Encephalitis
A severe inflammation of the brain, encephalitis is usually caused by a mosquito-borne or, in some areas, a tick-borne virus. Viruses transmitted by arthropods are arboviruses (arthropod-borne). Transmission by means other than arthropod bites may occur through ingestion of infected goat’s milk and accidental injection or inhalation of the virus. Eastern equine encephalitis may produce permanent neurologic damage and is commonly fatal.
In encephalitis, intense lymphocytic infiltration of brain tissues and the leptomeninges causes cerebral edema, degeneration of the brain’s ganglion cells, and diffuse nerve cell destruction.
Causes
Encephalitis generally results from infection with arboviruses specific to rural areas. In urban areas, it’s most frequently caused by enteroviruses (coxsackievirus, poliovirus, and echovirus).
Other causes include herpesvirus, mumps virus, human immunodeficiency virus, adenoviruses, and demyelinating diseases after measles, varicella, rubella, or vaccination.
Between World War I and the Depression, a type of encephalitis known as lethargic encephalitis, von Econ-omo’s disease, or sleeping sickness occurred with some regularity. The causative virus was never clearly identified, and the disease is rare today. Even so, the term sleeping sickness persists and in many cases is mistakenly used to describe other types of encephalitis as well. The most recent outbreak of mosquito-borne encephalitis was West Nile encephalitis.
Signs and symptoms
All viral forms of encephalitis have similar clinical features, although certain differences do occur.
Usually, the acute illness begins with sudden onset of fever, headache, and vomiting and progresses to include signs and symptoms of meningeal irritation (stiff neck and back) and neuronal damage (drowsiness, coma, paralysis, seizures, ataxia, and organic psychoses). After the acute phase of the illness, coma may persist for days or weeks.
The severity of arbovirus encephalitis may range from subclinical to rapidly fatal necrotizing disease. Herpes encephalitis also produces signs and symptoms that vary from subclinical to acute and commonly fatal fulminating disease. Associated effects include disturbances of taste or smell.
Diagnosis
During an encephalitis epidemic, diagnosis is easily based on clinical findings and patient history. Sporadic cases are difficult to distinguish from other febrile illnesses, such as gastroenteritis and meningitis. When possible, identification of the virus in cerebrospinal fluid (CSF) or blood confirms the diagnosis.
The common viruses that also cause herpes, measles, and mumps are easier to identify than arboviruses. Arboviruses and herpesviruses can be isolated by inoculating young mice with specimens taken from patients. In herpes encephalitis, serologic studies may show rising titers of complement-fixing antibodies. Virus-specific indirect fluorescent antibody assays have improved diagnosis.
In all forms of encephalitis, CSF pressure is elevated, and despite inflammation, the fluid is clear in many cases. White blood cell and protein levels in CSF are slightly elevated, but the glucose level remains normal. An EEG reveals abnormalities. Occasionally, a computed tomography scan may be ordered to rule out cerebral hematoma.
Treatment
The antiviral agent acyclovir is effective only against herpes encephalitis. Treatment of all other forms of encephalitis is entirely supportive.
Drug therapy includes phenytoin or another anticonvulsant, usually given I.V.; glucocorticoids to reduce cerebral inflammation and edema; furosemide or mannitol to reduce cerebral swelling; sedatives for restlessness; and aspirin or acetaminophen to relieve headache and reduce fever.
Other supportive measures include adequate fluid and electrolyte intake to prevent dehydration and antibiotics for an associated infection such as pneumonia. Isolation is unnecessary.
Special considerations
During the acute phase of the illness:
❑ Assess neurologic function often. Observe the patient’s mental status and cognitive abilities by performing a rapid neurologic examination. (See Performing a rapid neurologic examination.) If the tissue within the brain becomes edematous, changes in the patient’s mental status and cognitive abilities will occur.
CLINICAL TIP: Assessment should focus on early changes in intracranial dynamics. Continued swelling may result in cranial nerve compression, causing changes in pupillary reaction to light, ptosis, eyelid droop, and an eye rotating outward.
❑ Monitor for signs of progression of a herniation pattern (abnormal posturing movements, such as decerebration, decortication, and flaccidity, to noxious stimuli).
❑ Watch for cranial nerve involvement (ptosis, strabismus, diplopia), abnormal sleep patterns, and behavioral changes.
❑ Maintain adequate fluid intake to prevent dehydration, but avoid fluid overload, which may increase cerebral edema. Measure and record intake and output accurately.
❑ Give acyclovir by slow I.V. infusion only. The patient must be well hydrated and the infusion given over 1 hour to avoid kidney damage. Watch for adverse effects, such as nausea, diarrhea, pruritus, and rash, and adverse effects of other drugs. Check the infusion site often to avoid infiltration and phlebitis.
❑ Carefully position the patient to prevent joint stiffness and neck pain, and turn him often. Assist with range-of-motion exercises.
❑ Maintain adequate nutrition. It may be necessary to give the patient small, frequent meals or to supplement these meals with nasogastric tube or parenteral feedings.
❑ To prevent constipation and minimize the risk of increased intracranial pressure from straining during defecation, give a mild laxative or stool softener.
❑ Provide good mouth care.
❑ Maintain a quiet environment. Darkening the room may decrease photophobia and headache. If the patient naps during the day and is restless at night, plan daytime activities to minimize napping and promote sleep at night.
❑ Provide emotional support and reassurance because the patient is apt to be frightened by the illness and frequent diagnostic tests.
❑ If the patient is delirious or confused, attempt to reorient him often. Providing a calendar or a clock in the patient’s room may be helpful.
❑ Reassure the patient and his family that behavioral changes caused by encephalitis usually disappear. If a neurologic deficit is severe and appears permanent, refer the patient to a rehabilitation program as soon as the acute phase has passed. Consultation with a speech, occupational, or physical therapist may be indicated.
❑ Review prevention strategies, such as adequate immunizations and protection against mosquito bites.
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Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright Details: Handbook of Diseases, Copyright © 2008 Williams & Wilkins.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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