Encephalitis
DEBIKA DAS
M.SC (N) II YR
ROLL NO-MN1509
NEUROSCIENCE
NURSING
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Definition
• The Encephalitis is an acute inflammatory
process involving brain tissue.
• Meningoencephalitis is an acute
inflammatory process involving the meninges and, to
a variable degree, brain tissue.
• They are often found associated together.
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Encephalitis
Two Components:
1. Inflammation of brain,
and
2. Dysfunction of brain.
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Encephalopathy
• Dysfunction of brain
• Encephalopathy describes a clinical
syndrome of altered mental status,
manifesting as reduced consciousness or
altered behaviour.
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Causes of Encephalopathy
• Systemic infection,
• Metabolic derangement (e.g. DKA),
• Toxins,
• Drugs & Poisoning,
• Hypoxia,
• Trauma,
• Vasculitis,
• CNS infection.
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Acute Encephalitis Syndrome (AES)
Clinically, a case of acute encephalitis
syndrome is defined as a person of any age, at
any time of year with the acute onset of fever
and a change in mental status (including
symptoms such as confusion, disorientation,
coma or inability to talk) AND/OR new onset of
seizures (excluding simple febrile seizures)
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Conditions included in AES
• Viral Encephalitis,
• All causes of fever with altered sensorium:
– Bacterial Meningitis (Acute Pyogenic Meningitis),
– TBM,
– Cerebral Malaria,
– ADEM.
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Causes of Encephalitis
• Infectious causes:
– Viral
– Bacterial (TBM)
– Ricketssial,
– Fungal,
– Parasites (pl falciparum)
• Non-infectious causes.
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VIRAL CAUSES
• Enteroviruses: More than 80% of all cases.
• Arboviruses: e.g. Japanese-B Encephalitis which is
more common during summer months.
• Herpesvirus.
• CMV.
• EBV.
• Mumps.
• RSV, Rubeola, Rubella or Rabies (Occasionally).
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Viral Encephalitis
• Direct viral infection:
– Primary Viral Encephalitis.
• Indirect immune mediated mechanism:
– Post-infectious viral encephalitis.
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Viral Encephalitis
• Epidemic:
– Japanese Encephalitis,
– Dengue virus.
• Sporadic:
– Herpes simplex Encephalitis,
– Enterovirus (EV71),
– Chandipura virus,
– Nipah virus,
– Chikangunya virus.
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Other virus causing sporadic encephalitis
• Varicella zoster virus,
• Mumps,
• Human herpesvirus 6 & 7,
• EB virus,
• Herpes simplex virus.
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Non-Infectious Causes
1.Acute Disseminated Encephalomyelitis
(ADEM),
2.Antibody-associated encephalitis,
3.Allergy: Post Vaccine.
4.Heat Hyperpyrexia.
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Signs & Symptoms of Encephalitis
• Fever,
• Headache,
• Lethargy,
• Vomiting,
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Clinical Features (continued)
• Behavioural changes,
• Impairment of consciousness,
• Focal neurological signs,
• Seizures.
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Encephalitis associated with GIT symptoms
• Enteroviruses,
• Rotavirus,
• Parechovirus.
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Encephalitis associated with respiratory illness
• Influenza viruses:
– Myositis may also be associated.
• Paramyxoviruses,
• Bacteria.
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Clue on physical examination
• Pallor:
– Cerebral Malaria,
– Intracranial bleed.
• Icterus:
– Leptospirosis,
– Hepatic Encephalopathy,
– Cerebral Malaria.
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Clues (continued)
• Skin rash:
– Meningococcemia,
– Dengue,
– Measles,
– Varicella,
– Rickettsial diseases,
– Arboviral diseases,
– Enteroviral encephalitis.
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Clues (continued)
• Petechiae:
– Meningococcemia,
– Dengue,
– Viral Hemorrhagic Fever,
• Parotid swelling:
– Mumps.
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Clues (continued)
• Orchitis:
– Mumps
• Labial herpes in young children:
– Herpes simplex virus encephalitis.
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CSF in viral encephalitis
• Pressure: normal or slightly raised,
• Sugar: normal,
• Cells: acellular (no cell) or mild
leukocytosis (mostly lymphocytes)
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Imaging
• CT Scan:
– Normal.
• MRI:
– Localized areas of inflammation,
– Diffuse brain swelling.
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UK Regimen
(till culture-report is available)
• Aciclovir:
– to cover HSV,
• 3rd generation cephalosporin:
– to cover bacterial cause,
• Erythromycin:
– to cover mycoplasma.
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India
Add antimalarials
to UK protocol,
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Japanese-B
Japanese-B
Encephalitis
Encephalitis
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Japanese Encephalitis (JE)
• One of the commonest cause of AES.
• Year 2014:
– Cases: 1661
– Deaths: 293 (17.6%)
• Assam, West Bengal, Uttar Pradesh
and Jharkhand.
