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CNS CNS infectionsinfections

By By

Dr Muhammad Saleem Dr Muhammad Saleem LaghariLaghari

MBBS(KEMU), MCPS, FCPS (Paed) MBBS(KEMU), MCPS, FCPS (Paed)

Gold Medalist FCPS-IGold Medalist FCPS-I

Associate ProfessorAssociate ProfessorDepartment of pediatricsDepartment of pediatrics

SMC,RYKSMC,RYK

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CNS INFECTIONSCNS INFECTIONS MENINGITIS:MENINGITIS:

I) AcuteI) Acute Bacterial (Pyo)Bacterial (Pyo) Viral (Aseptic)Viral (Aseptic)

ii) Sub acute (Chronic)ii) Sub acute (Chronic) TB, Fungal, Neoplastic, TB, Fungal, Neoplastic, Parasitic, Parasitic,

Rickettsial Rickettsial

iii)iii) Partially treated Partially treated iv) Chemicaliv) Chemical ENCEPHALITIS ENCEPHALITIS CEREBRAL ABSCESSCEREBRAL ABSCESS

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Case ScenarioCase Scenario

A 2 years old boy presented with A 2 years old boy presented with history of fever, irritability & vomiting. history of fever, irritability & vomiting. Examination revealed semiconscious Examination revealed semiconscious child having temp.102Fchild having temp.102F00

decrebrate posturing .Rest of systemic decrebrate posturing .Rest of systemic examination unremarkable. examination unremarkable.

Q - write 3 differential diagnosis.Q - write 3 differential diagnosis.

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Key.Key.

1- pyomeningitis1- pyomeningitis

2- Encephalitis2- Encephalitis

3- cerebral malaria3- cerebral malaria

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Case ScenarioCase Scenario

A 7 year old boy brought to emergency A 7 year old boy brought to emergency with high grade fever, headache for 2 with high grade fever, headache for 2 days & projectile vomiting since days & projectile vomiting since morning. Examination revealed morning. Examination revealed semiconscious child with positive neck semiconscious child with positive neck stiffness. stiffness.

1-1- What is the most likely diagnosis?What is the most likely diagnosis?

2-2- Write 3 relevant investigations to Write 3 relevant investigations to reach final reach final

diagnosis.diagnosis. 3-3- Write steps in the management of Write steps in the management of

this case.this case.

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Key:Key:1-1- Acute – pyogenic meningitis Acute – pyogenic meningitis 2-2- (i)(i) CSF examination & culture (after fundoscopy) CSF examination & culture (after fundoscopy)

(ii)(ii) CBCCBC(iii)(iii) Blood cultureBlood culture

3-3- Steps of TreatmentSteps of Treatment a. a. General Supportive MeasuresGeneral Supportive Measures

Maintain I/V line, Monitor vitals, Fluids balance, IOP Maintain I/V line, Monitor vitals, Fluids balance, IOP record, Control of fever.record, Control of fever.

b. b. Specific treatmentSpecific treatment(i)(i)Either combination of B. Penicillin + Either combination of B. Penicillin +

Chloramphenicol orChloramphenicol or(ii)(ii) Vancomycin + Cefotaxime / CeftriaxoneVancomycin + Cefotaxime / Ceftriaxone(iii)Duration of Treatment: 7 – 10 days(iii)Duration of Treatment: 7 – 10 days cc. . SteroidsSteroids: Dexamethasone 0.6 mg/kg/day in 2 – 4 : Dexamethasone 0.6 mg/kg/day in 2 – 4

divided doses for 2- 4 days divided doses for 2- 4 days d.d.Monitor and treatment of complicationsMonitor and treatment of complications. .

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Case ScenarioCase Scenario 8 year old girl presented to emergency 8 year old girl presented to emergency

department with complaint of progressive department with complaint of progressive loss of weight & low grade fever for 2 loss of weight & low grade fever for 2 months, lethargy, off & on headache & months, lethargy, off & on headache & vomiting for 2 weeks and now vomiting for 2 weeks and now unconsciousness for last 5 days. unconsciousness for last 5 days. Examination revealed unconscious, Examination revealed unconscious, emaciated girl having 10 Kg weight. No emaciated girl having 10 Kg weight. No BCG scar. CNS examination revealed BCG scar. CNS examination revealed right sided uncrossed hemiplegia. Her right sided uncrossed hemiplegia. Her grand father died 2 months back.grand father died 2 months back.

