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8/12/2019 ENCEPHALITIS Presentation
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ENCEPHALITIS
-GUNASEELAN KUMAR
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DEFINITION
Acute central nervous system (CNS)
dysfunction with radiographic or laboratory
evidence of brain inflammation
CNS dysfunction includes seizures
focal neurologic findings
alteration in mental status.
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CAUSES
VIRUS Arboviruses
examples: Japanese encephalitis; West Nile encephalitis virus;Eastern,Western and Venzuelan equine encephalitis virus; tick
borne encephalitis virus Herpes viruses
Eg: HSV-1, HSV-2, varicellazoster virus, cytomegalovirus,Epstein-Barr virus
Adenoviruses
Influenza A Enteroviruses, poliovirus
Measles, mumps, and rubella viruses
Rabies
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CAUSE- VIRUS (JE)
Most important cause of arboviral encephalitisworldwide, with over 45,000 cases reportedannually
Transmitted by culex mosquito (breeds in ricefields)
Mosquitoes become infected by feeding ondomestic pigs and wild birds infected withJapanese encephalitis virus
Infected mosquitoes transmit virus to humans andanimals during the feeding process
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CAUSES
Bacteria H. influenza
S. pneumoniae
N. meningitidis
M. tuberculosis Mycoplasma pneumoniae
Others Rickettsia, Spirochete & Malaria
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TYPES
Two forms
Primary encephalitis
Post or parainfectious encephalitis
(secondary)
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TYPES-
PRIMARY ENCEPHALITIS
Primary encephalitis
Results from direct CNS invasion by the offending
agent
the gray matter often is targeted.
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TYPES-
PRIMARY ENCEPHALITIS
Organisms gain entry to the CNS directly
Eg. arboviruses initially cause bloodstream infection, thenenter the CNS via endothelial cell infectioncell transport,or carriage in cells enteringthe CNS. An alternativemechanism
Eg. herpes simplex virus (HSV), rabies, and possiblypoliovirus is retrograde transport in neurons (less immunesurveillance)
Eg. amoeba Naegleria fowleri is entry through the olfactorymucosa.
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TYPES-
PRIMARY ENCEPHALITIS
Variety of anatomic sites can be infected
HSVneurons in the temporal lobe
Rabiespons, medulla, cerebellum,
hippocampus Japanese encephalitis brainstem and basal
ganglia
Neurologic signs and symptoms develop afterinfection result of direct
neuronal injury,
the host inflammatory response (include
perivascular inflammation, gliosis, and brain
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TYPES-
SECONDARY ENCEPHALITIS
Post/parainfectious (secondary)
not caused by direct CNS infection
neurologic effects are the consequence of the
hosts immune response faulty immune systemreaction in response to an infection elsewhere in
the body)
often affects the white matter
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TYPES-
SECONDARY ENCEPHALITIS
occurs days to weeks after the onset of aninfection
pathogen is not detected in the CNS inpostinfectious encephalitis
hypothesized to be caused by an aberrantimmune response against brain antigens such asmyelin basic protein
Subsequent demyelination causes focal or globalCNS dysfunction
Postinfectious encephalitis often is called acutedisseminated encephalomyelitis (ADEM).
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CLINICAL MANIFESTATION
Initial Signs
Fever (usually high grade)
Headache
Malaise
Anorexia
Nausea and Vomiting
Abdominal pain
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CLINICAL MANIFESTATION
Developing Signs
Altered LOC
mild lethargy to deep coma
confused, delirious, disorientedMental aberrations :
Hallucinations
personality change
behavioral disorders ; occasionally frankpsychosis
Focal or general seizures in >50% severe cases.
