Herpes Zoster
An acute unilateral and segmental inflammation of the dorsal root ganglia, herpes zoster (shingles) produces localized vesicular skin lesions confined to a dermatome. The patient with shingles may have severe neuralgic pain in the areas bordering the inflamed nerve root ganglia. (See Tracing the path of herpes zoster, pages 402 and 403.)
The infection, found primarily in adults older than age 50, seldom recurs. The prognosis is good, and most patients recover completely unless the infection spreads to the brain. Herpes zoster is more severe in the immunocompromised patient but is seldom fatal.
Causes
The varicella–zoster virus, a herpesvirus, causes shingles. For unknown reasons and by an unidentified process, the disease erupts when the virus reactivates after dormancy in the cerebral ganglia (extramedullary ganglia of the cranial nerves) or the ganglia of posterior nerve roots. Although the process is unclear, the virus may multiply as it reactivates, and antibodies remaining from the initial infection may neutralize it. Without opposition from effective antibodies, the virus continues to multiply in the ganglia, destroys neurons, and spreads down the sensory nerves to the skin. Herpes zoster may be more prevalent in people who had chickenpox at a very young age.
Complications
Herpes zoster ophthalmicus may result in vision loss. Complications of generalized infection may involve acute urine retention and unilateral paralysis of the diaphragm. In postherpetic neuralgia (most common in elderly patients), intractable neurologic pain may persist for years, and scars may be permanent. In rare cases, herpes zoster may be complicated by generalized central nervous system (CNS) infection, muscle atrophy, motor paralysis (usually transient), acute transverse myelitis, and ascending myelitis.
Assessment
The typical patient reports no history of exposure to others with the varicella–zoster virus. He may complain of fever, malaise, pain that mimics appendicitis, pleurisy, musculoskeletal pain, or other conditions. In 2 to 4 days, he may report severe, deep pain; pruritus; and paresthesia or hyperesthesia (usually affecting the trunk and occasionally the arms and legs). Pain—described as intermittent, continuous, or debilitating—usually lasts from 1 to 4 weeks.
During examination of the patient within 2 weeks after his initial symptoms, you may observe small, red, nodular skin lesions spread unilaterally around the thorax or vertically over the arms or legs. Alternatively, instead of nodules, you may see vesicles filled with clear fluid or pus. About 10 days after they appear, these vesicles dry, forming scabs. The lesions are most vulnerable to infection after rupture; some even become gangrenous.
During palpation, you may detect enlarged regional lymph nodes.