05/09/2023, 08:25 Tratamento do herpes zoster - UpToDate

Treatment of herpes zoster

AUTOR: Mary A Albrecht, MD
EDITORES DE SEÇÃO: Martin S Hirsch, MD, Kenneth E Schmader, MD
EDITOR ADJUNTO: Jennifer Mitty, MD, MPH

Divulgações do Colaborador

Todos os tópicos são atualizados à medida que novas evidências são disponibilizadas e nosso processo de revisão por
pares é concluído.

Revisão da literatura atualizada até:  agosto de 2023.

Este tópico foi atualizado pela última vez:  24 de agosto de 2023.

INTRODUÇÃO

A infecção pelo vírus varicela-zoster (VZV) causa duas doenças. A infecção primária pelo
VZV resulta em varicela, também conhecida como varicela, caracterizada por lesões
vesiculares de base eritematosa em diferentes estágios de desenvolvimento na face,
tronco e extremidades. Durante a varicela, o VZV estabelece uma infecção latente nos
gânglios sensoriais. O herpes zoster, também conhecido como herpes zoster, resulta da
reativação desse VZV latente.

O herpes zoster é uma erupção vesicular unilateral e dolorosa, que ocorre no dermátomo,
inervado pelo gânglio no qual ocorre a reativação [ 1 ]. Embora o herpes zoster possa
ocorrer em qualquer idade, é mais comumente uma doença em adultos com mais de 50
anos de idade. Além disso, a gravidade e as complicações do herpes zoster são muito mais
comuns nesta faixa etária.

O tratamento do herpes zoster será revisto aqui. A epidemiologia, as manifestações

clínicas, o diagnóstico e a prevenção do herpes zoster são discutidos em outra parte. (Ver
"Epidemiologia, manifestações clínicas e diagnóstico de herpes zoster" e "Infecção pelo
vírus varicela-zoster na gravidez" e "Vacinação para a prevenção do herpes zoster (herpes
zoster)" e "Prevenção e controle do vírus varicela-zoster em hospitais" .)

Erupção dermatológica

A maioria dos pacientes com herpes zoster apresenta erupção cutânea vesicular
dermatomal e neurite aguda; a neurite aguda geralmente precede (“dor prodrômica”) a
erupção cutânea em um a três dias. A erupção geralmente é limitada a um dermátomo,
mas freqüentemente afeta dermátomos contíguos. Alguns pacientes também podem

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apresentar algumas vesículas dispersas localizadas a alguma distância do dermátomo

envolvido. (Consulte "Epidemiologia, manifestações clínicas e diagnóstico de herpes
zoster" .)

Terapia antiviral

Objetivos da terapia  —  O tratamento do herpes zoster não complicado inclui:

● Antiviral therapy to hasten healing of cutaneous lesions, decrease the duration and
severity of acute neuritis, and prevent new lesion formation [2,3]. (See 'Antiviral
therapy' above.)

● Analgesia for patients with moderate to severe acute neuritis. (See 'Management of
acute neuritis' below.)

Several lines of evidence suggest that antiviral therapy hastens resolution of cutaneous
lesions and the pain of herpes zoster [4-6]. Antiviral therapy likely decreases viral shedding
and may reduce the risk of transmission of varicella-zoster virus (VZV).

However, it is unclear if antiviral therapy prevents postherpetic neuralgia (PHN) because of

conflicting study results, which are due in part to different methodologies of pain
assessment, definitions of PHN, and length of follow-up [4-7]. The treatment of established
PHN is discussed elsewhere. (See "Postherpetic neuralgia", section on 'Treatment'.)

Indications — The indications for treatment depend upon duration of symptoms and the
presence or absence of comorbid conditions.

Patients who present within 72 hours of onset — We recommend antiviral therapy

for all patients with herpes zoster who present within 72 hours of clinical signs and
symptoms. Antiviral therapy should be initiated as soon as possible to maximize the
potential benefits of treatment. (See 'Regimen selection' below.)

