LecturerLecturer(Deptt. of pediatrics)(Deptt. of pediatrics)MGIMS SevagramMGIMS Sevagram

n An inflammatory process that affects the brain tissue.n It is almost always accompanied by inflammation of adjacent meninges ,thus the term meningoencephalitis.meningoencephalitis.

n Encephalopathy implies cerebral dysfunction due to circulating toxins, poisons, abnormal metabolites, or intrinsic biochemical disorders affecting the neurons but without inflammatory response.

A. Viruses: spread person to person:Harpies simplex1 &2.Varicella zoster.

B. Spread by mosquitoes or ticksJapanese B encephalitisKyasanur forest disease.

Mumps, Measles, VariolaEpstien -Barr Virus, CMVInfluenza virus, EnterovirusRubella, AdenovirusHHV6

Dengue virusWest Nile virusEquine encephalitis virusSt.louis encephalitis

Etiology cont…..Spread by warm blooded mammals

Others

Rabies Lymphocytic

HIVSlow virus infections, prion Lymphocytic

Choriomeningitis virusSlow virus infections, prion disease

Etiology cont…..Bacteria:H.InfluenzaeN.MeningitidisS.pneumonae, M.tuberculosisSpirochetes; borrelia,leptospira,

Others:Chlamydia, Rickettsia, mycoplasma.Fungi: Cryptococus neoformans, coccidiodomycosis, blastomycosis.Spirochetes; borrelia,leptospira,

Trponema pallidum.

coccidiodomycosis, blastomycosis.

Protozoa:Plasmodium falciparum, Acanthamoeba, Naegleria

Helminths:Schistosoma

n Factors affect the epidemiology are; age, geographical location, season, climate, and host immunocompetence.

n Incidence of encephalitis differs greatly in different countries and in different seasons of the year.countries and in different seasons of the year.

n JE transmitted in our country by female mosquitoes Culex triaenorhynchus and culex vishnui.

n Herpies tends to occur worldwide with little seasonal variation.

n Primary: direct invasion and replication of virus leading to tissue necrosis.

n Para infectious: A post infectious inflammatory response characterized by immune mediated CNS damage, demyelination with preservation of neurons damage, demyelination with preservation of neurons and axones.

n Many viruses caused widespread inflammation ,cerebral edema and necrosis.

n Some such as rabies and harpies virus have predisposition to involve specific areas of the brain namely basal ganglia and temporal lobe.

n Harpies virus have predisposition to involve specific areas involve specific areas of the brain namely temporal lobe.

n Determined by the:1.severelty of involvement and anatomic location of affected portion of the nervous system.2.Inherent pathogenesis of offending agent.3.Immune and other reactive mechanisms of the patient.3.Immune and other reactive mechanisms of the patient.

n Clinical manifestations may vary from inapparent mild abortive illness or aseptic meningitis syndrome to severe encephalopathy with or without radiculitis.

n Onset usually acute, but sign and symptoms of CNS involvement often are preceded by a non specific ,acute febrile illness.

Clinical features cont……n In Older children: headache and malaise.n Infants are typically are irritable and lethargic.n Fever, nausea, vomiting, neck pain, and photophobia are common.n Alteration of consciousness ranges from mild lethargy and confusion to

coma.coma.n Evidence of brain parenchymal involvement is the hallmark of

encephalitis.n Children with encephalitis may demonstrate evidence of diffuse disease

e.g. behavioral or personality changes ,decreased consciousness, and generalized seizures or localized changes e.g. focal seizures , hemi paresis, movement disorders ,cranial nerve deficits and ataxia.

