Herpes zoster

[Anonymous]

Herpes zoster involves one of the divisions of
the trigeminal nerve in 18 to 20% of cases, but the ophthalmic
branch is affected several times more frequently than are the
second or third divisions. HZ of the first division can lead to
blindness secondary to corneal scarring and should be managed
by an ophthalmologist. Facial and intraoral lesions are
characteristic of HZ involving the second and third divisions
of the trigeminal nerve.
Each individual oral lesion of HZ resembles lesions seen
in herpes simplex infections. The diagnosis is based on a history
of pain and the unilateral nature and segmental distribution
of the lesions (Figures 4-7 and 4-8).When the clinical
appearance is typical and vesicles are present, oral HZ can be
distinguished clinically from other acute multiple lesions of
the mouth,which are bilateral and are not preceded or accom-
56 Diagnosis and Management of Oral and Salivary Gland Diseases
panied by pain along the course of one trigeminal nerve
branch.
HZ has been associated with dental anomalies and severe
scarring of the facial skin when trigeminal HZ occurs during
tooth formation. Pulpal necrosis and internal root resorption
have also been related to HZ. In immunocompromised
patients, large chronic HZ lesions have been described that have
led to necrosis of underlying bone and exfoliation of teeth.
HZ of the geniculate ganglion, Ramsay Hunt syndrome, is
a rare form of the disease characterized by Bell’s palsy, unilateral
vesicles of the external ear, and vesicles of the oral mucosa.
Because oral lesions occurring without facial lesions are
rare, isolated oral HZ can be misdiagnosed, particularly when
erythema, edema, and nonspecific ulceration are seen without
the presence of intact vesicles. In these cases, a cytology
smear or viral culture is often necessary for diagnosis. An
incorrect diagnosis can be made when prodromal pain is
present prior to the appearance of the characteristic lesions.
During this period, endodontic therapy, extractions, or other
surgery may be performed unnecessarily. Similar problems
occur in zoster sine eruptione.

        

[sushantpatel_doc]

MANAGEMENT
Episodes of herpes zoster are generally self-limited and resolve without intervention. However, effective treatments do exist and can reduce the extent and duration of symptoms, and possibly the risk of chronic sequelae (ie, postherpetic neuralgia) as well. Treatment is of most benefit in those patient populations at risk for prolonged or severe symptoms, specifically, immunocompromised people and persons older than 50 years. The benefit of treating younger and healthier populations is unclear.

Uncomplicated zoster does not require inpatient care. Patients at high risk for disseminated zoster may benefit from intravenous (IV) acyclovir. Patients with disseminated zoster usually require admission for IV acyclovir. Inpatient care is also recommended for any patient demonstrating disseminated disease or ophthalmic or meningoencephalopathic involvement.

Pain Management for Acute Herpes Zoster
The majority of patients with acute herpes zoster experience pain. Primary treatments for acute zoster-associated pain include narcotic and non-narcotic analgesics (both systemic and topical), neuroactive agents, and anticonvulsant agents. While the efficacy of these treatments for general neuropathic pain has been well established, only a few of these modalities have been evaluated specifically for acute zoster-associated pain in controlled studies.

The oral narcotic oxycodone and the oral anticonvulsant gabapentin, as well as the topical analgesics aspirin and lidocaine, have all demonstrated the ability to reduce acute zoster-associated pain in double-blind, placebo-controlled studies. On the other hand, the oral anticonvulsant pregabalin failed to show any statistically significant effect in relieving acute zoster pain in a small double-blind, placebo-controlled study. Although, it should be noted this medication has demonstrated efficacy in treating the pain of postherpetic neuralgia in other controlled studies.

Antivirals and corticosteroids have also been shown to accelerate resolution of zoster-associated pain.

Nonpharmacologic therapies for acute zoster-associated pain include sympathetic, intrathecal, and epidural nerve blocks and percutaneous electrical nerve stimulation. Although well-controlled studies are few, meta-analyses and clinical trials suggest these treatments are effective in treating acute zoster-associated pain.

Antiviral Therapy for Uncomplicated Herpes Zoster
The goals of antiviral therapy in herpes zoster are to decrease pain, inhibit viral replication and shedding, promote healing of skin lesions, and prevent or reduce the severity of postherpetic neuralgia. Three antiviral agents, acyclovir, valacyclovir, and famciclovir, have been approved for treatment of herpes zoster in the United States. The mechanism of action for all of these agents is the prevention of varicella-zoster virus (VZV) replication through inhibition of the viral DNA polymerase.

Oral forms of all 3 agents have been shown in clinical trials to reduce viral shedding and accelerate resolution of symptoms, including pain, in uncomplicated herpes zoster. Some studies have suggested superiority of valacyclovir and famciclovir compared with acyclovir in terms of resolution of pain and acceleration of cutaneous healing. In addition, both valacyclovir and famciclovir have increased bioavailability over acyclovir and, as a result, require less frequent dosing.

The controlled studies of antiviral use in herpes zoster have only evaluated the efficacy of initiation of therapy within 48-72 hours of rash onset, and they have demonstrated no loss of effectiveness when medications are started at any point during that period. Several observational studies have shown antiviral therapy capable of reducing zoster pain, even when started beyond the traditional 72-hour therapeutic window. Thus, antiviral therapy should be considered for acute zoster treatment regimens, regardless of the time of presentation.