The benefit of antiviral therapy appears to be greatest in patients older than 50 years of
age, in whom the pain of herpes zoster is generally greater and persists longer and in
whom complications of herpes zoster are more likely [4,8]. Although the efficacy of antiviral
therapy in immune-competent patients less than 50 years of age has not been as well
studied, the risk of adverse events secondary to antiviral therapy is very low. Efficacy has
been demonstrated in younger patients who are immune compromised.

More detailed information on the efficacy of antiviral therapy is found below. (See
'Approach for most patients' below and 'Immunocompromised patients' below.)

Selected patients who present after 72 hours — We suggest antiviral therapy in

certain patients with herpes zoster even if >72 hours have passed ( algorithm 1). This

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primarily includes persons who have, or are likely to have, an impaired immune response
to VZV infection. However, there is no benefit of antiviral therapy after all the lesions have
crusted, regardless of the patient's underlying condition.

These patients include:

● Immunocompromised persons – We administer antiviral therapy to

immunocompromised patients who present after 72 hours of symptoms, particularly
those at risk for disseminated disease. This includes hematopoietic cell transplant or
solid organ transplant recipients, persons with hematologic malignancies, those with
solid tumor malignancies receiving chemotherapy, persons with advanced HIV
infection (eg. CD4 count <200 cells/microL, especially those not receiving
antiretroviral therapy), persons receiving high-dose glucocorticoids (eg, >20 mg/day
of prednisone for more than two weeks) or immunomodulatory therapy (eg,
rituximab or TNF inhibitors) [9,10].

● Pregnant persons – We treat pregnant women with herpes zoster to hasten healing
of cutaneous lesions and reduce the severity and duration of pain. However, there is
no evidence to suggest that herpes zoster is more severe during pregnancy or that
the fetus is at risk.

● Selected immunocompetent persons – We treat certain immunocompetent

persons, even if they present after 72 hours. This includes patients who have
advanced age (eg, >65), those who are frail, and/or those who are forming new crops
of lesions after 72 hours. These groups of patients likely have decreased immunity to
VZV [11]. Although the utility of initiating antiviral therapy more than 72 hours after
the onset of lesions in such persons is unknown since clinical trials did not evaluate
the efficacy of treatment initiated beyond this time period [4], treatment may be of
some benefit.

Regimen selection

Approach for most patients

● Choice of agent – The nucleoside analogues acyclovir, valacyclovir, and famciclovir

are the preferred antivirals for treatment of herpes zoster. For most patients, oral
therapy is sufficient. Intravenous treatment is reserved for patients who have
complications of herpes zoster (eg, acute retinal necrosis, encephalitis) or severe
immune compromise. (See 'Complicated zoster' below and 'Immunocompromised
patients' below.)

Of the available agents, we generally prefer valacyclovir or famciclovir given their

superior bioavailability and the need for less frequent dosing compared with
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acyclovir, although small comparative trials do not support the efficacy of one over
the other [12-14], as described below. However, acyclovir is often preferred in persons
who are pregnant. (See 'Pregnancy' below.)

Brivudine is another effective antiviral against VZV that is not available in the United
States but is often used in other countries. It is a nucleoside analog that is mono-
phosphorylated by a unique VZV-specified enzyme and changed into the triphosphate
by cellular enzymes. Brivudine triphosphate is incorporated into VZV DNA and also is
a competitive inhibitor of VZV DNA synthesis. However, the primary metabolic
product of brivudine is bromovinyluracil, which inhibits enzymes degrading other
fluoropyrimidines (eg, 5 fluorouracil and other bone marrow-suppressing
chemotherapeutic drugs), and thus could be extremely toxic in certain clinical
situations when these agents are used.

● Dosing – The doses used for oral treatment of herpes zoster are:

• Valacyclovir: 1000 mg three times daily

• Famciclovir: 500 mg three times daily
• Acyclovir: 800 mg five times daily

The typical course of treatment is seven days. (See 'Expected response to treatment'
below.)

Acyclovir and its analogues are dependent upon renal function for clearance, and
dose adjustment is needed in moderate to severe renal insufficiency. Dosing
information can be found in the Lexicomp drug information topics within UpToDate.

