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Encephalitis

It is an acute inflammation of the brain.

Encephalitis with meningitis is known as


meningoencephalitis.
Types of Encephalitis
• Herpes Simplex Virus Encephalitis

• Arthropod-Borne Virus Encephalitis

• Fungal Encephalitis
Clinical Manifestations
• Fever
• Headache
• Stiff neck
• Vomiting
• Drowsiness
• Dysphasia
• Focal Seizure
• Hemiparesis
• Altered LOC
• Personality Changes
• Maculopapular Rash
• SIADH with hyponatremia
• Increased ICP
Pathophysiology
Nsg Diagnosis:
• Acute Pain may be related to
inflammation/irritation of the brain and
cerebral edema, possibly evidenced by
verbal reports of headache, distraction
behaviors, restlessness, and autonomic
response (changes in vital signs).
Nsg Interventions:
• INDEPENDENT:
• Anticipate need for pain relief.
• * Respond immediately to complaint of pain. In
the midst of painful experiences a patient’s
perception of time may become distorted.
* Eliminate additional stressors or sources of
discomfort whenever possible.

• * Provide rest periods to facilitate comfort,


sleep, and relaxation.
o Imagery The use of a mental picture or an imagined
event involves use of the five senses to distract
oneself from painful stimuli.
o Distraction techniques Heighten one’s concentration
upon nonpainful stimuli to decrease one’s awareness
and experience of pain.

o Relaxation exercises Techniques are used to bring


about a state of physical and mental awareness and
tranquility. The goal of these techniques is to reduce
tension, subsequently reducing pain.

o Biofeedback, breathing exercises, music therapy


Dependent:
• Give analgesics as ordered, evaluating
effectiveness and observing for any signs and
symptoms of untoward effects. Pain
medications are absorbed and metabolized
differently by patients, so their
effectiveness must be evaluated from patient
to patient. Analgesics may cause side effects
that range from mild to life-threatening.
* Notify physician if interventions are
unsuccessful or if current 
Nsg Diagnosis:
• Hyperthermia may be related to
increased metabolic rate, illness, and
dehydration, possibly evidenced by
increased body temperature,
flushed/warm skin, and increased pulse
and respiratory rates.
Nsg Interventions:
Nsg Diagnosis
• Risk for Trauma/Suffocation: risk
factors may include restlessness,
altered LOC, cognitive impairment;
generalized weakness
Nsg Interventions
• INDEPENDENT:
• 1. Explore with client the various stimuli that may precipitate seizure
activity.
• Rationale: Alcohol, various drugs, and other stimuli, such as loss of sleep,
flashing lights, and prolonged television viewing, may increase the potential
for seizure activity. Client may or may not have control over many
precipitating factors, but may benefit from becoming aware of risks.

• 2. Discuss seizure warning signs, if appropriate, and usual seizure pattern.


Teach SO to recognize warning signs and how to care for client during and
after seizure.
• Rationale: Can enable client or SO to protect individual from injury and to
recognize changes that require notification of physician and further
intervention. Knowing what to do when seizure occurs can prevent injury or
complications and decreases SO’s feelings of helplessness.

• 3. Keep padded side rails up with bed in lowest position, or place bed up
against wall, and add floor pad if rails are not available or appropriate.
• Rationale: Minimizes injury should frequent or generalized seizures occur
while client is in bed.
• 4. Maintain strict bedrest if prodromal signs or aura is
experienced. Explain necessity for these actions.
• Rationale: Client may feel restless, need to ambulate or even
defecate during aural phase, thereby inadvertently removing
self from safe environment and easy observation. Understanding
importance of providing for own safety needs may enhance client
cooperation.

• 5. Stay with client during and after seizure.


• Rationale: Promotes client safety and reduces sense of isolation
during event.

