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NCC0316_Encephalitis_Yogesh.inddEncephalitis
in adults Outcomes in critical care By Vincent M. Vacca, Jr.,
MSN, RN, CCRN, SCRN
Abstract: Encephalitis is defined as inflammation of brain tissue
leading to alterations in level of consciousness, cognition, and
behavior. Encephalitis can range from mild with full recovery to
fulminant leading to death in 4% to 30% of those affected.
Approximately one-half of encephalitis survivors have permanent
neurologic deficits and require long-term care. Keywords: bacteria,
cerebrospinal fluid, encephalitis, inflammation, virus
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Encephalitis is an inflammation of brain tissue that leads to
alterations in level of consciousness (LOC), cognition, and
behavior. It can also cause fever, headache, seizures, cranial
nerve disorders, and motor def- icits, including paralysis.
Encephalitis results from various identifiable etiologies,
including viruses, bacteria, fungi, parasites, and autoimmune
disorders; however, the specific cause remains undetermined in more
than 50% of cases.1-5
This article reviews the types, causes, presentation, diagnostics,
and treatment of encephalitis with a focus on nursing assessment in
the critical care setting.
A global health concern Encephalitis is a major public health
concern worldwide. From 1998 to 2010, an estimated 263,352
encephalitis-associated hospitalizations occurred in the United
States, and the annual incidence of encephalitis worldwide is
estimated to be 0.07 to 12.6 cases per 100,000 people.6-10
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Encephalitis in adults: Outcomes in critical care
Currently, over 20,000 encephalitis-associated hospitalizations
occur in the United States each year. However, this number is
likely to be signifi- cantly higher because of undiagnosed cases.
Encephalitis can range from mild (leading to full recovery) to
severe (resulting in permanent disabili- ty) to fulminant (leading
to death in 4% to 30% of individuals affected). Approximately
one-half of encephalitis survivors will have permanent neuro- logic
deficits and require long-term care, which is estimated to cost as
much as $3 million per patient over the rest of their lives. The
cost to provide care to all individuals in the United States with
enceph- alitis-associated hospitalizations in 2010 was
approximately $2 billion.6-10
Causes of encephalitis Encephalitis can occur from noninfectious,
infec- tious, or postinfectious causes (see Etiologies of infec-
tious and noninfectious encephalitis). The most com- mon causes of
encephalitis are from viral infections and autoimmune disorders
such as Hashimoto encephalopathy.11 Encephalitis can be
transmitted: • via airborne droplets from infected persons to
noninfected persons • person to person through oral contact • by
eating or drinking contaminated food or bever- ages (including
water) • via mosquito or tick bites or infected animal
bites.12
Regardless of cause, prompt diagnosis and initia- tion of
appropriate treatments can improve patient outcomes.4,5,13
Clinical presentation Encephalitis is characterized by inflammation
of brain tissue and is almost always accompanied by
meningoencephalitis (see Defining terms). Presence of normal brain
function is the important distin- guishing feature between
encephalitis and meningitis.12 Patients with meningitis may be
uncomfortable, lethargic, or distracted by a head- ache, but they
retain normal neurologic func- tion.5,12 Encephalopathy may occur
with or with- out inflammation of brain tissue. Encephalopathy
without inflammation can be triggered by a number of metabolic or
toxic conditions such as acute toxic-metabolic
encephalopathy.12
Other signs and symptoms secondary to encepha- litis include
altered mental status, sensory deficits, behavior and personality
changes, and speech or movement disorders. Nuchal rigidity and
seizures may also be present. Motor and sensory effects associated
with encephalitis may include paresthe- sia and spastic or flaccid
paralysis. Patients may also exhibit signs and symptoms such as
oliguria, weight gain, hyponatremia, and hypo-osmolality. The
lasting effects of encephalitis can include sig- nificant
neurologic, motor, sensory, and cognitive deficits.4,5,12
Encephalitis can cause brain tissue edema, resulting in increased
intracranial pressure (ICP). Increased ICP can cause brain tissue
to shift with- in the skull, resulting in herniation. If severe,
her- niation can cause cardiopulmonary dysfunction, which can lead
to death. Other complications associated with encephalitis include
systemic
Etiologies of infectious and noninfectious
encephalitis2,3,5,20,23
Viruses Bacteria Fungi Protozoa Noninfectious
HSV Haemophilus Cryptococcus Plasmodium Allergic reactions infl
uenzae neoformans falciparum to vaccinations
WNV Neisseria meningitidis Cryptococcus gattii Acanthamoeba
Cancer
JEV Streptococcus Blastomycosis Naegleria Prior exposure pneumoniae
to JEV
EEE Mycobacterium Coccidioidomycosis Toxoplasma Chemical exposure
tuberculosis gondii including alcohol and
drugs
16 l Nursing2016CriticalCare l Volume 11, Number 2
www.nursingcriticalcare.com
Copyright © 2016 Wolters Kluwer Health, Inc. All rights
reserved.
