- Is an inflammation of cerebral tissue typically accompanied by meningeal inflammation, caused by an infection or other source.
- It can present as acute viral encephalitis, most frequently caused by herpes virus and most commonly occurring in children.
- Cytomegalovirus (CMV) and toxoplasma are common causes in patients with acquired immunodeficiency syndrome.
- It may also present as post-infectious encephalitis, which follows a viral or bacterial infection, usually of the respiratory or GI tract.
- It may also present as an anthropod-borne infection such as West Nile Virus.
- The disease, which is commonly fatal, causes lymphocytic infiltration of the brain, which leads to cerebral edema, basal ganglia degeneration, and diffuse nerve cell destruction.
- Complications include motor and sensory deficits, amnesia syndrome, syndrome of inappropriate antidiuretic hormone (SIADH), coma, and death.
- Fever, headache, nausea and vomiting, mental status changes.
- Meningeal signs – nuchal rigidity (stiff neck), photophobia.
- Seizures, motor deficits, personality changes.
- Signs of brain stem involvement, such as nystagmus, extraocular nerve palsies, hearing loss, dysphagia, and respiratory dysfunction.
- Patients with hypothalamic-pituitary involvement may develop diabetes insipidus, hypothermia, or SIADH.
- Lumbar puncture evaluates cerebrospinal fluid (CSF) for increased cell count; polymerase chain reaction analysis of CSF for viral antibodies.
- Electroencephalogram may reveal abnormalities.
- Gadolinium-enhanced magnetic resonance imaging can detect different patterns of inflammation to differentiate type of encephalitis.
- Blood cultures rarely identify causative organism, but brain-tissue biopsy may indicate presence of microorganism.
- West Nile virus serologic testing on blood or CSF.
- Antiviral agent acyclovir given I.V. for 10 days to 3 weeks for herpes simplex virus.
- Blood cultures and foscarnet I.V. for CMV encephalitis.
- Anticonvulsants to treat seizures, corticosteroids to reduce cerebral edema, and sedatives and analgesics as supportive therapy.
- Monitoring pupils and vital signs frequently for increased intracranial pressure (ICP; irregular pupils, widening pulse pressure, tachycardia, irregular breathing hyperthermia).
- Monitor the patient’s response to medications and observe for adverse reactions.
- Monitor neurologic status closely. Watch for subtle changes, such as behavior or personality changes, weakness, or cranial nerve involvement.
- Monitor fluid intake and output to ensure adequate hydration.
- Maintain quiet environment and provide care gently, to avoid excessive stimulation and agitation, which may cause increase ICP.
- Maintain seizure precautions; pad side rails of bed and have airway and suction equipment available at bedside.
- Maintain standard precautions and additional isolation according to hospital policy to prevent transmission.
- Administer antipyretics and other cooling measures as indicated.
- Provide fluid replacement through I.V. lines as needed.
- Reorient patient frequently.
- Provide supportive care if coma develops; may last several weeks.
- Encourage significant others to interact with patient with even while in coma and to participate in care to promote rehabilitation.