Severe focused neurologic deficits
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CLINICAL MANIFESTATION
Neurologic Signs
Most Common
Aphasia
Ataxia
Hemiparesis with hyperactive tendon reflexes
Involuntary movements
Cranial nerve deficits (ocular palsies, facialweakness)
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DIAGNOSIS
PATIENT HISTORY
PHYSICAL EXAM
LABORATORY AND RADIOLOGICAL
INVESTIGATIONS
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DIAGNOSIS-
PATIENTS HISTORY
Recent travel and the geographical : Africa Cerebral malaria
Asia Japanese encephalitis
High risk regions of Europe and USA Lyme disease
Recent animal bites Tick borne encephalitisorRabies
Occupation Forest worker, exposed to mosquitoes Medical personnel, possible exposure
to infectiousdiseases
Farmers- pig farms (nipah virus), japanese encephalitis
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DIAGNOSIS
PHYSICAL EXAM
Focal neurological deficit HSV encephalitis
Hallucination or aphasia HSV encephalitis
Local paresthesia Rabies encephalitis
Brain stem signs, Unilateral peripheral motorweakness or Cerebellar sign Meliodosis
Eschar Scrub typhus
ParotitisMumps
Systemic sign eg. Rash Mycoplasma &Enterovirus
Regional adenopathiesherpangina, HFMD(enterovirus)
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DIAGNOSIS-
LABORATORY
FBC : usually within the reference range
Electrolytes :usually within reference range
Syndrome of inappropriate secretion of antidiuretic
hormone (SIADH) Serum glucose: Use this level as a baseline for
determining normal CSF glucose values
RP / LFT :Assess organ function and the need to
adjust the antibiotic dose Coagulation profile : if DIC is suspected
Urinary electrolyte test: if SIADH is suspected
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DIAGNOSIS-
LABORATORY (NON-CNS)
Cultures of body fluid specimens (e.g., from blood,stool, nasopharynx, or sputum)
to identify various viral, bacterial, and fungal etiologies ofencephalitis Lumbar puncture- CSF examination(Polymorphonuclear cells may predominate early in the illness
but are replaced by mononuclear cells within hours)
Viral culture
Viral PCR may identify the virusbody fluids other than CSF
Serology tests antibodies to an specific virus (IgM)
JEV,Dengue, Mycoplasma (4 fold rising)
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DIAGNOSIS-
LAB (CNS)
CSF- virus-specific IgM in CSF specimens may be indicative
of CNS disease caused
by that pathogen
Nucleic acid amplification tests (such as PCR)
Herpes simplex PCR should be performed on all CSF
specimens in patients with encephalitis . In patients with
encephalitis who have a negative herpes simplex PCR
result, consideration should be given to repeating the test
37 days later in those with a compatible clinical syndromeor temporallobe localization on neuroimaging
Viral cultures of CSF specimens (not routinely recommended)
Brain biopsy (rarely done;unknown etiology whose condition
deteriorates despite aggressive treatment with acyclovir
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DIAGNOSIS-
IMAGING
Imaging- to rule out SOL and other causes of
CNS disturbance
MRI is the most sensitive to evaluate patient
with encephalitis (CT/CECT only if MRI notavailable/cant be performed)
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DIAGNOSIS-
IMAGING
EEG-needed to assess seizure activity and
may help localize the region of encephalitic
involvement
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TREATMENT
EMPERICAL THERAPHY
Acyclovir should be initiated to all patient
suspected encephalitis, pending results
Other antimicrobial esp presumed bacterialmeningitis should be started if clinically
suggestive
In case postinfectious encephalitis orencephalitis unknown cause- Intravenous
Ig/corticosteroid should be started after
consulting ID specialist
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TREATMENT
SPECIFIC THERAPHY
Herpes simplex - Acyclovir
Varicella ZosterAcyclovir
CMV- Ganciclovir
Mycoplasma pneumonia-azithromycin,
doxycycline, or a fluoroquinolone
Mycobacterium TB- 4 drug anti TB withdexamethasone
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TREATMENT
SUPPORTIVE TREATMENT
Reduce intracranial pressure : restrict fluid,
hyperventilation( if on ventilator), lower body
temperature , Rest, nutrition, fluids (SIADH), antipyretic,
Anticonvulsant
Acute psychosis : haloperidol
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PROGNOSIS
Depends the virulence of the virus and on
variables associated with the patient's health
status, such as extremes of age,
immune status, and preexistingneurologicconditions
Rabies, EEE, JE, and untreated HSE have
high rates of mortality and severe morbidity,
including mental retardation, hemiplegia, and
seizures
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Acute Disseminated
Encephalomyelitis (ADEM)
Postinfectious encephalitis often features thatpermit classification as ADEM. infection that occurred days to weeks before the onset
of neurologic symptoms.
The infectionmay be memorable measles, or
minor, such as a respiratory tract infection
The diagnosis usually is considered because ofthe distinctive findings on MRI of the brain andspine
Classically, white matter is affected more thangray matter, but basal ganglion and thalamiclesions often are described
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Acute Disseminated
Encephalomyelitis (ADEM)
Distinguishing ADEMimportant to optimize
therapy
high doses of glucocorticoids to limit further,
presumed immune-mediated, damage to the CNSAlternative are IVIG
Most patients who have ADEM make a clear
and often complete recovery (however, the
prognosis should be guarded)
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CONCLUSION
Encephalitis is an uncommon and disturbing illnesswhose cause often remains enigmatic despiteextensive diagnostic efforts.
Clinicians should focus
treatable and common causes; empiric therapy for bacterial meningitis and herpes simplex
encephalitis should be started while awaiting results
Many patients will not receive a specific diagnosis
Duration of therapy should be decided in consultation
with neurology and infectious disease specialists. Supportive care and early referral for rehabilitation
maximize functional recovery.
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THANK YOU
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