disorders that can affect brain function, such as hypoglycemia,
fever, and fluid and electrolyte abnormalities. Systemic infections
must be consid- ered because they can also be associated with,
cause, or worsen encephalitis. An altered LOC can lead to impaired
airway protection reflexes that can result in aspiration pneumonia,
causing hypoxia. Seizures are common in patients with encephalitis,
and status epilepticus associated with encephalitis is present in
approximately 15% of patients.13 Mild encephalitis lasts for 7 to
10 days after which a gradual recovery is seen with or without
sequelae. Fulminate encephalitis can result in death in 2 to 4
days.2,4,5
Most common types of encephalitis Viral encephalitis. Many viruses
are transmitted to humans by arthropods, such as mosquitoes and
ticks, and are called arthropod-borne viruses, or arboviruses.
Arboviruses include Japanese enceph- alitis virus (JEV), West Nile
virus (WNV), Eastern equine encephalitis virus (EEEV), St. Louis
encephalitis virus (SLEV), chikungunya virus (CKNV), and others.2
Arbovirus infections such as WNV, EEEV, and SLEV are designated by
the Council of State and Territorial Epidemiologists and the CDC as
nationally notifiable infectious diseases.4,14
JEV is the leading cause of encephalitis, with an estimated 67,900
annual cases worldwide. The Advisory Committee on Immunization
Practices (ACIP) recommends JEV vaccination for all travel- ers who
plan to spend 1 month or more in JEV- endemic regions (Asia) during
the transmission sea- son (in temperate regions of China, Japan,
the Korean peninsula, and eastern parts of Russia, transmission
occurs mainly during the summer and fall; it may take place
year-round in southeast Asia).15 Since a JEV vaccine was licensed
in the United States in 1992, only eight cases of JEV have been
reported among U.S. travelers.16 The ACIP also recommends that the
JEV vaccine be consid- ered for short-term (less than 1 month)
travelers going to rural areas of affected regions whose itiner-
aries or activities place them at increased risk for JEV exposure.
ACIP also recommends vaccination for short-term travelers going to
areas with known outbreaks, and short-term travelers who are unsure
of their itineraries.2,17
Defi ning terms Encephalitis: inflammation of brain tissue that
leads to alterations in level of consciousness, cognition, and
behavior
Encephalopathy: a clinical state of altered mental status,
manifesting as confusion, disorientation, behavioral changes, or
other cognitive impairments
Meningitis: an inflammatory process limited to the meninges
Meningoencephalitis: inflammation of the brain tissue and adjacent
meninges
WNV continues to pose a significant disease bur- den in human
populations, with new emerging or reemerging strains. Between 1999
and 2013, more than 39,000 cases of clinical WNV were reported to
the CDC. In 2012, the CDC reported the highest number of human WNV
cases in the United States since 2003. The majority of individuals
present with signs and symptoms such as fatigue, fever, and
headache. They may also present with myalgia, muscle weakness,
rash, difficulty concentrating, neck pain, arthralgia,
gastrointestinal symptoms, photophobia, and maculopapular or
morbilliform rash involving the neck, trunk, arms, or legs.18
Approximately 75% of individuals infected with WNV remain
asymptomatic. Those who progress to WNV encephalitis present for
clinical care with a prolonged altered mental status greater than
24 hours, seizures, and/or focal neurologic abnormalities.4,5
Of the 5,674 cases of WNV reported to the CDC in 2012, 51% were
determined to be West Nile neu- roinvasive disease (WNND),
amounting to the high- est number of human neuroinvasive cases
caused by a mosquito-borne or arbovirus in U.S. history. Prior to
2012, WNND accounted for less than 1% of symptomatic cases per
year. WNND is character- ized by meningitis, encephalitis, and/or
acute flaccid paralysis, and occurs in 1 in 150 WNV-infected indi-
viduals. In 2012, 286 deaths occurred from WNV/ WNND, the most
WNV-associated fatalities on record in the United States. Among
patients who meet clinical criteria for WNND, acute case fatality
is 5% to 10%.13,18-21
Herpes simplex virus type 1 (HSV-1), varicella- zoster virus (VZV),
