Treatment of herpes zoster ophthalmicus, 2014 cure for herpes - PDF Review

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. Herpes zoster infection (shingles) results from the reactivation of varicella zoster virus infection.
In excess of 60% of people older than 60 years, especially those with diminished immunity due to diabetes and cancers, are afflicted by herpes zoster. Prednisone use in conjunction with acyclovir resulted in the reduction of the pain associated with acute herpes zoster. The outcome of treatment of shingles is often unsatisfactory, although the antiviral medications reduce the duration of pain during the acute phase but do not prevent PHN complications and pain.
Most patients with herpes zoster ophthalmicus present with a periorbital vesicular rash distributed according to the affected dermatome.
Initially, the host is able to produce varicella zoster virus—specific, cell-mediated immunity during the infection.
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). Low levels of immune globulin have been shown to predispose patients to recurring herpes zoster infection. Despite the usefulness of prednisone in managing the associated pain with herpes zoster infection, it has not been shown to decrease or prevent the incidence of PHN. I believe it is a neurologic condition and that it should be aggressively treated with some kind of physiologic treatments by a neurologist. Permanent sequelae of ophthalmic zoster infection may include chronic ocular inflammation, loss of vision, and debilitating pain.

Postherpetic neuralgia is very resistant to treatment and results in decreased quality of life.
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. The CDC Advisory Committee on Immunization Practices recommends routine vaccination of all persons age >60 years with one dose of zoster vaccine. Timely diagnosis and management of herpes zoster ophthalmicus, with referral to an ophthalmologist when ophthalmic involvement is present, are critical in limiting visual morbidity. Occasionally, zoster can cause motor weakness in noncranial nerve distributions, calledzoster paresis. The pain is stipulated to be due to persistent C-fiber nociceptor activity in the nerve cells, although studies have shown chronic neural loss and scarring in nerves affected by herpes zoster injury.
Lidocaine patches were superior to both no treatment and vehicle patches in averaged category pain relief scores.
Combining TCAs with antiviral drugs during herpes zoster infection has been shown to decrease the intensity of PHN pain but does not prevent it.
One specific risk for patients who are immunocompromised is dissemination of the zoster rash. Zoster vaccination is not indicated to treat acute zoster, to prevent persons with acute zoster from developing PHN, or to treat ongoing PHN. It is a member of the same family (Herpesviridae) as herpes simplex virus, Epstein-Barr virus, and cytomegalovirus. Cutaneous dissemination generally occurs only among immunocompromised patients, occurring in up to 37% of zoster cases in the absence of antiviral treatment. Valacyclovir appears to be more efficacious in decreasing the severity of pain associated with acute herpes zoster and the duration of the PHN when compared to acyclovir. Before routine administration of zoster vaccine, it is not necessary to ask patients about their history of varicella (chickenpox) or to conduct serologic testing for varicella immunity. Reactivation of the latent virus in neurosensory ganglia produces the characteristic manifestations of herpes zoster, commonly known as shingles. 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.

Rarely, patients will experience acute focal neurologic deficits weeks to months after resolution of the zoster rash, involving the trigeminal distribution contralateral to the initial rash. 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. When antiviral therapy starts within 72 hours of the onset of herpes zoster, acyclovir, valacyclovir, and famciclovir have been shown to significantly shorten the periods of acute pain, virus shedding, rash, and acute and late-onset complications. Other rare neurologic complications of herpes zoster include myelitis, aseptic meningitis, and meningoencephalitis. Corneal complications occur in approximately 65 percent of cases of herpes zoster ophthalmicus.7Epithelial Keratitis.
The risk for neurologic zoster complications is generally increased in immunocompromised persons. 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. 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).
A chronic relapsing course is not unusual, especially without timely and adequate treatment. 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.
As with stromal keratitis, the course of disease may be prolonged, especially without timely, adequate treatment. 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.

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