The duration of antiviral treatment in studies has varied from 7-21 days. Based on current literature, for immunocompetent patients, acyclovir for 7-10 days or a 7-day course of the newer agents is appropriate. Longer courses may be needed in immunocompromised patients.

        

[sushantpatel_doc]

images

        

[Anonymous]

Treatment of Complicated Herpes Zoster
Individuals with altered cell-mediated immunity, due to an immunosuppressive condition (eg, HIV, cancer) or treatment (eg, extended corticosteroid use), are at increased risk for herpes zoster. Further, herpes zoster presentations in the immunocompromised population can be complicated by disseminated disease and visceral organ involvement.

Antiviral therapy has been demonstrated to halt progression and dissemination of acute herpes zoster in immunocompromised patients, even when initiated more than 72 hours after rash onset. As such, current expert opinion recommends the use of antiviral therapy in all immunocompromised zoster patients who present prior to full crusting of all lesions.

Intravenous acyclovir remains the drug of choice for selected populations of immunocompromised patients, as follows:

Patients with evidence of disseminated disease or visceral organ involvement
Patients with ophthalmic involvement
Patients with advanced HIV/AIDS with active opportunistic infections or prominent wasting
Transplant recipients soon after transplantation or when being treated for rejection
Patients without such risk factors can be treated with oral antivirals. Data on adjunctive therapy with corticosteroids are lacking, and this therapy is not currently recommended. Antiviral therapy should be continued until resolution of all lesions.

        

[Drsumitra]

Treatment of Chronic Herpes Zoster (Postherpetic Neuralgia)
Primary treatments for postherpetic neuralgia include neuroactive agents, such as tricyclic antidepressants; anticonvulsant agents, such as gabapentin and pregabalin; and narcotic and non-narcotic analgesics, both systemic, such as opioids, and topical, such as capsaicin. No standard treatment plans or protocols exist for treating the pain associated with postherpetic neuralgia. Consultation with pain specialists may be required.

Placebo-controlled trials of various antiviral agents in treating herpes zoster have shown clear reductions in the intensity and duration of acute zoster-associated pain among treated populations. However, whether the use of antivirals in acute zoster reduces the incidence or duration of postherpetic neuralgia is less clear. Meta-analyses and studies have given conflicting results, and the subject is still under debate in the literature. Treating established postherpetic neuralgia with antivirals has not been shown to be beneficial.

The use of oral or epidural corticosteroids in conjunction with antiviral therapy has been found to be beneficial in treating moderate-to-severe acute zoster, but to have no effect on the development or duration of postherpetic neuralgia.

Intrathecal administration of corticosteroids has also been attempted. A trial involving a series of 4 intrathecal injections of methylprednisolone and lidocaine in patients with established postherpetic neuralgia demonstrated a significant and persistent reduction in pain among corticosteroid-treated patients when compared with untreated patients or those treated with intrathecal lidocaine alone. However, as these results have not received independent confirmation, and there are significant safety concerns with administration of intrathecal steroids, this treatment modality is not recommended.

        

[Drsumitra]

Prevention of Herpes Zoster
Herpes zoster results from reactivation of a previous infection with varicella-zoster virus (VZV) due to altered cell-mediated immunity in the patient. As such, prevention of herpes zoster can be achieved by either avoiding initial infection, or, post infection, maintaining sufficient cell-mediated immunity against VZV to suppress reactivation of the virus. Currently, multiple vaccines are approved and used in the United States that address each of these pathways to prevention.

In regard to prevention of initial infection, multiple live, attenuated VZV vaccines, based on the Oka vaccine strain have been used for routine childhood immunization in the United States since 1995. This has led to a remarkable reduction in the incidence of primary varicella infection. Further, vaccinated children have demonstrated lower rates of herpes zoster than those infected with wild-type VZV. However, the effect of childhood vaccination on the incidence of herpes zoster in adult populations is still unclear.

Other methods of prevention of initial infection include contact and respiratory isolation of infected patients until full crusting of lesions is achieved, as well as post-exposure prophylaxis in select populations with varicella-zoster immune globulin (VZIG).

Another live, attenuated varicella-zoster vaccine (Zostavax) has been approved and used in the United States since 2006 for the prevention of herpes zoster and its complications in older adults. In a large, placebo-controlled trial, this vaccine demonstrated a reduction in the incidence of acute herpes zoster by more than 50% and a reduction in the incidence of postherpetic neuralgia by 67% in the treated population. The Advisory Committee on Immunization Practices (ACIP) has recommended that nonimmunocompromised, nonpregnant adults aged 60 years or older receive the vaccine, regardless of zoster history.

In March 2011, the Food and Drug Administration (FDA) lowered the approved age for use of Zostavax to 50-59 years. Zostavax was already approved for use in individuals aged 60 years or older. Annually, in the United States, shingles affects approximately 200,000 healthy people aged 50-59 years. Approval was based on a multicenter study, the Zostavax Efficacy and Safety Trial (ZEST). The trial was conducted in the United States and 4 other countries in 22,439 people aged 50-59 years. Participants were randomized in a 1:1 ratio to receive either Zostavax or placebo. Participants were monitored for at least 1 year to see if shingles developed. Compared with placebo, Zostavax significantly reduced the risk of developing zoster by approximately 70%.

        

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