c Is an inflammation of cerebral tissue typically accompanied by meningeal inflammation,

caused by an infection or other source.

c It can present as acute viral encephalitis, most frequently caused by herpes virus and most
commonly occurring in children.
c Cytomegalovirus (CMV) and toxoplasma are common causes in patients with acquired
immunodeficiency syndrome.
c It may also present as post-infectious encephalitis, which follows a viral or bacterial infection,
usually of the respiratory or GI tract.
c It may also present as an anthropod-borne infection such as West Nile Virus.
c 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.
c Complications include motor and sensory deficits, amnesia syndrome, syndrome of
inappropriate antidiuretic hormone (SIADH), coma, and death.




Assessment
. Fever, headache, nausea and vomiting, mental status changes.
2. Meningeal signs ± nuchal rigidity (stiff neck), photophobia.
3. Seizures, motor deficits, personality changes.
4. Signs of brain stem involvement, such as nystagmus, extraocular nerve palsies, hearing
loss, dysphagia, and respiratory dysfunction.
5. Patients with hypothalamic-pituitary involvement may develop diabetesinsipidus,
hypothermia, or SIADH.
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. Lumbar puncture evaluates cerebrospinal fluid (CSF) for increased cell count; polymerase
chain reaction analysis of CSF for viral antibodies.
2. Electroencephalogram may reveal abnormalities.
3. Gadolinium-enhanced magnetic resonance imaging can detect different patterns of
inflammation to differentiate type of encephalitis.
4. Blood cultures rarely identify causative organism, but brain-tissue biopsy may indicate
presence of microorganism.
5. West Nile virus serologic testing on blood or CSF.
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. Antiviral agent acyclovir given I.V. for  days to 3 weeks for herpes simplex virus.
2. Blood cultures and foscarnet I.V. for CMV encephalitis.
3. Anticonvulsants to treat seizures, corticosteroids to reduce cerebral edema, and sedatives
and analgesics as supportive therapy.
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. Monitoring pupils and vital signs frequently for increased intracranial pressure (ICP; irregular
pupils, widening pulse pressure, tachycardia, irregular breathing hyperthermia).
2. Monitor the patient¶s response to medications and observe for adverse reactions.
3. Monitor neurologic status closely. Watch for subtle changes, such as behavior or personality
changes, weakness, or cranial nerve involvement.
4. Monitor fluid intake and output to ensure adequate hydration.
5. Maintain quiet environment and provide care gently, to avoid excessive stimulation and
agitation, which may cause increase ICP.
6. Maintain seizure precautions; pad side rails of bed and have airway and suction equipment
available at bedside.
7. Maintain standard precautions and additional isolation according to hospital policy to prevent
transmission.
8. Administer antipyretics and other cooling measures as indicated.
9. Provide fluid replacement through I.V. lines as needed.
 . Reorient patient frequently.
. Provide supportive care if coma develops; may last several weeks.
2. Encourage significant others to interact with patient with even while in coma and to
participate in care to promote rehabilitation.