encephalitis presentation

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-


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-


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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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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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

encephalitis presentation

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