Herpes zoster (shingles)

Herpes zoster or shingles is an acute selflimiting vesicular eruption occurring in a dermatomal (localised area of skin that has its sensation via a single nerve from a single nerve root) distribution. It is caused by a reactivation of VZV. It is not known what causes this but is more likely in the elderly, those who are under stress or immunosuppressed.

It always occurs in people who have previously had varicella (chickenpox). The virus lies dormant in the sensory root ganglion of the spinal cord and when reactivated, the virus replicates and travels down the nerve to the skin to induce the cutaneous lesions of shingles. Viraemia (the presence of virus in the bloodstream) is frequent and involvement may be disseminated (Gawkrodger, 2003). The thoracic dermatomes are involved in 50% of cases. Involvement of the ophthalmic division of the trigeminal nerve is particularly common in the elderly.

Presentation
Pain, tenderness and paraesthesia in the dermatome may precede the eruption by 3–5 days. These are followed by erythema and groups of vesicles scattered in the dermatomal area. The vesicles become pustular and then form crusts (Figure 12.4). Secondary infection can occur. These separate after 2–3 weeks and leave scarring. Herpes zoster is usually unilateral and can involve adjacent dermatomes. Local lymphadenopathy is common. Shingles recurs in about 5% of cases.

Complications
Serious complications can occur depending on which nerve is involved (Gawkrodger, 2003).

Opthalmic disease: If the first trigeminal division is affected, corneal ulcers and scarring can result.
Motor palsy: The viral involvement may spread from the posterior horn of the spinal cord to the anterior horn which results in a motor disorder. Cranial nerve palsy or paralysis of the diaphragm or other muscle groups can happen.
Disseminated herpes zoster: Immunosuppressed patients can develop confluent haemorrhagic involvement which spreads and can become necrotic or gangrenous.
Postherpetic neuralgia: The pain of shingles may go on long after the rash has disappeared. Neuralgia is rare in patients under 40 years of age but affects a third of those over the age of 60 years and usually subsides within 6 months but may go on for more than a year.

Management

1. The goals of treatment are to shorten the attack, reduce pain, deal with complications and prevent postherpetic neuralgia if possible and to treat pain should it occur (BAD, 2004).
2. In mild disease, treatment is symptomatic with rest and analgesia. Basic hygiene should be maintained (Docherty, 2001) and the principles of care for chickenpox applied.
3. Any secondary bacterial infection may make the neuralgia worse and should be treated with antibiotics.
4. Patients should stay away from young babies and the immunocompromised and may need to stay off work for 2–3 weeks (BAD, 2004).
5. More severe cases may be treated if seen within 72 hours of onset with aciclovir or famciclovir to reduce the length of the attack and reduce viral shedding. Immunosuppressed patients will need intravenous aciclovir.
6. Except in the immunosuppressed, oral prednisolone can reduce the incidence of postherpetic neuralgia. There is evidence to show that gabapentin which was originally developed to treat epilepsy, but is now widely used to relieve neuropathic pain, may be effective but ineffective in acute pain (Wiffen et al., 2005). In severe cases, referral to pain clinics may be needed.