1-1- What is most likely diagnosis?What is most likely diagnosis?

2-2- Mention 4 investigations to reach final Mention 4 investigations to reach final diagnosis?diagnosis?

3-3- Write 4 steps of treatment of above Write 4 steps of treatment of above disease?disease?

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Key:Key:1-1- TBM TBM 2-2- (i)(i) CSF examination & CultureCSF examination & Culture

(ii)(ii) CBC + ESRCBC + ESR(iii)(iii) Chest X-rayChest X-ray

(iv)(iv) Mantoux testMantoux test (v)(v) CT Scan BrainCT Scan Brain3-3- (i)(i) General measuresGeneral measures

(ii)(ii) Anti tuberculosis treatment (INH, PZA, Anti tuberculosis treatment (INH, PZA,

Rifampicin, Streptomycin)Rifampicin, Streptomycin)(iii)(iii) CorticosteroidsCorticosteroids(iv)(iv) Monitor & treatment of complicationMonitor & treatment of complication

(v) Follow up(v) Follow up

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MENINGITISMENINGITIS

Meningitis is defined as Meningitis is defined as inflammation of the inflammation of the

membranes surrounding the membranes surrounding the brain & spinal cord.brain & spinal cord.

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MeningoencephalitisMeningoencephalitis

Inflammation of both the Inflammation of both the meninges & cortex of brain.meninges & cortex of brain.

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ROUTES OF INFECTIONROUTES OF INFECTION Nasopharyngeal.Nasopharyngeal. Paranasal sinuses.Paranasal sinuses. Blood stream Septicemia Blood stream Septicemia

Pneumonia, OsteomyelitisPneumonia, Osteomyelitis Skull Fracture, Meningocele, Skull Fracture, Meningocele,

EncephaloceleEncephalocele Middle Ear Infection/ Mastoiditis.Middle Ear Infection/ Mastoiditis. VentriculoPeritoneal ShuntsVentriculoPeritoneal Shunts Pilonidal SinusPilonidal Sinus

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ETIOLOGYOrganismsOrganisms

0-2months0-2months: E.coli, Group B streptococci, : E.coli, Group B streptococci, staylococcus aureus, Listeria staylococcus aureus, Listeria monocytogenes.monocytogenes.

2months -2 years2months -2 years: Hib, S. pneumoniae, : Hib, S. pneumoniae,

Neisseria meningitidis Neisseria meningitidis

2 years - 21 years2 years - 21 years :N. meningitidis, :N. meningitidis,

S. pneumoniae ,Hib.S. pneumoniae ,Hib.

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CLINICAL FEATURESCLINICAL FEATURESNEONATESNEONATES

Sick Baby /SepticemiaSick Baby /SepticemiaSubtleSubtle

INFANTS INFANTS Fever, Vomiting, Stiffness, Sensorial Fever, Vomiting, Stiffness, Sensorial

disturbance, Irritability, Excessive Cry, disturbance, Irritability, Excessive Cry, Seizures,Seizures,

Anterior Fontanel Full/Bulging.Anterior Fontanel Full/Bulging. Neck Retraction.Neck Retraction. Meningeal signs Less Reliable Meningeal signs Less Reliable PapillodemaPapillodema Tone/Reflexes Brisk Tone/Reflexes Brisk

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CLINICAL FEATURES IN CLINICAL FEATURES IN CHILDRENCHILDREN

Fever. Vomiting. Headache, Fever. Vomiting. Headache, DrowsinessDrowsiness

SeizuresSeizures Neck StiffnessNeck Stiffness Kernings, Brudzinki signsKernings, Brudzinki signs Rash (Petechial, purpural )Rash (Petechial, purpural ) Vitals instabilityVitals instability Cranial nerve palsy, hemiplegia, Cranial nerve palsy, hemiplegia,

ataxiaataxia Infection Source e.g. otitis media.Infection Source e.g. otitis media.