and enterovirus are three of the most commonly identified etiologic
agents
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Encephalitis in adults: Outcomes in critical care
associated with acute encephalitis. Herpes is the most common cause
of sporadic encephalitis in western countries, with an incidence of
approxi- mately two to four cases per million per year. Herpes
simplex virus encephalitis (HSE) is the most common nonepidemic
form of viral encepha- litis in Western countries.22 Affecting the
limbic structures of the brain, HSE causes fever, altera- tions in
LOC, personality change, memory dys- function, seizures, and focal
neurologic deficits. The most common focal neurologic findings
include aphasia, ataxia, involuntary movements including myoclonus,
and cranial nerve dysfunc- tion. However, HSV-1 can cause severe
necrotizing encephalitis with a high mortality approaching 70%
without treatment.19 Clinical presentation, brain imaging such as
magnetic resonance imaging (MRI) and cerebral spinal fluid (CSF)
analysis, are necessary for the diagnosis of HSE. Unilateral or
bilateral temporal lobe involvement is the classic finding of HSE
seen on MRI.1,23,24
Because HSV, VZV, and enterovirus are three of the most commonly
identified etiologic agents in acute encephalitis, they should be
routinely screened for in CSF analysis. If HSE is still suspect- ed
despite negative testing from the first CSF analysis, a second CSF
analysis should be repeated within 3 to 7 days.13
The prevalence of HSE is not increased in immu- nocompromised
hosts, but the presentation may be subacute or atypical in these
patients. HSE has a bimodal distribution by age, with the first
peak occurring in patients under age 20 and a second peak occurring
in patients over age 50. HSE in younger patients usually represents
primary infec- tion, whereas HSE in older patients typically
reflects reactivation of latent infection. Untreated HSE is
progressive and often fatal in 7 to 14 days. Even with treatment,
permanent neurologic deficits are com- mon, affecting more than 50%
of survivors.8,23,25
Bacterial encephalitis. Rates of bacterial encephali- tis in the
United States have declined in the last decade due in large part to
highly effective vaccina- tion programs. Because of vaccination,
the inci- dence of bacterial encephalitis fell from 0.44 cases per
100,000 between 1998 and 1999 to 0.19 cases between 2006 and
2007.22
Autoimmune encephalitis. Anti-N-methyl-d- aspartate receptor
(NMDAR) encephalitis is a severe
but treatable autoimmune disorder defined by the presence of
immunoglobulin G in serum and CSF. Anti-NMDAR syndrome is
characterized by a promi- nent change in behavior, memory deficits,
psychosis, autonomic dysfunction, seizures, abnormal move- ments,
and coma. Some patients, mainly young women, harbor an underlying
teratoma (germ cell tumors composed of multiple cell types derived
from one or more of the three germ layers), usually in the ovary.26
In others, the triggering factor for the NMDAR antibody production
is unknown. Prodromal symptoms such as headache, fever, diar- rhea,
or upper respiratory symptoms such as hypoventilation requiring
mechanical ventilation are frequently reported.17,27
In a large group of patients in whom both CSF and serum were tested
for NMDAR antibodies, approximately 15% had positive CSF antibodies
in the absence of serum antibodies. Thus, CSF testing by lumbar
puncture (LP) is recommended in patients with a compatible clinical
picture and neg- ative serum antibodies. Recent evidence has linked
the development of antibodies to NMDAR with pre- ceding or
concurrent HSE. These reports suggest that patients who experience
a neurologic decline following treatment for HSE should also be
tested for NMDAR antibodies.17,22,23
Diagnosing encephalitis A thorough health and travel history can
help iden- tify potential causes of encephalitis and should include
a review of all recent travel, infections, and vaccinations. The
history should also include any report of a recent bite from a
potentially rabid ani- mal or exposure to mosquitoes, ticks, or
rodents. In addition, the season in which illness occurs, and the
disease currently prevalent in the community, may provide clues to
the diagnosis. (See Encephalitis: Diagnostic criteria.)