The doses used to treat herpes zoster infection are higher than those typically
required for herpes simplex virus since VZV is less sensitive to nucleoside analogs.
However, these nucleoside analogs have well-established safety records at the
currently recommended doses. Adverse events are uncommon, but when present
typically include nausea, diarrhea, or headache. More detailed information about the
individual agents is found elsewhere. (See "Acyclovir: An overview" and "Valacyclovir:
An overview" and "Famciclovir: An overview".)

● Efficacy – Data supporting the efficacy of these agents for the treatment of herpes
zoster include:

• Oral acyclovir – Oral acyclovir was the first nucleoside analogue available for the
treatment of herpes simplex and herpes zoster. (See "Acyclovir: An overview".)

In a meta-analysis of four placebo-controlled trials involving 691 patients (mean

age 62 years), those who received acyclovir (800 mg five times daily) administered

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within 48 to 72 hours of the onset of rash were more likely to have resolution of
moderate/severe acute neuritis (hazard ratio [HR] 1.46; 95% CI 1.1-1.93) and PHN,
defined as the presence of pain at three and six months after resolution of the
rash (HR 1.8; 95% CI 1.35-2.43) [4]. In a subsequent meta-analysis, which included
one additional placebo-controlled trial, antiviral therapy decreased the risk of PHN
(as defined by any pain at six months) by 46 percent [5].

• Valacyclovir – The limited bioavailability of acyclovir necessitated frequent daily

dosing (800 mg five times daily), prompting the development of a prodrug with
improved absorption (valacyclovir). Valacyclovir is well absorbed from the
gastrointestinal tract and rapidly converted to acyclovir in vivo, thereby providing a
three- to fivefold increase in acyclovir bioavailability. This results in improved
pharmacokinetics and less frequent dosing. (See "Valacyclovir: An overview" and
"Valacyclovir: An overview", section on 'Basic pharmacokinetics'.)

A randomized, double-blind trial compared valacyclovir (1000 mg orally three

times daily for 7 or 14 days) with acyclovir (800 mg orally five times daily for seven
days) for treatment of herpes zoster in 1141 immunocompetent adults (mean age
68 years) [15]. Cutaneous lesions resolved at similar rates in all treatment groups;
however, valacyclovir for 7 or 14 days accelerated the resolution of acute neuritis
compared with acyclovir (median duration of pain 38 and 44 days for the 7 and 14
day course of valacyclovir, respectively, compared with 51 days for acyclovir).

• Famciclovir – Famciclovir, the prodrug of penciclovir, is well absorbed from the

gastrointestinal tract and rapidly converted in the intestinal wall and liver to
penciclovir, which has good activity against VZV [8,16]. (See "Famciclovir: An
overview", section on 'Mechanism of action'.)

A placebo-controlled clinical trial was conducted in 419 immunocompetent adults

(mean age 50 years) with uncomplicated zoster to evaluate the efficacy of
standard-dose and high-dose famciclovir (500 or 750 mg three times daily) with
placebo [8]. All patients initiated therapy within 72 hours of rash onset and were
treated for seven days. Famciclovir was associated with a modest improvement in
lesion-healing rates compared with placebo (median five to six versus seven days).
While there was no difference in the incidence of PHN among the three treatment
arms, the use of famciclovir therapy, regardless of dose, conferred a selective
reduction in the median duration of PHN compared with placebo (62 and 55 days
with low- and high-dose famciclovir, respectively versus 119 days).

Pregnancy — We prefer oral acyclovir (800 mg five times daily) rather than other
antiviral agents during pregnancy since there is the most experience with this medication
in pregnancy. Although there are no clinical trials evaluating specific antiviral agents in
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pregnant women with herpes zoster, experience with acyclovir in both herpes simplex
infection and varicella pneumonia, which is supported by a large registry of acyclovir
exposure during pregnancy, suggests that this drug is safe in pregnancy. (See "Acyclovir:
An overview", section on 'Use in pregnancy' and "Varicella-zoster virus infection in
pregnancy" and "Genital herpes simplex virus infection and pregnancy", section on 'Drug
choice, dose, and safety'.)

Immunocompromised patients — Regimen selection in immunocompromised

patients depends upon the degree of immunocompromise and the subsequent risk of
dissemination.