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MENINGOCOCCIMIAMENINGOCOCCIMIA

Fulminant Septicemia.Fulminant Septicemia. Acute Febrile Illness.Acute Febrile Illness. Petechial Haemorrhages.Purpura.Petechial Haemorrhages.Purpura. DIC.DIC. Adrenal Haemorrhage.Adrenal Haemorrhage. Peripheral Circulatory Failure.Peripheral Circulatory Failure. ShockShock

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DIAGNOSISDIAGNOSIS CBCCBC Blood CultureBlood Culture CSF examination CSF examination X-Ray chestX-Ray chest C T Scan brainC T Scan brain Rapid Diagnostic TestRapid Diagnostic Test

Counter current immuno electrophoresisCounter current immuno electrophoresis Latex particle agglutination Latex particle agglutination ELISA ELISA CSF, LDH CSF, LDH

Gram Staining / Smears of Gram Staining / Smears of Petechial / Purpural Lesions.Petechial / Purpural Lesions.

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CSF EXAMCSF EXAM

Color.Color. Pressure.Pressure. Cells. Cells. Gram stainingGram staining Proteins.Proteins. GlucoseGlucose Culture.Culture.

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COMPLICATIONSCOMPLICATIONS Seizures. Epilepsy.Seizures. Epilepsy. Cranial Nerve Palsies. Deafness Cranial Nerve Palsies. Deafness

(sensoneural). Blindness, Oculomotor, (sensoneural). Blindness, Oculomotor, Abducent, Facial ..Abducent, Facial ..

Raised ICP. Brain Herniation.Raised ICP. Brain Herniation. In Appropriate ADH syndromeIn Appropriate ADH syndrome Stroke. Cerebral Infarcts.Stroke. Cerebral Infarcts. DIC.DIC. Hydrocephalus.Hydrocephalus. Subdural Effusion.Subdural Effusion. Mental & Physical Handicap.Mental & Physical Handicap. Learning Disabilities.Learning Disabilities. Recurrences.Recurrences.

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MANAGEMENTMANAGEMENT

SUPPORTIVESUPPORTIVE Control Hyperpyrexia.Control Hyperpyrexia. Seizures Diazepam iv slow, Midzolam Seizures Diazepam iv slow, Midzolam

i. v, Phenobarbitone .i. v, Phenobarbitone . Resticted Fluid 800-1000ml/m.sq./day.Resticted Fluid 800-1000ml/m.sq./day. Airway, Bowel & Bladder, Posture, Wt. Airway, Bowel & Bladder, Posture, Wt.

H.CH.C Pupillary Reflex, Signs ICP, Fundoscpy..Pupillary Reflex, Signs ICP, Fundoscpy.. Feeding.Feeding. IOP.IOP.

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Specific Therapy

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CORTICOSTEROIDSCORTICOSTEROIDS

Dexamethasone iv Dexamethasone iv 0.15mg/kg/dose 6hr.2D.0.15mg/kg/dose 6hr.2D.

H Influenza type b.H Influenza type b. Inflammatory Mediators Inflammatory Mediators

reduction.reduction.Cerebral edema.Cerebral edema.

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PROGNOSISPROGNOSISConsiderable Age, Seizures, Considerable Age, Seizures,

Coma Coma MortalityMortality25% Pneumococcal.25% Pneumococcal.15%Meningococcal.15%Meningococcal.8% H. Influenza type b.8% H. Influenza type b.

MorbidityMorbidity35% Neurological Deficit.35% Neurological Deficit.

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PREVENTIONPREVENTION Vaccines. Vaccines.

Pneumococcal Pneumococcal polysaccharide.polysaccharide.

Meningococcal.Meningococcal.H. Influenza.H. Influenza.

Antibiotic Prophylaxis.Antibiotic Prophylaxis.Rifampicin oralRifampicin oralPatient & contactsPatient & contacts

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TUBERCULOUTUBERCULOUS S

MENINGITISMENINGITIS

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DefinitionDefinition

It is inflammation of the It is inflammation of the lepatomenings (pia-lepatomenings (pia-arachnoid) by arachnoid) by mycobacterium tuber-mycobacterium tuber-culosis.culosis.

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IncidenceIncidence Most serious complication of tuberculosis.Most serious complication of tuberculosis.

TBM complicates 1 of every 200 primary TBM complicates 1 of every 200 primary infections. infections.

It is not reported in infants below 4 months of It is not reported in infants below 4 months of age.age.

The maximum risk of TBM is within 6 months of The maximum risk of TBM is within 6 months of primary infection.primary infection.