6. Turn head to side and suction airway as indicated. Insert soft


bite block per facility protocol, only if jaw relaxed.
• Rationale: Helps maintain airway and reduces risk of oral trauma
but should not be “forced” or inserted when teeth are clenched
because dental and soft-tissue damage may result. Note:
Current practice is mixed regarding the use of airways during
seizure activity.
• 7. Cradle head, place on soft area, or assist to floor if out of
bed. Do not attempt to restrain.
• Rationale: Gentle guiding of extremities reduces risk of physical
injury when client lacks voluntary muscle control. Note: If
attempt is made to restrain client during seizure, erratic
movements may increase, and client may injure self or others.

• 8. Perform neurological and vital sign checks after seizure: level


of consciousness, orientation, ability to comply with simple
commands, ability to speak, memory of incident, weakness or
motor deficits, blood pressure (BP), pulse, and respiratory rate.
• Rationale: Documents postictal state and time and completeness
of recovery to normal state. May identify additional safety
concerns to be addressed.

• 9. Reorient client following seizure activity.


• Rationale: Client may be confused, disoriented, and possibly
amnesic after the seizure and need help to regain control and
alleviate anxiety.
Nsg Management:
• 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.
Pharmacologic Management
• Antiviral medications, such as acyclovir (Zovirax) and
foscarnet (Foscavir) -- to treat herpes encephalitis
or other severe viral infections (however, no specific
antiviral drugs are available to fight encephalitis)
• Antibiotics -- if the infection is caused by certain
bacteria
• Anti-seizure medications (such as phenytoin) -- to
prevent seizures.
• Steroids (such as dexamethasone) -- to reduce brain
swelling (in rare cases)
• Sedatives -- to treat irritability or restlessness
• Acetaminophen -- for fever and headache
Diagnostic Tools
• MRI
• CT scan
• Culture of cerebrospinal fluid (CSF),
blood, or urine (however, this test is
rarely useful)
• Electroencephalogram
• Lumbar puncture and CSF examination
• Tests that detect antibodies to a virus
(serology tests)
• Test that detects tiny amounts of virus
DNA (polymerase chain reaction -- PCR)
New Trends
Tobacco Plant-Made
Therapeutic Thwarts West Nile
Virus
• Feb. 3, 2010 -The study examined antibodies against West Nile
virus derived from mammalian cell lines and compared their
effectiveness with those extracted from plants. The plants used
to produce the antibodies are a relative of common tobacco, a
member of the Solanceae family of plants, which produce
abundant leaves for harvesting material and are also prolific
seed producers. Seven days after the introduction of antibody
genes into plants, the leaves are harvested, homogenized and
purified to remove extraneous material.
• The strategy for gene insertion is to use the specific machinery
of the tobacco mosaic virus and potato virus X (PVX) to carry
the genes of interest into the plants, where they can be
expressed, yielding a human monoclonal antibody known as hu-
E16. The gene expression occurs in just a week's time, making
the production process highly efficient.
• The monoclonal antibody, once injected into the recipient, binds
to a particular surface protein of the virus. That binding site is
also the one used by the virus to attach itself to mammalian
host cells, and once it is occupied, the virus' cell-binding (and
infectious) capacity is neutralized.
• Cell-derived versions of this antibody have already demonstrated impressive
effectiveness, protecting mice from WNV-induced mortality even several days
after infection. Chen's research shows comparable effectiveness using tobacco-
plant derived monoclonal antibodies. Indeed, the results in the groups of mice
tested, were essentially indistinguishable. The therapeutic, Chen emphasizes, is
effective in very small dosages, (50-200 micrograms), and only one dose is
required to clear the virus from an infected individual's system.
• The effectiveness of the plant expression system is dependent in part on the
optimization of the antibody DNA sequence, which helps to ensure a high level of
expression in the plants. "The goal is to make more of the protein and for it to
persist longer before it is degraded, " said Chen. "Optimization helps." The
strategy permitted the group to set a record for the antibody yield produced by
the transgenic tobacco plants -- an increase from 500 micrograms of antibody
per gram of leaf tissue to 800 micrograms per leaf.