Clinical features cont……n Neurological abnormalities may be stationary ,progressive ,or fluctuating.

n Sudden severe rise of ICT may result in decerebration cardio respiratory insufficiency, hyperventilation and autonomic dysfunction.

n Uncontrolled cerebral edema may lead to herniation at tentorial hiatus ,compression of the midbrain causing deterioration of consciousness, papillary changes,ptosis,6th

nerve palsy, Ophthalmoplegia, paralysis of upward gaze, cheyne-stroke breathing ,hyperventilation and bradycardia.

n Herniation of cerebellum through the foramen magnum causes distortion and compression of medulla oblongata with severe disturbances of vital centers leading to respiratory or cardiac arrest.

n Course of encephalitis varies from that of fulminating n Course of encephalitis varies from that of fulminating type, ending in death in 2 to 4 days,

n to that of a mild form in which illness subsides in 1 or 2 weeks with complete recovery.

n Typically this stage lasts for 7-10 days after which there is gradual recovery with or without sequelae.

n Ds usually made on clinical presentation of a non-specific prodrome followed by progressive CNS involvement.

n Presence of focal features favors the possibility of harpies encephalitis.

n History is taken for prior viral infections, exanthema (echovirus, coxsackievirus, varicella zoster virus, measles, rubella) or recent vaccination.

n History of bite from a potentially rabid animal, travel history, exposure to mosquitoes, rodents and ticks, the season in which illness occurs and the disease prevalent in community may provide clues to the diagnosis.

n Pressure: normal to slightly elevated.n Usually there is lymphocytic pleocytosis(5-500 cells/mm3).n Rarely more than 1,000 cells/mm3 may be seen in conditions

like eastern equine encephalitis and lymphocytic choriomeningitis.choriomeningitis.

n Early in the disease cells might be polymorphonuclear ,later mononuclear cells predominate.

n Some patients of HSE may show a xanthochromic or bloody CSF ,usually with less than 500 RBCs/cmm.

n Protein contents is mildly elevated (50-200mg/dl).n Glucose content is normal or slightly decreased.

n CSF should be cultured for viruses, bacteria, fungi and mycobacteria.n Lab methods include to diagnose CNS viral infection: isolation of

virus, detection of viral antigen, or its nucleic acids and serology.n Workup includes: viral culture of respiratory secretions ,throat swab,

CSF, blood ,urine, stool, swab from skin rash and brain tissue taken as early as possible in the illness.early as possible in the illness.

n Detection of viral antigen can be done in brain tissue or CSF.n Detection of antibodies in CSF and CSF to blood ratio of specific IgG

can be helpful in diagnosing the HSV infection.n Single serum IgM value or paired sera (acute and convalescent) to

show rising titers of IgG are also helpful.n PCR to detect viral nucleic acids in CSF is provide a rapid ,accurate

diagnosis.

n May be helpful in patients with:1.markedly neurological function,where it detect seizure and monitor the effect of antiepileptics.2.suspected HSV infection where characteristics periodic sharp waves repeating every 0.5-4 sec. are found.sharp waves repeating every 0.5-4 sec. are found.

n EEG abn. May be deffuse or temporo- frontal, unilateral, or bilateral, and are always accompanied by diffuse or temporally accentuated excess Delta activity.

n It is helpful to separate viral encephalitis from metabolic or toxic disorders.

n MRI is sensitive than CT scan to identifies the lesions of encephalitis.

n In JE, CT scan shows non-enhancing low density areas in n In JE, CT scan shows non-enhancing low density areas in thalamus, basal ganglia, midbrain, pons and medulla.

n Bilateral hemorrhagic thalamic involvement is characteristic of JE in endemic areas.

n HSE

.

n 3 y male presented with fever & unconscious. n Bilateral asymmetrical hypodense area in the temporal region with hyperdense focus. n Herpes encephalitis.

n Bilaterally hypo dense lesions in basal ganglia suggestive of JE.

n Bacterial or tuberculous meningitisn Cerebral malaria.n Encephalitis or meningoencephalitis due to leptospira spp, mycoplasma pneumonea Aracanthamoeba. mycoplasma pneumonea Aracanthamoeba.

n Brain abscess.n Reye syndrome.n Enteric encephalopathy.n Electrolyte and metabolic encephalopathy.n Drug ingestion.n Cerebral vascular disorders.

n Main objectives of treatment;1.To reduce the raised ICT.2.To optimize systemic arterial pressure to maintain adequate cerebral perfusion pressure.adequate cerebral perfusion pressure.