The highest incidence is recorded below 5 years The highest incidence is recorded below 5 years of age.of age.

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Pathogenesis Pathogenesis TMB is always a secondary lesion TMB is always a secondary lesion

with primary usually in the lungs.with primary usually in the lungs. Meningitis results from the Meningitis results from the

formation of a metastatic caseous formation of a metastatic caseous lesion (seeding of the bacilli) in the lesion (seeding of the bacilli) in the cerebral cortex, meninges and cerebral cortex, meninges and choroid plexus during the process of choroid plexus during the process of initial occult lympho-hematogenous initial occult lympho-hematogenous spread of the primary infection.spread of the primary infection.

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Within a short period of time, caseous foci Within a short period of time, caseous foci form on the surface of brain (Rich’s foci). form on the surface of brain (Rich’s foci). They increase in size and discharge bacilli in They increase in size and discharge bacilli in the CSF (subarachnoid space).the CSF (subarachnoid space).

A thick, gelatinous exudate may infiltrate A thick, gelatinous exudate may infiltrate the cortical or meningeal blood vessels, the cortical or meningeal blood vessels, producing inflammation, obstruction, or producing inflammation, obstruction, or infarction. Most commonly involved site is infarction. Most commonly involved site is the brain stem causing frequent involvement the brain stem causing frequent involvement of 3of 3rdrd, 6, 6thth, and 7, and 7thth cranial nerves. cranial nerves.

Basal cisterns are obstructed causing Basal cisterns are obstructed causing communicating hydrocephalus. Accompany-communicating hydrocephalus. Accompany-ing inflammation may cause cerebral edema.ing inflammation may cause cerebral edema.

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Clinical featuresClinical features In a classical case, onset is insidious but may be In a classical case, onset is insidious but may be

fulminant in certain cases.fulminant in certain cases. A more rapid progression of the disease may occur A more rapid progression of the disease may occur

in young infants in whom symptoms develop for in young infants in whom symptoms develop for only several days before the onset of acute only several days before the onset of acute hydrocephalus, brain infarction, or seizures.hydrocephalus, brain infarction, or seizures.

Classically, the onset is gradual (over several Classically, the onset is gradual (over several weeks).weeks).

History of measles may precede the onset of TBM.History of measles may precede the onset of TBM. The clinical manifestations may be divided into 3 The clinical manifestations may be divided into 3

stages and each stage lasts approximately 1 week. stages and each stage lasts approximately 1 week. There may be considerable overlap of the 3 stages. There may be considerable overlap of the 3 stages.

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Stage-1 (Prodromal stage).Stage-1 (Prodromal stage).(lasts for 1-2 weeks)(lasts for 1-2 weeks)

Initial symptoms are non-specific.Initial symptoms are non-specific. The child becomes listless or irritable, The child becomes listless or irritable,

loses interest in play, have fever, loses interest in play, have fever, anorexia, vomiting, constipation and anorexia, vomiting, constipation and weight loss.weight loss.

Some children may complain of Some children may complain of headache and drowsiness. headache and drowsiness.

There are no focal neurologic signs. There are no focal neurologic signs. There may be loss of or stagnation of There may be loss of or stagnation of

the developmental milestones. the developmental milestones.

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Stage – 2 Stage – 2 Onset of 2Onset of 2ndnd stage is more abrupt. stage is more abrupt. During this stage, During this stage, signs of meningeal irritation signs of meningeal irritation

(neck stiffness) appear with increased CSF (neck stiffness) appear with increased CSF pressure. Positive kerning and Brudzinski pressure. Positive kerning and Brudzinski signs develop with increased tendon jerks and signs develop with increased tendon jerks and extensor plantar responses. There may be extensor plantar responses. There may be generalized hypertonia. generalized hypertonia.

Headache is the cardinal symptoms in the 2Headache is the cardinal symptoms in the 2ndnd week of illness in older children. Fever is week of illness in older children. Fever is constant and headache is severe, persistent constant and headache is severe, persistent and often occipital. and often occipital.

Vomiting and constipation may become severe. Vomiting and constipation may become severe. Exudate develops at the base of brain Exudate develops at the base of brain

involving cranial nerves and brain stem. involving cranial nerves and brain stem.

