneal stromal involvement presents during the second week of disease, occurring in 25 to 30 percent of patients with herpes zoster ophthalmicus. Most of the infiltrates lie directly beneath pre-existing dendrites or areas of punctate epithelial keratitis. The infiltrates are thought to arise from antigen-antibody interaction resulting from viral proliferation in the overlying epithelium.
Slit lamp examination of a patient with nummular keratitis as a result of herpes zoster virus infection. Subepithelial infiltrates are located in the anterior stroma below areas of previous epithelial keratitis. Stromal Keratitis—Deep Stromal Keratitis. This later stage of stromal keratitis is relatively uncommon and typically develops three to four months after the initial acute episode, but development can range from one month to many years later.
The keratitis may present as a lesion consisting of a localized area of inflammation affecting all levels of the stroma, or as peripheral infiltrates that may have a surrounding immune ring.
Corneal edema may be a prominent feature at this stage, usually with associated anterior chamber inflammation. A rare necrotizing form can also occur. A chronic relapsing course is not unusual, especially without timely and adequate treatment. Corneal neovascularization and lipid infiltrates may occur in patients with uncontrolled chronic disease. The pathogenesis of stromal disease probably involves a delayed cell-mediated hypersensitivity reaction. Neurotrophic Keratopathy. Neurotrophic keratitis is the end result of decreased corneal sensation from herpes zoster virus-mediated destruction, including susceptibility to mechanical trauma, decreased lacrimation, and delayed epithelial healing.
Such patients are at high risk for developing a secondary bacterial infection. Using preservative-free lubricating drops and ointment can prevent the development of epithelial defects.
Anterior uveitis, which is diagnosed by slit lamp examination, refers to inflammation of the iris and ciliary body and occurs frequently with herpes zoster ophthalmicus.
It may be isolated or associated with keratitis. The inflammation is generally mild and transient, but it frequently causes a mild elevation in intraocular pressure. Zoster uveitis can result in iris atrophy and an irregular pupil. As with stromal keratitis, the course of disease may be prolonged, especially without timely, adequate treatment. Herpes zoster uveitis may cause glaucoma and cataract formation.
Chronic inflammation can lead to endothelial cell injury, resulting in corneal edema. Findings of episcleritis include localized or diffuse redness, as well as pain and swelling of the conjunctiva and episclera. Scleritis is a more serious condition with involvement of the sclera.
Both conditions may be accompanied by localized stromal keratitis. Herpes zoster virus is considered the offending agent in most cases of acute retinal necrosis and progressive outer retinal necrosis syndromes.
Compared with acute retinal necrosis, progressive outer retinal necrosis is a more severe viral retinitis observed in immunocompromised persons, often in patients with acquired immunodeficiency syndrome. Acute retinal necrosis is characterized by peripheral patches of retinal necrosis that rapidly coalesce Figure 4 , occlusive vasculitis, and vitreous inflammation. Conversely, immunocompromised patients with progressive outer retinal necrosis are unable to mount a vitreous inflammatory response, leading to rapid involvement of the macula.
Both conditions commonly cause retinal detachment. The prognosis is extremely poor in patients with progressive outer retinal necrosis; most patients have no light perception vision. Postherpetic neuralgia affects about 7 percent of patients and is characterized by varying degrees of constant or intermittent pain in the distribution of the affected dermatome.
It generally improves with time but may last for months to years. In severe cases, patients may be depressed and suicidal. Treatment includes topical capsaicin cream, over-the-counter analgesics, tricyclic antidepressants, and anticonvulsants. Cranial nerve palsies involving the third most common , fourth, and sixth nerves may occur rarely Figure 5. If a team cannot play in the title game, the available team will be declared national champion. If neither team has enough available players by Jan.
For the semifinals, if both teams scheduled to play each other are unavailable, that game shall be declared a no contest and the winner of the the other semifinal will be declared national champion. If three semifinal teams are unavailable to play on Dec.
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