3.Prevention of secondary complications.

n 1.avoiding situations that increases the ICP.

n 2.Therapeutic measures to decrease ICP.

n 1.Position and general care of patient- A 15-300 head up tilt with head kept in the midline position facilitates venous return from head, decreases ICP and improves cerebral perfusion pressure.

n 2.Temperature control: Raised temp. increases the ICP by increasing cerebral metabolism ,cerebral blood flow and cerebral edema.

n It should be controlled by cooling mattresses and paracetamol. n It should be controlled by cooling mattresses and paracetamol. n 3.Role of sedation: Pain and arousal cause elevated ICP by increasing

cerebral blood flow.n It play a imp. role in prevention of worsening of ICP by this

mechanism.n Seizure control: Seizure increases ICP by increasing cerebral

metabolism and cerebral blood flow.n Midazolam and diazepam is effective for emergency use.

n Pt. should kept nil by orally for first 24 hours.n Pt. should receive IV fluids as n.5 in 5% dextrose in normal maintenance requirement.

n If pt, develop SIADH than 2/3 of maintenance are given.

n 1. Hyperventilation: After Endotracheal intubation with maintenance of Paco2 between 25-30 mmHg effectively reduces ICP by causing cerebral vasoconstriction.

n Drop in ICP occur within 1 to 5 minutes of initiation of hyperventilation.

n 2.Mannitol:it is most commonly used agent for control of raised ICP.

n DOSE: 0.25 to 1.0 g/kg body weight every 4-6 hours, or 20% mannitol 5 ml/kg over 5-10 min. followed by 3 ml/kg BW 6 hourly till 48 hours.

n Acetazolamide in dose of 20-50 mg/kg /day in 3 to 4 doses .oral glycerol 1ml/kg/dose 8 hourly may be used if ICP is elevated beyond 48 hours.

n Furosemide can be used in a dose of 1 mg/kg IV q 12 hourly.n Barbiturates are generally used only when standard therapy consisting Barbiturates are generally used only when standard therapy consisting

of osmotic agents, hyperventilation and head position failed to control the ICP.

n Dexamethasone: use of corticosteroid is controversial.n CSF removal by an external ventricular drain: can be used only when it

has reached dangerous levels. it gives only a temporary relief for raised ICP in pt. with acute hydrocephalus.

n Maintenance of cerebral perfusion: it is essential to prevent cerebral ischemia.

n Normal cerebral perfusion in an infant is in the range of 30 mmHg.

n Hence it should be:n Hence it should be:n >30 mmHg in infants <6mon.n >40 mmHg in older children.n >60 mmHg in adolescents.n Feeding; should be started once the sensorium improved.

n Pt. should be managed in ICU.n Aim is to evaluate cardio-respiratory stability and detect acute life threatening.

n Vitals including; temp. pulse, respiration, BP, neurological status, head size, body weight, and urine are recorded carefully.

Virus Drug Dose

HSV Acyclovir 10 mg/kg, q 8 hr, IV for 14-21 days.

VZV Acyclovir 10-15 mg/kg, q 8 hr, IV for VZV Acyclovir 10-15 mg/kg, q 8 hr, IV for 7-10 days.

CMV Gancyclovir 7.5 mg/ k/ d, q 8hr, for14-21days.

Influenza Amantadine

Rimantadine

100 mg twice daily,for 5-7 days.<14 yrs not recommended.

n Prognosis in all encephalitis is guarded with respect to immediate outcome and sequelae.

n Sequelae involving CNS include intellectual, motor, psychiatric, epileptic, visual or auditory.psychiatric, epileptic, visual or auditory.

n Predictor of poor outcome are: young age, low GCS, abn. oculocephalic response, focal neurological signs, reduction in cerebral perfusion pressure, abn. Neuroimaging study, and unilateral hyper perfusion on SPECT suggest a poor prognosis.