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Abducent nerve paralysis is common. Abducent nerve paralysis is common. Oculomotor lesion causes internal Oculomotor lesion causes internal squint. Facial palsy is also common.squint. Facial palsy is also common.

Some children may have disorientation, Some children may have disorientation, and speech and movement disorders. and speech and movement disorders.

In infants anterior fontanelle may be In infants anterior fontanelle may be bulging and sutures become separated bulging and sutures become separated with “crackpot” sign.with “crackpot” sign.

In older children, papilledema In older children, papilledema develops. Head circumference starts develops. Head circumference starts enlarging rapidly.enlarging rapidly.

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Choroid tubercles may be seen.Choroid tubercles may be seen. Child is semiconscious and may Child is semiconscious and may

shriek loud noises and develops shriek loud noises and develops convulsions.convulsions.

All the above clinical features are All the above clinical features are due to the development of due to the development of hydrocephalus and increased hydrocephalus and increased intracanial pressure along with intracanial pressure along with meningeal irritation. meningeal irritation.

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Stage – 3 Stage – 3 Child rapidly becomes comatose during 3Child rapidly becomes comatose during 3rdrd

week.week. He is emaciated with scybalous masses in He is emaciated with scybalous masses in

the abdomen. the abdomen. Child starts getting high-grade irregular Child starts getting high-grade irregular

fever and convulsions. fever and convulsions. There may be hemiplegia or paraplegia.There may be hemiplegia or paraplegia. With extreme neck stiffness opisthotonus With extreme neck stiffness opisthotonus

develops with decerebrate rigidity and develops with decerebrate rigidity and pupil becomes dilated and fixed. pupil becomes dilated and fixed.

There is deterioration of the vital signs There is deterioration of the vital signs especially hypertension. especially hypertension.

Death may occur if treatment is started late Death may occur if treatment is started late during this stage. during this stage.

Tache-cerebrale is sometimes seen in Tache-cerebrale is sometimes seen in children. children.

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Diagnosis Diagnosis Clinical suspicion + Fundoscopy.Clinical suspicion + Fundoscopy. CBC, ESRCBC, ESR X-ray chestX-ray chest Mantoux / Acc. BCGMantoux / Acc. BCG Lumber puncture (CSF examination)Lumber puncture (CSF examination) Gastric lavage or sputum Gastric lavage or sputum

examinationexamination Lymph node biopsy Lymph node biopsy CT scan / MRI brainCT scan / MRI brain

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ManagementManagementGeneral measuresGeneral measures1.1. Careful record of vital signsCareful record of vital signs

2.2. Daily monitoring of the Daily monitoring of the complications complications

3.3. Phenobarbitone: Dose 5mg/kg/day Phenobarbitone: Dose 5mg/kg/day to control convulsions.to control convulsions.

4.4. Antipyretics: Paracetamol Antipyretics: Paracetamol

5.5. corticosteroidscorticosteroids

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6.6. Pyridoxine 10mg daily to prevent Pyridoxine 10mg daily to prevent polyneuritis.polyneuritis.

7.7. Feeding: Give tube feeding Feeding: Give tube feeding according to the requirement.according to the requirement.

8.8. Bed sores: Change posture every Bed sores: Change posture every two hours to prevent bed sores.two hours to prevent bed sores.

9.9. Care of comatose patientCare of comatose patient10.10. Care of bowel and bladder.Care of bowel and bladder.11.11. It is also important to screen to It is also important to screen to

screen the family members for screen the family members for tuberculosis and treat the infected tuberculosis and treat the infected persons. persons.

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Specific managementSpecific management..

1.1. Isoniazid (INH)Isoniazid (INH)

2.2. RifampicinRifampicin

3.3. PyrazinamidePyrazinamide

4.4. Streptomycin /orStreptomycin /or

5.5. Ethambutol Ethambutol

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ComplicationsComplications Mental retardation Mental retardation Cranial nerve palsies (3Cranial nerve palsies (3rdrd, 6, 6thth & 7 & 7thth)) Blindness (optic atrophy)Blindness (optic atrophy) Deafness.Deafness. HydrocephalusHydrocephalus Hemiplegia, paraplegia, or monoplegia.Hemiplegia, paraplegia, or monoplegia. EpilepsyEpilepsy Endocrine disturbances (diabetes Endocrine disturbances (diabetes

insipidus).insipidus). Tuberculoma Tuberculoma

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Prognosis Prognosis It depends upon two factors:It depends upon two factors:

1.1. Age of the patientAge of the patient2.2. Stage of the disease at which treatment is Stage of the disease at which treatment is

started.started. Without treatment it is invariably fatal.Without treatment it is invariably fatal. In stage-1, 100% cure rate is expected.In stage-1, 100% cure rate is expected. Even with optimal therapy mortality ranges Even with optimal therapy mortality ranges

from 30-50% and incidence of neurologic from 30-50% and incidence of neurologic squelae is 75-80% especially in stage-3. squelae is 75-80% especially in stage-3. there may be blindness, deafness, there may be blindness, deafness, paraplegia, mental retardation and diabetes paraplegia, mental retardation and diabetes inspidus. inspidus.

Infants and young children have poor Infants and young children have poor prognosis as compared to older children. prognosis as compared to older children.

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ENCEPHALITISENCEPHALITIS

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DEFINITION.DEFINITION.The inflammation of the The inflammation of the brain tissue is known as brain tissue is known as Encephalitis.Encephalitis.

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It results in It results in marked cerebral dysfunction marked cerebral dysfunction and and early loss of consciousnessearly loss of consciousness. .

It is usually caused by viruses e.g. influenza, It is usually caused by viruses e.g. influenza, herpes simplex but brain tissue is also involved herpes simplex but brain tissue is also involved as part of bacterial meningitis (e.g. tuberculous as part of bacterial meningitis (e.g. tuberculous meningoencephalitis, etc.) meningoencephalitis, etc.)

Sometimes features of encephalitis occur after Sometimes features of encephalitis occur after few days of known viral infection or vaccination few days of known viral infection or vaccination and it is then called “Postinfectious” encephalitis. and it is then called “Postinfectious” encephalitis.

Neuro-logic manifestations suggestive of Neuro-logic manifestations suggestive of encephalitis but occurring in the absence of encephalitis but occurring in the absence of inflammation indicate encephalopathy. inflammation indicate encephalopathy.

General General ConsiderationConsideration

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Etiology.Etiology. Encephalitis is mainly caused by viruses. Encephalitis is mainly caused by viruses. It is caused by direct viral infection of the brain It is caused by direct viral infection of the brain

via a hematogenous or neuronal route. via a hematogenous or neuronal route. Arboviruses and enteroviruses are most Arboviruses and enteroviruses are most

commonly responsible for epidemics of acute commonly responsible for epidemics of acute encephalitis. encephalitis.

Herpes simplex is the most common cause of Herpes simplex is the most common cause of sporadic encephalitis. sporadic encephalitis.

Varicella virus commonly causes cerebellar Varicella virus commonly causes cerebellar ataxia. ataxia.

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Table shows the Causes of Viral Meningitis / Table shows the Causes of Viral Meningitis / Encephalitis.Encephalitis.

Infections Infections Post-infections Post-infections

Entero-viruses.Entero-viruses.Coxsackie.Coxsackie.

Polimyelitis.Polimyelitis.

Echo-Virus.Echo-Virus.

Myxovirus:Myxovirus:MumpsMumps

Rabies.Rabies.

Herpes Virus.Herpes Virus.Herpes Simplex.Herpes Simplex.

Herpes Zoster.Herpes Zoster.

Arthropod-borne:Arthropod-borne:Yellow Fever.Yellow Fever.

Dengue Fever.Dengue Fever.

Others.Others.LymphocyticLymphocytic

Chriomeningitis.Chriomeningitis.

Psittacosis.Psittacosis.

MeaslesMeasles

RubellaRubella

VaricellaVaricella

Pox virusPox virus

VacciniaVaccinia

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Pathophysiology.Pathophysiology.

Following ingestion or mosquito bite, the virus Following ingestion or mosquito bite, the virus infects several organs, where it multiples infects several organs, where it multiples causing a systemic febrile illness. causing a systemic febrile illness.

CNS is involved in the secondary viraemia if the CNS is involved in the secondary viraemia if the virus continues to multiply in the primary organs. virus continues to multiply in the primary organs.