● Patients at high risk for dissemination – Intravenous (IV) acyclovir (10 mg/kg every
eight hours) is used as initial therapy in patients who are at high risk for
dissemination [3]. This includes hematopoietic cell (HCT) or organ transplant
recipients with significant immunosuppression (eg, HCT recipients in the pre- or post-
transplant period, those with graft versus host disease, or cancer patients with
leukopenia). Clinical trials have found that IV acyclovir substantially reduces the risk
for cutaneous and visceral dissemination in highly immunocompromised patients
[17-21].

After initial clinical improvement, patients may be switched to an oral agent with
good bioavailability, such as valacyclovir or famciclovir. Patients should be treated
until all lesions have crusted (typically 10 to 14 days).

● Other immunocompromised patients – For other immunocompromised patients,

oral therapy with valacyclovir (1 g three times daily) can be used. In a randomized trial
of 87 immunocompromised patients with clinical evidence of localized herpes zoster,
patients who received this regimen had the same median time to full crusting of
lesions as those who received valacyclovir 2 g three times daily [22].

Expected response to treatment — The expected response to treatment is for new

vesicles to stop forming within five to seven days of therapy. (See 'Regimen selection'
above.)

If there is a delayed response to treatment, antiviral therapy treatment should be extended

until new vesicle formation has ceased. The patient should also be evaluated to ensure
there are no complications associated with herpes zoster (eg, secondary bacterial
infection). (See 'Secondary bacterial infection' below.)

Patients with a delayed response to treatment generally have decreased immunity to VZV
infection. Thus, when evaluating the patient, clinicians should assess for clinical
manifestations that would suggest underlying immune suppression. We do not routinely

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do additional work-up to search for immunocompromising conditions unless the initial

clinical evaluation is suggestive of a certain disease.

Adjunctive therapies — For patients with uncomplicated zoster, we suggest against the

routine use of adjunctive agents (eg, gabapentin, tricyclic antidepressants, or
glucocorticoids) in the acute setting. However, some of these agents may have a role in
select patients with acute neuritis, as discussed below. (See 'Management of acute neuritis'
below.)

There are no definitive data to suggest these adjunctive agents prevent PHN from
developing [23], and the risk of adverse events can be increased by adjunctive agents in
elderly patients. Although some early trials suggested glucocorticoids in addition to
acyclovir made people feel better sooner [24-28], a subsequent meta-analysis did not
demonstrate any benefit of combination therapy on quality of life or the incidence of PHN
[25]. In addition, their role in hastening the resolution of the rash is unclear.

Assessing and managing pain

Patient monitoring — After treatment for herpes zoster has been initiated, patients
should be assessed for improvement in their clinical symptoms, including worsening or
persisting pain. Serial patient monitoring should include standardized pain measures and
frequent follow-up to assess efficacy in relief of symptoms [3].

Approximately 10 to 15 percent of patients may develop PHN, defined as pain (defined as

severity of 3 out of 10) which interferes with daily activity that is present 90 days after the
onset of rash (or begins after this interval) in the distribution of the documented episode of
acute herpes zoster. This a more frequent problem in patients over the age of 60 years
[29].

Management of acute neuritis — Although antiviral therapy reduces pain associated

with acute neuritis, pain syndromes associated with herpes zoster can still be severe.
Management of acute neuritis must be individualized and requires the same principles as
managing any pain: use of standardized pain measures, scheduled analgesia, and
consistent and frequent monitoring to adjust dosing to the needs of the patient and to
avoid side effects.

● For patients with mild pain, nonsteroidal anti-inflammatory drugs and

acetaminophen can be useful agents to alleviate pain.

● For those with moderate to severe pain that disturbs sleep, management can be
more difficult, and additional agents may be needed. The choice of treatment is
based upon the patient's comorbidities, concurrent medications, pain intensity, and
preferences. Options include [30]:
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• The use of agents such as short-acting narcotics (see "Prescription of opioids for
acute pain in opioid naïve patients") or a 10- to 14-day tapering course of oral
prednisone (starting at 60 mg/day and administered in combination with antiviral
therapy).

• If short-acting narcotics or prednisone are unsuccessful, treatments that are used

for management of postherpetic neuralgia (eg, gabapentin or tricyclic
antidepressants) can be tried. (See "Postherpetic neuralgia".)