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Japanese Encephalitis (JE)
• Leading viral cause of acute encephalitis syndrome
(AES) in Asia.
• Primarily affects children under age 15.
• Acute onset, fulminant course, and high mortality &
morbidity.
• 70% of patients either die or survive with long term
neurological disability.
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JE
• Group-B arbovirus (Flavivirus).
• Mosquito borne Encephalitis.
• Transmitted by Culicine (culex) mosquitoes.
• Zoonotic Disease.
• Rice or Pig Farming.
• Peak season: JUN – SEP.
SEP
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Virus
• Japanese Encephalitis Virus (JEV),
• Single stranded RNA virus,
• Genus: flaviviridae
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Spread
• Spreads by mosquito bite only,
• Man is an incidental dead end host,
• Man-to-man transmission not reported.
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Japanese-B
Encephalitis
• Incubation Period: 5-15 days.
• Ratio of overt disease to unapparent infection =
1:300 to 1: 1000.
• Cases represent tip of iceberg.
• Case Fatality Rate: 10 –70%.
• Incidence: 1- 10/10, 000 population.
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Pathology
• Mosquito bite transmission to man JEV
multiplies Neurologic invasion enters CNS
JEV replicates in endoplasmic reticulum and Golgi
apparatus and destroys them.
• Changes mainly in gray matter.
• Growth of the virus across vascular endothelium
mainly thalamus, basal ganglia, brain-stem,
cerebellum, hippocampus and cerebral cortex.
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Pathology outside CNS
• Hyperplasia of germinal centers of lymph-nodes,
• Enlargement of malpigian bodies in spleen.
• Interstitial myocarditis, swelling and hyaline
changes in Kuffer’s cells of liver, pulmonary
interalviolitis, and focal hemorrhages in kidneys.
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Clinical Features.
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Japanese-B Encephalitis
• Abortive.
• Aseptic Meningitis.
• Severe Encephalomyelitis.
– With Radiculitis.
– Without Radiculitis.
• Sudden onset with high fever, headache, vomiting,
Mental Confusion, Irritability, Loss of consciousness.
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3 Stages
1. Prodromal Illness [2 - 3 days]
2. Encephalitis stage
• Acute Stage [3 - 4 days]
• Sub-acute Stage [7 - 10 days]
3. Convalescence [4 - 7 weeks]
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Prodromal Stage
• High grade fever +/- rigor,
• Headache,
• General malaise,
• Nausea and Vomiting.
• During this stage, a definitive clinical
diagnosis is not possible.
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Encephalitic Stage
• Altered mental status:
– Confusion, agitation, coma
• Generalized weakness,
• Hypertonia & Hyper-reflexia,
• Seizures,
• Papilloedema and/or Cr. N. involvement,
• GIT bleed & Pulmonary Hemorrhage.
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Late Stage
• Stage of convalescence,
• Recovery,
• Persistence of signs of CNS injury:
– Residual neurological impairments
• Secondary infections are frequent in this stage.
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Residual neurological impairments
• Involuntary movements:
– Choreoathetosis or extrapyramidal symptoms,
• Paralysis & Paresis,
• Speech disorders.
• Decorticate or Decerebrate Posturing.
• Post-Encephalitis Cerebral Palsy.
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Clinical Manifestations
• Altered sensorium.
• Headache.
• Convulsions.
• Fever.
• Vomiting/Nausea.
• Photophobia.
• Abnormal movements.
• Signs of raised ICT.
• Altered Tone and Reflexes
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Diagnosis
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DIAGNOSIS
• Clinical Manifestations.
• CSF:
– Pleocytosis: Initially Polymorphs then Lymphocytes.
– Increased protein.
– Normal sugar.
• EEG: Diffuse slow-wave activity.
• CT or MRI: Swelling of the brain parenchyma.
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Diagnosis (Contd)
• Virus isolation
• Detection of viral component
(antigen detection)
• Viral serology
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Virus Isolation
• CSF
• Nasopharynx
• Faeces
• Urine
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Viral Serology
IgM & IgG:
IgM appears early within 2 weeks of infection
IgG appears later, peaking around 8 weeks.
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Management
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Principles of Management
• Hospitalization.
• Line-listing with correct address.
• Save Life.
• Prevent neurological residues.
• Relieve symptoms.
• Provide specific treatment.
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Steps of evaluation
and management
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6 steps
• Step 1: Rapid assessment and
stabilization.
• Step 2: Clinical evaluation:
– History & Physical Examination.
• Step 3: Investigations.
• Step 4: Empirical Treatment
• Step 5: Supportive care and treatment.
• Step 6: Complications and Rehabilitation.
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Step 1: Rapid Assessment & Stabilization
• Maintain ABC.
• Intubate SOS (children with GCS < 8).
• Oxygen.
• Ventilation.
• Establish IV line and take samples.
• Fluid bolus (RL/NS 20 ml/kg) SOS.
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Step 1 (continued)
• Fluid bolus (RL/NS 20 ml/kg) SOS.