Other relevant history that can provide clues to diagnosis include
drug and alcohol use, occupa- tional or recreational exposure to
rural or outdoor settings (farmers, hunters, campers, forest work-
ers), and the immune status of the patient. Although pathologic
examination and testing of brain tissue is considered to be the
diagnostic gold standard for encephalitis, it is rarely done due to
potential morbidity associated with an invasive neurosurgical
procedure. In the absence
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Copyright © 2016 Wolters Kluwer Health, Inc. All rights
reserved.
of pathologic brain tissue confirmation, encephali- tis is
diagnosed on the basis of selected clinical, lab,
electroencephalography (EEG), and neuroim- aging features.2 In
addition to brain imaging, CSF polymerase chain reaction (PCR)
analysis is con- sidered a standard diagnostic study for HSE. The
benefit of PCR is that replication of viral DNA can result in both
a rapid and specific diagnosis that can facilitate targeted
therapies early.3
An LP is the most common approach to access CSF for pressure
measurement and sample analy- sis. Prior to performing an LP,
evidence of a space- occupying brain lesion causing suspected or
known increased ICP should first be ruled out because removal of
CSF could precipitate cerebral bleeding or brain
herniation.28
Because the spinal cord terminates at the L-2 level, the spinal
needle used for an LP enters or punctures the L4-5 intervertebral
space to avoid damage to the spinal cord. The subarachnoid space of
the lumbar cistern is punctured and accessed. This location is used
to both measure spinal fluid opening and closing pressure, and to
remove CSF for analysis.29,30
The spinal fluid is normally clear and opening pressure is normally
10 to 20 cm H2O. Elevated opening pressure may contribute to the
neurologic dysfunction in encephalitis and must be managed as part
of the treatment plan.25
Acute management and goals of care The immediate goals of care are
to ensure patient safety along with rapid and accurate diagnosis
and appropriate treatment. Assessment and support of airway,
breathing, and circulation are an essential first step. The
inability to maintain a patent airway and evidence of hypoxemia
and/or hypercarbia may necessitate endotracheal intubation with
mechanical ventilatory support.6,7
Fever can increase cerebral metabolism, oxygen demand, and
accumulation of leukocytes, which also increases with temperature.
These changes in inflammatory processes could worsen neurologic
condition by disrupting the blood-brain barrier leading to brain
tissue edema. Inflammation also increases the viscosity of CSF,
which can interfere with absorption, leading to increased ICP,
cerebral edema, and hydrocephalus.5,13,31,32 Concerns for ICP
elevation and cerebral mass effect due to brain
Encephalitis: Diagnostic criteria3-5,33
Major diagnostic criteria (required):
Altered mental status ≥ 24 hours duration such as altered LOC,
lethargy, or personality change
Minor diagnostic criteria (2 required for possible; ≥ 3
required for probable or confi rmed)
• Fever ≥ 38.0° C (100.4° F) within 72 hours before or after
presentation
• Generalized or partial seizures not attributable to pre- existing
seizure disorder
• New onset of focal neurologic fi ndings • CSF leukocyte count ≥ 5
cells/microL • Abnormality of brain parenchyma on brain
imaging
suggestive of encephalitis that is either new or acute •
Abnormality on EEG consistent with encephalitis and
not attributable to another cause.
tissue edema from inflammation should prompt rapid bedside
assessment and immediate neurolog- ic imaging such as a noncontrast
head computed tomography (CT) scan. Rapidly evolving hydro-
cephalus, seen on CT scan, typically requires the placement of a
ventriculostomy for CSF drainage and ICP monitoring.13
Altered LOC associated with unilateral or bilateral pupillary
dilation and sluggish reaction or nonreactivity to light may
indicate a neurologic emergency such as transtentorial brain tissue
herniation from increased ICP.