• If pain medications are used, they should be carefully titrated because of

associated side effects, especially in older patients. (See "Geriatric health
maintenance".)

● For patients with unrelenting pain, neural blockade with a long acting agent like
bupivacaine can also be considered [30,31].

Management of postherpetic neuralgia — PHN (pain which interferes with daily activity

that is present 90 days after the onset of rash in the distribution of the documented
episode of acute herpes zoster) can be difficult to treat, and some patients require
multimodal therapy for symptomatic management as well as referral to a pain
management center, if available. The approach to treatment of PHN should be
individualized according to severity and location of pain, comorbid conditions, medication
side effect profile, treatment cost and availability, and patient values and preferences. This
is discussed in detail in a separate topic review. (See "Postherpetic neuralgia".)

Additional considerations

Secondary bacterial infection — Although uncommon, secondary bacterial infections of

the zoster rash can occur. Patients should be counseled to contact their clinician if they
observe increased erythema, warmth, or purulence surrounding any lesions, which could
suggest secondary bacterial skin infection.

Should a bacterial infection be suspected at the time of the initial evaluation or during
follow-up visits, the patient should receive appropriate antibiotic coverage in addition to
antiviral therapy; regimens should include coverage for both staphylococcal and
streptococcal species. (See "Acute cellulitis and erysipelas in adults: Treatment".)

Treatment failure — On rare occasion, a patient may have persistence or progression of

lesions on treatment. There is no standard approach to managing treatment failure. In this
setting, the lesions should be cultured and the virus isolated should be sent for resistance
testing. If drug resistant virus is present, alternative agents can be used (eg, foscarnet).
Such patients should be managed in conjunction with an infectious diseases specialist.

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Recurrent zoster — Patients with recurrent zoster should be treated with antiviral

therapy using the recommended dose and duration for treatment of an initial episode of
herpes zoster. (See 'Antiviral therapy' above.)

Since episodes of recurrent zoster are uncommon, it is important that clinicians assess the
patient to determine the certainty of the diagnosis [32-34]. A common error is to mistake
recurrent herpes simplex for herpes zoster when the lesions are in the perioral or
perigenital area, including the buttock. If the diagnosis is uncertain, confirmatory testing is
warranted. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster",
section on 'Recurrent herpes zoster'.)

In addition, clinicians should assess patients with recurrent zoster for clinical features that
would suggest underlying immune suppression. However, we do not routinely do
additional work-up to search for immunocompromising conditions unless the initial clinical
evaluation is suggestive of a certain disease.

COMPLICATED ZOSTER

Certain patients with herpes zoster will have ocular, otic, or neurologic manifestations.
Such patients may require intravenous (IV) and/or prolonged therapy. In addition, there
may be a role for adjunctive glucocorticoids in certain conditions.

Disseminated infection — Disseminated zoster includes extensive cutaneous involvement

(>2 contiguous dermatomes or the presence of lesions at a distant site from the primary
dermatome) and/or visceral involvement. Disseminated zoster almost always occurs in
those who are immunocompromised. (See "Epidemiology, clinical manifestations, and
diagnosis of herpes zoster", section on 'Special considerations in immunocompromised
hosts'.)

In such patients, IV acyclovir (10 mg/kg every eight hours) should be initiated. When
lesions are improving the patient can be transitioned to oral treatment such as valacyclovir
(1 g three times daily). The duration of therapy is typically 10 to 14 days but may need to be
extended in those with ongoing symptoms. The use of IV therapy is based upon early data
that found IV acyclovir accelerates the rate of clearance of virus from vesicles, as compared
with no therapy or therapy with vidarabine [19,35]. Studies comparing oral therapy versus
IV acyclovir for disseminated disease have not been conducted.

Patients with disseminated infection are typically managed in the hospital setting. For such
persons, appropriate infection control precautions (eg, standard, droplet, and airborne)
should be implemented. (See "Prevention and control of varicella-zoster virus in hospitals",
section on 'Infection control measures'.)