• Because the monoclonal antibody therapeutic binds to a conserved region of the
viral surface, it can be effective against a variety of West Nile virus stains and
potentially against other flaviviral strains. Here, another advantage of plant-
derived as opposed to animal-derived antibodies becomes important. If an
individual is exposed to a variant strain of virus differing in some particulars
from the antibody used to treat it, there is a chance in the case of the
mammalian cell-derived therapy to actually worsen the condition, through an
effect known as antibody dependent enhancement. The process has been studied
in some detail in dengue fever, a related flavivirus. Chen emphasizes that plant-
based antibodies lack the capacity to bind with a critical receptor implicated in
the antibody dependent enhancement effect, making them potentially safer for
use.
• The completion of this research relied on the efforts of a large,
interdisciplinary team, including lead author Huafang "Lily" Lai. Michael Diamond
of Washington University collaborated in studies with the mouse model. In
addition to Chen's ASU scientist colleagues, Thomas Keller, an undergraduate in
ASU's School of Life Sciences Undergraduate Research program appears as a
co-author of the PNAS paper, having carried out much of the critical protein
expression and characterization work. "This was a very remarkable achievement
for an undergraduate student," Chen points out. The research was supported by
grants from the National Institute of Allergy and Infectious Diseases, and
Keller's work was supported in part through the Howard Hughes Fellowship for
Undergraduate Research.
• While the group's focus has been on West Nile Virus, Chen believes the plant-
based antibody approach could provide highly effective, cost efficient
therapeutics for other diseases, including related flavivirus infections such as
dengue fever and Japanese encephalitis, if the successes in mice can be
replicated in humans.
• One challenge in treating a virus like West Nile, which targets the central
nervous system, is that current antibody therapeutics are unable to pursue the
virus into its sanctuaries in the human brain, due to the existence of the blood
brain barrier. If this obstacle can be overcome, it may be possible to produce
therapeutics capable of eradicating the infection even after 6 or 7 days, when a
significant amount of virus has colonized brain tissue.
• Toward this end, Chen is now working on bifunctional antibodies, capable of
binding with virus particles as well as attaching to receptors in the brain,
allowing the antibody to migrate past the blood brain threshold. If successful,
the technique may allow treatment of other, currently intractable infectious and
neurological diseases. "If we can find a way to deliver therapeutics of this sort
into the brain it will be really significant," said Chen.
Visualizing Brain Invasion by a
Fungus
• Apr. 27, 2010) — Infection with the fungus  Cryptococcus neoformans can cause
meningitis (inflammation of the membranes surrounding the brain) and
encephalitis (inflammation of the brain itself), conditions that are often lethal.
To elicit these effects, the fungus must somehow leave the blood stream and
enter the brain, but little is known about how it does this.
• A team of researchers, at the University of Calgary, Canada, has now used a
form of microscopy known as intravital microscopy, which enables researchers to
observe events in real-time in live animals, to visualize in mice the process of
brain invasion by Cryptococcus neoformans.
• A key observation of the team, led by Christopher Mody, was that  Cryptococcus
neoformans stops suddenly in mouse brain capillaries that are similar or smaller
in diameter than it is. Only after stopping abruptly was the fungus seen to cross
the wall of the blood vessel and enter the brain. Interestingly, the protein
urease was required for Cryptococcus neoformans to invade the brain, and
treatment with a urease inhibitor reduced brain infection. The authors
therefore suggest that therapeutics that inhibit urease might help prevent
meningitis and encephalitis caused by infection with  Cryptococcus neoformans.
• In an accompanying commentary, Arturo Casadevall, at Albert Einstein College of
Medicine, New York, suggests that such inhibitors might not be applicable in the
clinic, because most patients already have substantial brain infection when they
first seek medical help. However, he highlights that the study opens up numerous
new avenues of research that could be exploited in the clinic in the future.
Fin…

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