• Treat/Prevent hypoglycemia.
• Identify signs of cerebral herniation and raised ICP.
• Manage fever.
• Control seizure.
• Correct acid-base and electrolyte imbalance, if any.
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Step 2
• Clinical evaluation:
– History including environmental details and
– Thorough Physical Examination.
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History
• Onset & duration,
• Fever, headache, vomiting, diarrhoea,
irritability, seizures, and rash.
• Contact with TB, Chicken Pox, Mumps,
• Place of residence
– Endemic for JE?
– Near rice-field?
– Cattle, Pigs?
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Physical Examination
• Vitals, GPE, and Systemic,
• Thorough CNS evaluation,
• GCS,
• Pupil:
– size, shape, symmetry, and response to light.
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Clue!
Unilateral pupillary dilatation in the
comatose patient should be
considered as evidence of 3rd Nerve
compression from ipsilateral uncal
herniation, unless proved otherwise.
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Step 3: Investigations
• CSF,
• Blood/Serum, Urine,
• Throat Swab, Nasopharyngeal Swab,
• MRI (if available), avoid sedation.
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Basic Investigations
• CBC including platelet count,
• Blood Glucose,
• Serum Electrolytes,
• Liver & Kidney Function Test,
• Blood C/S,
• ABG,
• P/S for MP.
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CSF
• Gross appearance: colour, transparency
• Chemistry including CSF: Blood Sugar,
• Cytology,
• C/S,
• Latex Agglutination,
• PCR for HSV 1 & 2,
• IgM antibodies for JE & Dengue.
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Step 4: Empirical Treatment
• Do not wait for report, start treatment
immediately.
• Ceftriaxone + Acyclovir + Artesunate
(stop artesunate if P/S and RDT are
negative).
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Step 5: Supportive Care & Treatment
1. Maintain airway, breathing and circulation.
2. Control of seizures.
3. Treatment of raised ICT.
4. Manage fever (Never give aspirin).
5. Maintain fluid & electrolyte balance.
6. Maintain blood-sugar level.
7. Feeding: NPO initially then NG Tube Feeding.
8. Specific Treatment.
9. Methylprednisolone or dexamethasone must be
given to children with suspected ADEM.
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Step 6: Prevention/Treatment of
complications and rehabilitation
• Physiotherapy, posture change, prevent bed-
sore and exposure keratitis.
• Prevent complications: aspiration pneumonia,
nosocomial infection, coagulation
disturbances.
• Nutrition: early feeding.
• Psychological support to patient and family.
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Features of raised ICP
• Asymmetric pupil,
• Tonic posturing,
• Papilloedema
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Treatment of raised
ICT
• Proper positioning: Head elevated 15-300.
• Fluid Restriction: 2/3rd of maintenance.
• 20% Mannitol 5 ml/kg over 10 – 15 min followed by 3
ml/kg every 6 hourly for 48 hrs then SOS, or
• Acetazolamide: 50 – 75 mg/kg/day, or
• Glycerin: 1 ml/kg/day through NG Tube.
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Raised ICT (continued)
• Hyperventilation,
• Furosemide
– Persistence of ICT after mannitol therapy.
– 1-2 mg/kg/dose every 12 hourly.
• Ventilation
• While tracheal suctioning, boluses of i. v. lignocaine
0.5-1 mg/kg may be used to prevent rise of ICP.
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Dosage
• Inj. Chloramphenicol:
– 100 mg/kg/day in 4 divided doses for 10 days.
• Inj. Ceftriaxone:
– 100 mg/kg/day in 2 divided doses for 10 days.
• Inj. Cefotaxime:
– 200 mg/kg/day in 3-4 divided doses for 10-14 days..
• Inj. Ampicillin:
– 300 mg/kg/day in 4 divided doses for 10 days.
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Prevention
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Control Measures
a. Vector Control:
1. Fogging.
ULV
2. Indoor mosquito spray
b. Vaccination.
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Personal
Protection
• Avoid mosquito bites:
– Use mosquito-net
– House Screening
– Mosquito Repellents.
– Avoid evening outdoor
exposure.
– Cover body with clothing
• Vaccination
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Vaccines
• Inactivated Mouse Brain Vaccine (JE-VAX),
JE-VAX
• Inactivated Primary Hamster Kidney Cells-P3-China,
• Live Attenuated Primary Hamster Kidney (PHK) Cells-
SA14-14-2 strain – China: Marketed for both domestic
use and for use in Nepal, S. Korea, Sri Lanka and India.
• Inactivated Vero Cell Culture Derived SA-14-14-2 JE vaccine
(IC51)-(IXIARO)
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Live Attenuated SA-14-14-2 Vaccine
• Launched in India in 2006.
• Single Dose.
• Efficacy: 94.5% (95% CI, 81.5 to 98.9).
• JE Vaccine efficacy:
– 60% in UP and 70% in Assam
– Results better in Nepal.
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Nursing management.
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