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Ocular disease — Ocular manifestations of herpes zoster include herpes zoster

ophthalmicus (HZO) and acute retinal necrosis (ARN). (See "Epidemiology, clinical
manifestations, and diagnosis of herpes zoster", section on 'Herpes zoster ophthalmicus'
and "Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on
'Acute retinal necrosis'.)

Patients with these conditions should be managed in conjunction with an ophthalmologist.

Immediate treatment is required since they can be associated with loss of vision.
Treatment includes antiviral therapy, and in some cases, additional therapies may be
warranted (eg, corticosteroids for selected patients with HZO or intravitreal foscarnet for
ARN) [36,37].

Ramsay Hunt syndrome — The major otologic complication of varicella-zoster virus (VZV)

reactivation is the Ramsay Hunt syndrome, which typically includes the triad of ipsilateral
facial paralysis, ear pain, and vesicles in the auditory canal and/or auricle. (See
"Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on 'Ramsay
Hunt syndrome (herpes zoster oticus)'.)

● For most patients, we administer valacyclovir (1 g three times per day) for 7 to 10
days and prednisone (1 mg/kg for five days, without a taper).

● In severe cases (eg, vertigo, tinnitus, or hearing loss), IV therapy can be initiated, and
the patient can then be transitioned to an oral antiviral agent when the lesions begin
to crust.

There are few data to guide treatment decisions about management of this complication.
Although a systematic review found no evidence that antiviral agents have a beneficial
effect on outcomes in Ramsay Hunt syndrome [38], a subsequent retrospective review of
101 patients found that patients who received acyclovir and glucocorticoids recovered
significantly more than those who had only one or no pharmacologic treatment [39].

Neurologic complications — IV acyclovir (10 mg/kg IV every eight hours) should be

administered to patients with neurologic complications where viral replication likely plays
an important role (eg, symptomatic meningitis, encephalitis, and myelitis) [3]. Treatment is
generally administered for 10 to 14 days. This approach is supported by expert opinion. An
additional discussion of the neurologic manifestations of VZV is found elsewhere. (See
"Varicella zoster virus vasculopathy".)

PREVENTING TRANSMISSION TO OTHERS

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Patients with herpes zoster can transmit varicella-zoster virus (VZV) to individuals who have
not had varicella and have not received the varicella vaccine. VZV is transmitted by direct
contact or by aerosolization of virus from skin lesions. In general, VZV is much less
transmissible from a person presenting with herpes zoster than from a person presenting
with varicella (chickenpox). (See "Epidemiology, clinical manifestations, and diagnosis of
herpes zoster", section on 'Transmission'.)

Patients with localized zoster (ie, a dermatomal rash) are not infectious before vesicles
appear and are no longer infectious when the lesions have crusted. Patients should be
counseled about the risk of viral transmission to others [3]. In addition, until the rash has
fully crusted, patients should be advised to:

● Keep the rash covered to reduce the risk of spreading the virus to others.
● Avoid contact with individuals who have never had chickenpox or the varicella vaccine
[40].

More detailed discussions of how to prevent transmission of VZV are found elsewhere. (See
"Prevention and control of varicella-zoster virus in hospitals" and "Post-exposure
prophylaxis against varicella-zoster virus infection".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and

regions around the world are provided separately. (See "Society guideline links: Varicella-
zoster virus".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces
are longer, more sophisticated, and more detailed. These articles are written at the 10th to
12th grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

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● Basics topic (see "Patient education: Shingles (The Basics)")

● Beyond the Basics topic (see "Patient education: Shingles (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

● Dermatomal zoster – Reactivation of latent varicella-zoster virus (VZV) infection

within the sensory ganglia may result in herpes zoster or "shingles." Uncomplicated
herpes zoster typically presents with prodromal pain and a dermatomal vesicular rash
and acute neuritis.

• Whom to treat – For patients with uncomplicated herpes zoster who present
within 72 hours of clinical symptoms, we recommend antiviral therapy (Grade 1B).
Antiviral therapy promotes more rapid healing of skin lesions, lessens the severity
and duration of pain associated with acute neuritis, and potentially reduces the
incidence or severity of chronic pain (ie, postherpetic neuralgia). (See 'Patients who
present within 72 hours of onset' above.)