A recent review addressed interventions designed to manage acute
brain tissue hernia- tion.13 Normal oxygenation (oxygen saturation
greater than 90%) and hyperventilation to a PaCO2 of 30 ± 2 mm Hg
(normal 35 to 45 mm Hg) and mean arterial pressure of at least 60
mm Hg are recommended. Hyperosmolar therapy with I.V. mannitol or
hypertonic saline may also be indicat- ed. When administering I.V.
mannitol, it is impor- tant to anticipate and correct subsequent
diuresis with 0.9% sodium chloride solution to avoid dehy-
dration.13 Head-of-bed elevation to greater than or equal to 30
degrees can be effective in reducing or controlling increased
ICP.5,33 Despite interven- tions, brain tissue edema, ICP
elevation, and herniation may progress. Initiation of a pharmaco-
logic-induced barbiturate coma with endotracheal intubation and
mechanical ventilation, if not
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Encephalitis in adults: Outcomes in critical care
already done, or a surgical hemi- craniectomy to relieve global
ICP, may be necessary.13
Encephalitis-associated seizure activity can worsen the patient’s
neurologic status and should be recognized and treated immedi-
ately. EEG monitoring is essen- tial, and continuous EEG (cEEG) is
recommended to improve diagnosis and to monitor the effect of
antiepileptic drugs (AEDs) in real time.13
For individuals with suspected or diagnosed seizures, first-line
benzodiazepine agents such as lorazepam or midazolam are
administered. Second-line AEDs, such as fosphenytoin, levetirace-
tam, or valproic acid, can be tailored to the specific clinical
situation.13
For patients who progress to medically refractory seizures, a
third-line AED with anesthetic properties, such as barbiturates
including pentobarbital or phenobarbital, or other agents such as
propofol or ketamine, may be necessary. Depending on individual
response to AEDs, it may be necessary to temporarily induce a
pharmacologic burst-suppression pattern on EEG using third-line
agents as therapeutic serum levels of second-line AEDs are reached.
Burst sup- pression, although not a specific treatment for
long-term control of medically refractory seizures, can be
beneficial to help recovery after brain inju- ries and to treat
epilepsy that is refractory to con- ventional drug therapies.34 On
cEEG, burst sup- pression is characterized by alternating patterns
of generalized electrical silence, seen as a flat EEG pattern,
which is interrupted by generalized bursts of chaotic electrical
activity seen as spikes and waves. The goal of burst suppression on
cEEG is from one to three bursts every 10 seconds.35
Aggressive seizure treatment and management requires ICU support
due to potential complica- tions from the seizure activity or the
medications administered to control seizures such as hypoten- sion,
loss of protective airway reflexes, and impaired respiratory
drive.13
Encephalitis is diagnosed on the basis of selected clinical, lab,
EEG, and neuroimaging
features.
Treating encephalitis At time of presentation, it is important to
consider empiric and broad-spectrum management for common
etiologies of encephalitis. Foremost consideration is for HSV and
the need to start I.V. antiviral medication (acyclovir) as early as
possible. A delay in I.V. acyclovir treatment in individuals with
sus- pected or known HSV-1 infection can result in increased risk
of severe permanent disability and death.13
Any suspicion of bacterial infection may necessitate broad- er
coverage with appropriate antibiotics and corticosteroids.13
In addition, results of the diag- nostic evaluation may prompt
administration of other appropri- ate antibacterial or antifungal
agents.
For individuals with an autoimmune etiology, appropriate strategies
for immune modulation are indicated. First-line immunotherapies for
acute immune-mediated encephalitis generally include
corticosteroids, I.V. immunoglobulin (IVIG), and plasmapheresis,
either alone or in combination. Response to these agents is
typically monitored over several weeks and, if suboptimal,
second-line treatments, including cyclophosphamide or ritux- imab,
are recommended.10
For anti-NMDAR encephalitis, identification and resection of the
offending teratoma is necessary for achieving control of brain
tissue inflammation. 13
Empiric immunosuppressive therapy may be con- sidered in patients
with encephalitis of unknown etiology. Clinical and/or radiologic
deterioration in these patients should prompt consideration of a
brain biopsy.10,12,13,17
Nursing considerations Encephalitis and its many potential
complications require comprehensive nursing assessment and care.
