Managing Herpes Zoster

Managing Herpes Zoster

A common problem in the elderly

by Dr Lee Haur Yueh

Herpes zoster, also commonly known as shingles, occurs secondarily to the reactivation of the varicella-zoster virus (VZV). The estimated lifetime incidence is 10% and there is a doubling of risk for every decade after age 50.

Clinical Features

Figure 1: Unilateral, grouped vesicles and blisters over an erythematous base in a dermatomal distribution

The prodrome of herpes zoster may be characterised by headache, photophobia or malaise. Localised abnormal pain and paraesthesia may precede the cutaneous lesions by one to five days. This pain may be intermittent or constant and is often accompanied by cutaneous hyperaesthesia. The cutaneous eruption is characterised by grouped vesicles over an erythematous base [Figure 1].

These lesions are unilateral and distributed in a dermatomal distribution. The most common dermatomes affected are the areas supplied by the trigeminal nerve and the trunk from T3 to L2. Over the next few days, the vesicles evolve into haemorrhagic vesicles/blisters or pustules before forming crusts. As the crusts fall, the patient is left with residual pigmentary changes or scarring. The entire course of disease may last between two to four weeks.

In immunocompetent individuals, the eruption is unilateral and does not cross the midline, although adjacent dermatomes are involved in about 20% of patients. In immunocompromised patients, disseminated forms of zoster may occur.

The most common complication of herpes zoster is post-herpetic neuralgia (PHN). This is typically defined as pain that persists for longer than one month after resolution of the rash. The incidence of PHN ranges from 8% to 70%. The characteristic of the pain may be lancinating or burning in nature, and may be triggered even by non-noxious stimuli such as clothing or slight pressure.

Other rarer complications include encephalitis, myelitis, cranial nerve/peripheral nerve palsies, pneumonitis or hepatitis. Mortality rate from herpes zoster with visceral dissemination is between 5% and 15%.


The clinical features of zoster are distinct enough for a clinical diagnosis to be made. Laboratory tests such as viral culture, VZV antigen detection by direct immunofluorescence or viral DNA by polymerase chain reaction (PCR) analysis can be performed to confirm the diagnosis, or may be indicated in atypical presentations (particularly in immunocompromised hosts).


Following an initial infection of varicella, the VZV passes from the skin lesions into the sensory ganglia via the sensory nerve endings. In the ganglia, the virus establishes a latent infection that persists for life, and reactivates when the host immune system is low.

Risk factors for reactivation include old age – more than 50% of all cases of zoster occur in patients who are older than 60 years old. Other factors include immunosuppressed individuals (e.g. HIV patients, organ or bone marrow transplant recipients), and use of cancer chemotherapy, corticosteroids or other immunosuppressants.

The exact cause of post-herpetic neuralgia is unclear. However, it is postulated that damages to the sensory nerve, dorsal ganglia and the dorsal horns of the spinal cord occur during viral reactivation.

Risk of Transmission

Patients with herpes zoster are less infective compared to varicella, and it has been estimated that the percentage of household contacts developing varicella after zoster exposure is about one-third compared to varicella. The disease is spread via direct contact, although in patients with disseminated zoster, there is a possibility of airborne transmission.


The aims of treatment include treatment of the acute viral infection, treatment of the acute pain associated with herpes zoster and the prevention of PHN.

Antiviral Agents

Table 1. First-line treatment for acute herpes zoster

Early treatment within the first 72 hours of vesicle formation is important for antiviral efficacy, time to lesion healing, and minimising zoster-associated pain. Antiviral agents include acyclovir, valacyclovir and famciclovir [Table 1].

Acyclovir, a DNA polymerase inhibitor, may be administered orally and intravenously. The usual oral dosage is 800mg, five times daily for one week. Intravenous acyclovir is given at a dose of 10mg/kg tds for one week. The main indications for intravenous treatment are immunocompromised individuals, those with disseminated disease or those who are unable to take medications orally.

Valacyclovir is the prodrug of acyclovir and is administered at a dose of 1,000mg tds for one week. It has a greater bioavailability and oral administration produces levels comparable to that of intravenous administration of acyclovir.

Famciclovir is given at a dose of 500mg tds for one week. It has longer intracellular half-life compared with acyclovir, and has better bioavailability compared with both acyclovir and valacyclovir.

All three antiviral agents have similar efficacy and are generally well tolerated. Most common adverse effects are headache, nausea, vomiting and gastric symptoms. Although valacyclovir and famciclovir have superior pharmacokinetic profiles and simpler dosing regimens compared to acyclovir, costs of the medications may be a consideration.


Corticosteroids have been given concurrently with antivirals. This combination has been shown to decrease pain and improve quality of life during the acute episode. However, the incidence or duration of PHN is not reduced. Common dosage ranges from 0.5mg/kg to 1.0mg/kg, which is tapered over two to three weeks. Corticosteroid therapy should not be used in patients at risk of corticosteroid-induced toxicity, and monotherapy with corticosteroids is not recommended.

Supportive Care

Saline or potassium permanganate soaks (two to three times a day) are effective in decreasing the inflammation and to promote drying of lesions. Sterile, non-occlusive, non-adherent dressing placed over the involved dermatome will protect the lesions from adhering to clothes or trauma. Topical or systemic antibiotics may be indicated in secondary bacterial infection. Analgesics should be given to control the acute pain.

Treatment of PHN

Table 2. Treatment for PHN

Opioids, tricyclic antidepressants, gabapentin and pregabalin [Table 2] have been shown to be effective in reducing the severity or duration of PHN, either as a single agent or in combination therapy. A recent study suggest that valacyclovir (1g tds x one week) in combination with gabapentin (300mg/day adjusted to 3,600mg/day over four to eight weeks) during the acute illness may reduce the chance of developing PHN.
Dr Lee Haur Yueh is an Associate Consultant at the Dermatology Unit, Singapore General Hospital. He completed his dermatology training in Singapore and has undergone further fellowship training in France, Switzerland and the United Kingdom. His clinical interests include medical dermatology, immunodermatology and drug allergies.


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