Herpes zoster
Herpes zoster: Excerpt from Professional Guide to Diseases (Eighth Edition)
Herpes zoster (also called shingles) is an acute unilateral and segmental inflammation of the dorsal root ganglia caused by infection with the herpesvirus varicella-zoster, which also causes chickenpox. This infection usually occurs in adults. It produces localized vesicular skin lesions, confined to a dermatome, and severe neuralgic pain in peripheral areas innervated by the nerves arising in the inflamed root ganglia.
The prognosis is good unless the infection spreads to the brain. Eventually, most patients recover completely, except for possible scarring and, in corneal damage, visual impairment. Occasionally, neuralgia may persist for months or years.
Causes and incidence
Herpes zoster results from reactivation of varicella virus that has lain dormant in the cerebral ganglia (extramedullary ganglia of the cranial nerves) or the ganglia of posterior nerve roots since a previous episode of chickenpox. Exactly how or why this reactivation occurs isn’t clear. Some believe that the virus multiplies as it's reactivated and that antibodies remaining from the initial infection neutralize it. However, if effective antibodies aren't present, the virus continues to multiply in the ganglia, destroy the host neuron, and spread down the sensory nerves to the skin.
Herpes zoster occurs primarily in adults, especially those older than age 50. It seldom recurs. It's also seen in patients with human immunodeficiency virus and other immunodeficiency disorders.
Signs and symptoms
Herpes zoster begins with fever and malaise. Within 2 to 4 days, severe deep pain, pruritus, and paresthesia or hyperesthesia develop, usually on the trunk and occasionally on the arms and legs in a dermatomal distribution. Pain may be continuous or intermittent and usually lasts from 1 to 4 weeks. Up to 2 weeks after the first symptoms, small red nodular skin lesions erupt on the painful areas. (These lesions typically spread unilaterally around the thorax or vertically over the arms or legs.) Sometimes nodules don't appear at all, but when they do, they quickly become vesicles filled with clear fluid or pus. About 10 days after they appear, the vesicles dry and form scabs. (See Recognizing shingles.) When ruptured, such lesions usually become infected and, in severe cases, may lead to the enlargement of regional lymph nodes; they may even become gangrenous. Intense pain may occur before the rash appears and after the scabs form.
Occasionally, herpes zoster involves the cranial nerves, especially the trigeminal and geniculate ganglia or the oculomotor nerve. Geniculate zoster may cause vesicle formation in the external auditory canal, ipsilateral facial palsy, hearing loss, dizziness, and loss of taste. Trigeminal ganglion involvement causes eye pain and, possibly, corneal and scleral damage and impaired vision. Rarely, oculomotor involvement causes conjunctivitis, extraocular weakness, ptosis, and paralytic mydriasis.
In rare cases, herpes zoster leads to generalized central nervous system infection, muscle atrophy, motor paralysis (usually transient), acute transverse myelitis, and ascending myelitis. More commonly, generalized infection causes acute urine retention and unilateral diaphragm paralysis. In postherpetic neuralgia, most common in elderly persons, intractable neurologic pain may persist for years. Scars may be permanent.
Patients with immunodeficiency disorders may develop disseminated zoster. Lesions are bilateral and not limited to dermatomal distribution.
Diagnosis
Diagnosis of herpes zoster usually isn’t possible until the characteristic skin lesions develop. Before then, the pain may mimic that of appendicitis, pleurisy, or other conditions. Individuals who are susceptible to varicella may develop a varicella infection following exposure to patients with zoster. Examination of vesicular fluid and infected tissue shows eosinophilic intranuclear inclusions and varicella virus. Also, a lumbar puncture shows increased pressure; examination of cerebrospinal fluid shows increased protein levels and, possibly, pleocytosis. Differentiation of herpes zoster from localized herpes simplex requires staining antibodies from vesicular fluid and identification under fluorescent light.
Treatment
Antiviral therapy is the mainstay of treatment. Acyclovir seems to stop the rash’s progression and prevent visceral complications. Capsaicin, transcutaneous electrical nerve stimulation, and low-dose amitriptyline are the current treatments of choice for postherpetic neuralgia. Topical antiviral ointment is helpful if started early in the disease process.
Herpes zoster can resolve spontaneously and may only require symptomatic treatment, the goal of which is to relieve itching and neuralgic pain with calamine lotion or another antipruritic; aspirin, possibly with codeine or another analgesic; and, occasionally, collodion or compound benzoin tincture applied to unbroken lesions.
If bacteria have infected ruptured vesicles, the treatment plan usually includes an appropriate systemic antibiotic.
Trigeminal zoster with corneal involvement calls for instillation of idoxuridine ointment or another antiviral agent. To help a patient cope with the intractable pain of postherpetic neuralgia, the physician may order systemic corticosteroids — such as cortisone or possibly corticotropin — to reduce inflammation (although their use is controversial). He also may prescribe tranquilizers, sedatives, or tricyclic antidepressants with phenothiazines. In some immunocompromised patients — both children and adults — acyclovir I.V. appears to prevent disseminated, life-threatening disease. High doses of interferon (an antiviral glycoprotein) have been used in patients with cancer when the herpetic lesions are limited to the dermatome.
Special considerations
Your care plan should emphasize keeping the patient comfortable, maintaining me-ticulous hygiene, and preventing further infection. During the acute phase, adequate rest and supportive care can promote proper healing of lesions.
❑If calamine lotion has been ordered, apply it liberally to the lesions. If lesions are severe and widespread, apply a wet dressing. Drying therapies, such as oxygen or air-loss bed, and Silvadene ointment, may also be used.
❑Instruct the patient to avoid scratching the lesions.
❑If vesicles rupture, apply a cold compress as ordered.
❑To decrease the pain of oral lesions, tell the patient to use a soft toothbrush, eat soft foods, and use a saline or bicarbonate mouthwash.
❑To minimize neuralgic pain, never withhold or delay administration of analgesics. Give them exactly on schedule because the pain of herpes zoster can be severe. In postherpetic neuralgia, consult a pain specialist to maximize pain relief without risking tolerance to the analgesic.
❑Repeatedly reassure the patient that herpetic pain will eventually subside. Encourage diversionary or relaxation activity.
❑Institute droplet and contact precautions. Disseminated zoster requires the same isolation precautions as primary varicella.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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