The neurologic damage occurs either (1) by The neurologic damage occurs either (1) by direct invasion and destruction of neural tissues direct invasion and destruction of neural tissues by actively multiplying viruses, (2) or by reaction by actively multiplying viruses, (2) or by reaction of the patient tissues to antigens of the virus.of the patient tissues to antigens of the virus.

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Pathology.Pathology. The brain is swollen with marked vascular The brain is swollen with marked vascular

congestion, and initial polymorph response is congestion, and initial polymorph response is followed by mononuclear, lymphocyte and followed by mononuclear, lymphocyte and plasma cells infiltration. There is degeneration of plasma cells infiltration. There is degeneration of the neuronal cells and interanuclear inclusion the neuronal cells and interanuclear inclusion bodies may be present. bodies may be present.

Certain viruses appear to have an affinity for Certain viruses appear to have an affinity for invading certain parts of the brain, e.g. herpes invading certain parts of the brain, e.g. herpes simplex for fronto-temporal lobe, mumps virus is simplex for fronto-temporal lobe, mumps virus is often associated with transverse myelitis, often associated with transverse myelitis, chickenpox for cerebellum. chickenpox for cerebellum.

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Clinical Features.Clinical Features. All viruses, which cause encephalitis, can All viruses, which cause encephalitis, can

also cause meningitis. Encephalitic picture also cause meningitis. Encephalitic picture may predominate or a combined picture of may predominate or a combined picture of meningo-encephalitis may occur if meningo-encephalitis may occur if meninges are also inflamed. The clinical meninges are also inflamed. The clinical features are extremely variable. features are extremely variable.

A sudden onset of high fever and A sudden onset of high fever and headache are the first signs of the illness. headache are the first signs of the illness.

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Features of encephalitis `Features of encephalitis `

Most Common causesMost Common causes

Herpes Herpes

MeaslesMeasles

Chicken PoxChicken Pox

Polio.Polio.

Clinical featuresClinical features

FeverFever

DisturbedDisturbed

ConsciousnessConsciousness

ConvulsionConvulsion

Focal neurologic signsFocal neurologic signs

Encephalitis; Direct invasion of gray matter by infectious agent.Encephalitis; Direct invasion of gray matter by infectious agent. Post-infectious; Delayed immunologicaly mediated demyelination.Post-infectious; Delayed immunologicaly mediated demyelination. Encephalopathy: Encephalitis like illness without fever or aseptic Encephalopathy: Encephalitis like illness without fever or aseptic

meningitis (inflammation) is called encephalopathy and is due to meningitis (inflammation) is called encephalopathy and is due to toxic or metabolic causes.toxic or metabolic causes.

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Signs of central nervous system involvement Signs of central nervous system involvement occur early which vary from mild drowsiness to occur early which vary from mild drowsiness to deep coma. deep coma.

Headache, fever, irritability, mental confusion or Headache, fever, irritability, mental confusion or abnormal behavior may be marked. abnormal behavior may be marked.

Headache is common in older children whereas Headache is common in older children whereas infants may have gross irritability and feeding infants may have gross irritability and feeding difficulty. difficulty.

Focal neurological signs may occur, cranial Focal neurological signs may occur, cranial verve palsies (squint or facial palsy) speech, verve palsies (squint or facial palsy) speech, disturbances (aphasia), spastic palsies disturbances (aphasia), spastic palsies (hemiplegia, tetraplegia), cerebellar (hemiplegia, tetraplegia), cerebellar disturbances (ataxia) and abnormalities or disturbances (ataxia) and abnormalities or various reflexes. various reflexes.

Meningeal infammation may produce neck Meningeal infammation may produce neck rigidity and stiffness of back. rigidity and stiffness of back.

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some children may present with abnormal some children may present with abnormal behavior screaming spells, irritability, behavior screaming spells, irritability, confusion, tremors and stupor, muscle confusion, tremors and stupor, muscle weakness and occasionally paralysis may weakness and occasionally paralysis may occur. occur.

Spastic paraplegia with loss of bowel and Spastic paraplegia with loss of bowel and bladder control indicates spinal cord bladder control indicates spinal cord involvement. involvement.

Sensory disturbances may be present in Sensory disturbances may be present in some. Respiratory irregularities and visual some. Respiratory irregularities and visual disturbances may occur. disturbances may occur.

Occasionally myocarditis and hypotension Occasionally myocarditis and hypotension may complicate the picture. may complicate the picture.

