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Send Home Our method Usage examples Index Contact StatisticsWe do not evaluate or guarantee the accuracy of any content in this site. A retrospective study of the clinical presentation and outcome of herpes zoster in a tertiary dermatology outpatient referral clinic. Herpes zoster ophthalmicus in patients at risk for the acquired immune deficiency syndrome (AIDS).
Natural history of herpes zoster ophthalmicus: predictors of postherpetic neuralgia and ocular involvement. Varicella zoster virus retrobulbar optic neuritis preceding retinitis in patients with acquired immune deficiency syndrome. Valaciclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Comparison of the efficacy and safety of valaciclovir and acyclovir for the treatment of herpes zoster ophthalmicus. Incidence of herpes zoster ophthalmicus: results from the Pacific Ocular Inflammation Study. Herpes zoster is an infection resulting from reactivation of the varicella-zoster virus (VZV) that affects peripheral or cranial nerves and usually occurs years after primary infection with the varicella (chickenpox) virus or receipt of the live, attenuated varicella vaccine. Effect of varicella vaccine on incidence of herpes zoster in various age groups in the years after vaccination.
Psychological Stress As A Trigger For Herpes Zoster: Might The Conventional Wisdom Be Wrong?
It is a member of the same family (Herpesviridae) as herpes simplex virus, Epstein-Barr virus, and cytomegalovirus.
Because the nasociliary branch innervates the globe, the most serious ocular involvement develops if this branch is affected. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference.
Cost-benefit analysis of universal varicella vaccination in the US taking into account the closely related herpes-zoster epidemiology. Most patients with herpes zoster ophthalmicus present with a periorbital vesicular rash distributed according to the affected dermatome. Reactivation of the latent virus in neurosensory ganglia produces the characteristic manifestations of herpes zoster, commonly known as shingles. Classically, involvement of the tip of the nose (Hutchinson's sign) has been thought to be a clinical predictor of ocular involvement. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP. Herpes zoster, also known as zoster and shingles, is caused by the reactivation of the varicella-zoster virus (VZV) , the same virus that causes varicella (chickenpox). Clinical Manifestations of Herpes Zoster Ophthalmicus (includes Images) Yanoff: Ophthalmology, 4th ed.


Medical records were reviewed for all 173 cases of herpes zoster diagnosed among residents of Rochester, Minnesota, less than 20 years of age during the period 1960 through 1981. A minority of patients may also develop conjunctivitis, keratitis, uveitis, and ocular cranial-nerve palsies.
Normal aging, poor nutrition, and immunocompromised status correlate with outbreaks of herpes zoster, and certain factors such as physical or emotional stress and fatigue may precipitate an episode.Herpes zoster ophthalmicus occurs when reactivation of the latent virus in the trigeminal ganglia involves the ophthalmic division of the nerve. Treatment includes topical capsaicin cream, over-the-counter analgesics, tricyclic antidepressants, and anticonvulsants.18Cranial nerve palsies involving the third (most common), fourth, and sixth nerves may occur rarely (Figure 5). CDC continues to study the epidemiology of herpes zoster among adults and children and to monitor the effects of the U. Permanent sequelae of ophthalmic zoster infection may include chronic ocular inflammation, loss of vision, and debilitating pain. All patients with acute herpes zoster ophthalmicus should receive antiviral therapy with the goal of preventing ocular complications. Herpes zoster ophthalmicus occurs when HZ presents in the ophthalmic division of the fifth cranial nerve.
Antiviral medications such as acyclovir, valacyclovir, and famciclovir remain the mainstay of therapy and are most effective in preventing ocular involvement when begun within 72 hours after the onset of the rash.
Direct ocular involvement is not specifically correlated with age, gender, or severity of disease. Optic neuritis has been noted in about one in 400 cases and may precede retinal disease or follow acute herpes zoster ophthalmicus infection (Figure 6).17,19,20The rightsholder did not grant rights to reproduce this item in electronic media. Oral acyclovir may be beneficial as an adjunct to topical antivirals and topical steroids in severe cases of zoster keratouveitis. Timely diagnosis and management of herpes zoster ophthalmicus, with referral to an ophthalmologist when ophthalmic involvement is present, are critical in limiting visual morbidity. Patients may develop blepharitis and present with ptosis secondary to edema and inflammation. TOPIC: The incidence and morbidity of herpes zoster (HZ) and HZ ophthalmicus (HZO) , and the potential impact of varicella vaccine on their epidemiology. 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.9 The findings usually resolve within one week.
The clinical features of corneal disease include direct viral infection, antigen-antibody reactions, delayed cell-mediated hypersensitivity reactions, and neurotrophic damage.7 Patients with corneal disease present with varying degrees of decreased vision, pain, and light sensitivity.
Corneal complications occur in approximately 65 percent of cases of herpes zoster ophthalmicus.7Epithelial Keratitis. The earliest corneal finding is punctate epithelial keratitis.10 On slit lamp examination, this appears as multiple, focal, swollen lesions that stain with rose bengal or fluorescein dye. 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.11Herpes 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. 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.13 The condition, known as anterior stromal keratitis or nummular keratitis, is characterized by multiple fine granular infiltrates in the anterior corneal stroma below the epithelial layer (Figure 3).
Most of the infiltrates lie directly beneath pre-existing dendrites or areas of punctate epithelial 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.7 It is usually central and preceded by anterior stromal keratitis. 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 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.7 Corneal thinning is a serious complication that may lead to corneal perforation. Using preservative-free lubricating drops and ointment can prevent the development of epithelial defects.UVEITISAnterior uveitis, which is diagnosed by slit lamp examination, refers to inflammation of the iris and ciliary body and occurs frequently with herpes zoster ophthalmicus. The inflammation is generally mild and transient, but it frequently causes a mild elevation in intraocular pressure. As with stromal keratitis, the course of disease may be prolonged, especially without timely, adequate treatment.
Chronic inflammation can lead to endothelial cell injury, resulting in corneal edema.EPISCLERITIS AND SCLERITISFindings of episcleritis include localized or diffuse redness, as well as pain and swelling of the conjunctiva and episclera. Both conditions may be accompanied by localized stromal keratitis.ACUTE RETINAL NECROSIS AND PROGRESSIVE OUTER RETINAL NECROSIS SYNDROMESHerpes zoster virus is considered the offending agent in most cases of acute retinal necrosis and progressive outer retinal necrosis syndromes.
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.



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