Evaluation of neurologic status using a stan- dardized assessment
scale, such as the Glasgow Coma Scale, can provide a baseline to
rapidly identify changes. Assess for signs and symptoms
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of increasing ICP such as decreased LOC, dilated pupils, widening
pulse pressure, or respiratory pattern irregularity. Prepare
patients for diagnostic procedures including LP and neuroimaging
studies such as a CT scan, MRI, or neurosurgery.
Notify the healthcare provider of any signs of dete- rioration in
clinical status such as fever, mental status changes, seizure
activity, or altered respirations. Ensure airway patency and
adequate gas exchange. Avoid dehydration and fluid volume overload
by assessment of daily weights, intake and output, and central
venous pressure measurements, if indicated. Maintain normothermia
and manage fever with tem- perature management interventions
including anti- pyretics, an external cooling device, or chilled
I.V. solutions.
Assess for pain using a standardized pain assess- ment scale
appropriate for the patient’s clinical sta- tus. Use a combination
of pharmacologic and non- pharmacologic interventions to control
pain to a level that is acceptable to the patient. Avoid or limit
the use of analgesic or sedative agents that may mask neurologic
changes. Darken the room if the patient is experiencing
photophobia. Assist with positioning to promote comfort and relief
for neck stiffness or pain. Maintain the patient’s head and neck in
neutral alignment.
Promote patient safety to decrease the risk of harm or injury.
Offer reassurance, redirection, and reorientation. Modify the
patient’s surroundings for safety and therapeutic benefit.
Promote nutrition management by assisting with and providing a
balanced dietary intake of foods and fluids. Assess the patient’s
swallowing ability and consider enteral feedings, if indicat- ed,
due to dysphagia and aspiration risk. Encourage active or perform
passive range-of- motion exercises and promote early and ongoing
mobility progression.
Utilize a standard assessment scale to identify and manage the
patient’s risk of pressure ulcers. Maintain skin and mucous
membrane integrity. Minimize pressure to body parts through
protective body and device positioning.
Provide patient and family education about encephalitis as
appropriate. Enforce transmission- based precautions as directed by
infection control experts as well as strict hand hygiene for all
staff and visitors. Report cases of encephalitis to the
department of public health and the CDC as indicated.4-7
Conclusion Encephalitis remains an important public health issue.
Although knowledge of encephalitis has increased substantially,
mortality has changed lit- tle across the past two decades.
Outcomes of encephalitis vary according to the etiology, timeli-
ness of diagnosis, and comorbidities. Viral causes account for the
majority of cases in which an etiol- ogy is identified, with a
substantial proportion of cases being associated with other
specified, pre- dominantly autoimmune, causes. Despite advances in
technology and pharmacology, encephalitis remains challenging to
diagnose and difficult to treat. The main indicators of poor
outcomes asso- ciated with encephalitis include advanced age (age
65 and older) or immunocompromised state (such as from medications,
coma, and ICU admission), especially if the patient requires
mechanical venti- lation. A specific etiologic agent or process is
iden- tified in approximately 50% of encephalitis cases, which
points to the need for further research. The mortality of
encephalitis is relatively low and near- ly two-thirds of patients
achieve a good outcome upon post- hospitalization follow-up.
Therefore, aggressive treatment should be pursued even in patients
with severe presentation and poor prog- nostic indicators because
of the possibility of favorable recovery.1,4,36
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Vincent M. Vacca, Jr., is a clinical nurse educator, Neuroscience
Intensive Care Unit, Brigham & Women’s Hospital, Boston, Mass.
He is also a member of the Editorial Advisory Board of Nursing2016
Critical Care.
The author has disclosed that he has no financial relationships
related to this article.
DOI-10.1097/01.CCN.0000480745.92978.ea