HERPES SIMPLEX VIRUS ENCEPHALITIS
Encephalitis is an acute inflammatory process of the brain tissue. Herpes simplex virus (HSV) is the most common cause of acute encephalitis in the United States (Levitz, 1998). There are two herpes simplex viruses, HSV-1 and HSV-2. HSV-1 typically affects children and adults.
There are two possible modes of HSV-1 infection. In most cases, primary HSV-1 infection of the buccal mucosa occurs, followed by retrograde spread along the trigeminal nerve to the brain. It is also believed that latent virus in brain tissue may reactivate and result in encephalitis (Roos, 1999). HSV-2 most commonly affects neonates and is discussed in pediatric textbooks (Gutierrez & Prober, 1998).
HSV-1 encephalitis causes inflammation and necrosis in the tem-poral lobe, frontal lobe, and limbic system. The initial symptoms include fever, headache, confusion, and behavioral abnormalities (Roos, 1999). Focal neurologic symptoms reflect the areas of cere-bral inflammation and necrosis and include behavioral change, focal seizures, dysphasia, hemiparesis, and altered level of con-sciousness. Focal symptoms are present within 7 days of infection and progress for 14 to 21 days.
Neuroimaging studies, electroencephalography (EEG), and CSF examination are used to diagnose HSV encephalitis. MRI is the neuroimaging study of choice in the diagnosis of HSV encephali-tis as it can help identify lesions in the temporal lobe.
The EEG demonstrates a specific wave pattern in 66% of cases of biopsy-proven HSV encephalitis. CSF reveals a high opening pressure and low glucose and high protein levels. Viral cultures are almost always negative. Since 1996, the polymerase chain reaction (PCR) technique has been used to diagnose HSV en-cephalitis (Roos, 1999). PCR will identify the DNA bands of the HSV specifically. The validity of PCR is very high between the third and tenth day of symptom onset.
Acyclovir (Zovirax), an antiviral agent, is the medication of choice in HSV treatment (Karch, 2002). The mode of action is the inhibition of viral DNA replication. It is usually well toler-ated by the patient. To prevent relapse, treatment should con-tinue for up to 3 weeks. Slow administration over 1 hour will prevent crystallization of the medication in the urine. The usual dose of acyclovir is decreased if the patient has a history of renal insufficiency (Karch, 2002). In the rare case of acyclovir resis-tance, foscarnet sodium (Foscavir) is prescribed (Roos, 1999).
Assessment of neurologic function is key to monitoring the pro-gression of disease. Comfort measures to reduce headache include dimming the lights, limiting noise, and administering analgesic agents. Opioid analgesic medications may mask neurologic symptoms; therefore, they are used cautiously. Focal seizures and altered level of consciousness require care directed at injury pre-vention and safety. Nursing care addressing patient and family anxiety is ongoing throughout the illness. Monitoring of blood chemistry test results and urinary output will alert the nurse to the presence of renal complications related to acyclovir therapy.
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