For selected patients who present after 72 hours, we also suggest antiviral therapy
(Grade 2C). This includes immunocompromised patients (particularly those at risk
for disseminated disease) as well as patients who have advanced age (eg, >65
years), those who are frail, and/or those who are forming new crops of lesions
after 72 hours ( algorithm 1). There is no benefit of antiviral therapy if all lesions
have already crusted. (See 'Selected patients who present after 72 hours' above.)

• Regimen selection – The nucleoside analogues acyclovir, valacyclovir, or

famciclovir can be used for treatment of acute herpes zoster. (See 'Regimen
selection' above.)

- For most patients we initiate oral therapy. We prefer valacyclovir (1000 mg

three times daily) or famciclovir (500 mg three times daily) because of their
lower dosing frequency compared with acyclovir (800 mg five times daily). The
duration of treatment is usually seven days. (See 'Approach for most patients'
above.)

- However, for immunocompromised patients at high risk for dissemination (eg,

hematopoietic stem cell or organ transplant recipients with significant
immunosuppression or cancer patients with leukopenia), we initiate
intravenous (IV) acyclovir (10 mg/kg every eight hours). After initial clinical
improvement, patients may be switched to an oral agent until all lesions have
crusted (typically 10 to 14 days). (See 'Immunocompromised patients' above.)

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• Considerations in pregnancy – We treat pregnant women with localized herpes

zoster to hasten healing of cutaneous lesions and reduce the severity and
duration of acute pain. Although there are no clinical trials examining the role of
antiviral therapy in pregnant woman with herpes zoster infection, extensive
experience with acyclovir suggests that this drug is safe in pregnancy. (See
'Pregnancy' above.)

• Role of adjunctive therapies - In patients with uncomplicated zoster, we suggest

against the routine use of adjunctive therapies, such as gabapentin, tricyclic
antidepressants, or glucocorticoids (Grade 2C). The clinical benefit of these agents
in reducing the risk of acute neuritis has not been clearly demonstrated and there
are significant risks associated with these medications. (See 'Adjunctive therapies'
above.)

• Management of acute or postherpetic neuralgia – Most patients with herpes

zoster experience acute neuritis. For patients with mild pain, nonsteroidal anti-
inflammatory drugs and acetaminophen can be useful. However, for those with
moderate to severe pain that disturbs sleep, additional agents may be needed.
(See 'Management of acute neuritis' above.)

Some patients will experience post herpetic neuralgia (PHN), which may interfere
with daily activity and is present 90 days after the onset of rash in the distribution
of the documented episode of acute herpes zoster. PHN may be difficult to treat
and require multimodal therapy. This is discussed in detail elsewhere. (See
"Postherpetic neuralgia".)

• Secondary bacterial infections – If a secondary bacterial infection occurs,

patients should receive an antibiotic regimen that includes coverage for both
staphylococcal and streptococcal species. (See 'Secondary bacterial infection'
above.)

● Management of complicated disease – Patients with herpes zoster can present with
disseminated infection and/or localized ocular, otic, or neurologic manifestations.
(See 'Complicated zoster' above.)

Some patients may require IV therapy. As an example, in patients with disseminated

infection, we suggest initial treatment with IV acyclovir rather than oral therapy
(Grade 2C). (See 'Disseminated infection' above.)

We also administer adjunctive therapies in certain settings. In patients with Ramsay

Hunt syndrome, we suggest adjunctive glucocorticoids in addition to antiviral therapy
(Grade 2C). (See 'Ramsay Hunt syndrome' above.)

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Patients with ocular disease (eg, herpes zoster opthalmicus, post herpetic neuralgia)
should be managed in conjunction with an ophthalmologist. Immediate treatment is
required since these conditions can be associated with loss of vision. (See 'Ocular
disease' above.)

● Preventing transmission to others – Patients with herpes zoster can transmit VZV to
individuals who have not had varicella and have not received the varicella vaccine.

To reduce the risk of transmitting VZV to others, patients should keep the rash
covered until all lesions have crusted.

They should also avoid contact with individuals who have never had chickenpox or
received the varicella vaccine. (See 'Preventing transmission to others' above.)

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