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The clinical features usually do The clinical features usually do not point to a specific viral not point to a specific viral etiology but some types of etiology but some types of encephalitis present distinct encephalitis present distinct clinical features e.g. Herpes clinical features e.g. Herpes simplex, since it is treatable it simplex, since it is treatable it is described further.is described further.

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Herpes Simplex Encephalitis.Herpes Simplex Encephalitis.

Type-1:Type-1: infants and children typically present with fever, infants and children typically present with fever,

vomiting, and lethargy and proceed to coma and vomiting, and lethargy and proceed to coma and focal fits. focal fits.

It usually produces features of a space-It usually produces features of a space-occupying lesion in the temporal lobe like occupying lesion in the temporal lobe like hemiparesis, focal fits and raised intracranial hemiparesis, focal fits and raised intracranial pressure tentorial herniation, papilledema and pressure tentorial herniation, papilledema and decerebrate posturing may occur. decerebrate posturing may occur.

CSF examination may show xanthochromia and CSF examination may show xanthochromia and in some cases RBSs. Cell count varies between in some cases RBSs. Cell count varies between 50-5000, CSF protein is normal or moderately 50-5000, CSF protein is normal or moderately elevated with normal glucose.elevated with normal glucose.

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Type-2:Type-2:

Herpes virus type 2 causes Herpes virus type 2 causes encephalitis in the newborn following encephalitis in the newborn following vaginal delivery. Virus is acquired from vaginal delivery. Virus is acquired from maternal birth canal and results in typical maternal birth canal and results in typical

vesicular skin eruptions and encephalitis.vesicular skin eruptions and encephalitis.

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Chicken Pox Encephalitis. (1 in 1000-5000).Chicken Pox Encephalitis. (1 in 1000-5000).

Occurs 4 – 6 days after the rash but it can Occurs 4 – 6 days after the rash but it can produce the rash in some. CSF shows produce the rash in some. CSF shows 10 – 15 cells/mm3 with polys initially and 10 – 15 cells/mm3 with polys initially and lymphos later. Protein is normal or lymphos later. Protein is normal or moderately elevated with normal glucose. moderately elevated with normal glucose.

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Measles Encephalitis. Measles Encephalitis. (1 in 600-1000 with a high mortality rate)(1 in 600-1000 with a high mortality rate)

It usually develops 2 days to 2 weeks after the It usually develops 2 days to 2 weeks after the appearance of rash, rarely even before. Spinal appearance of rash, rarely even before. Spinal cord involvement with paraplegia and neurologic cord involvement with paraplegia and neurologic bladder may occur with inappropriate ADH bladder may occur with inappropriate ADH secretion. CSF reveals lymphocytic pleocytosis secretion. CSF reveals lymphocytic pleocytosis of 20 – 250 cells with slightly raised protein and of 20 – 250 cells with slightly raised protein and normal glucose. normal glucose.

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Polio – Encephalitis.Polio – Encephalitis. Occurs in 1 – 5 percent of patients showing Occurs in 1 – 5 percent of patients showing

neurological manifestation of polio infection. neurological manifestation of polio infection. Drowsiness, irritability, coarse tremors, coma Drowsiness, irritability, coarse tremors, coma

and fits indicated encephalitis in addition to the and fits indicated encephalitis in addition to the usual symptoms of paresis of limbs or brain usual symptoms of paresis of limbs or brain stem involvement.stem involvement.

Although sensory deficits are rare but these can Although sensory deficits are rare but these can occur in the presence of transverse myelitis or occur in the presence of transverse myelitis or following involvement of the posterior hours of following involvement of the posterior hours of the gray mater. the gray mater.

CSF shows mild pleocytosis of 50 – 200 cells, CSF shows mild pleocytosis of 50 – 200 cells, initially polys and later lymphos. Protein in CSF initially polys and later lymphos. Protein in CSF is moderately elevated and glucose normal. is moderately elevated and glucose normal.

Polio-encephalitis should always be considered Polio-encephalitis should always be considered in differential diagnosis, as it is common here. in differential diagnosis, as it is common here.

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MumpsMumpsMumps is commonly associated with Mumps is commonly associated with aseptic meningitis, which occurs 2 – 3 aseptic meningitis, which occurs 2 – 3 days after the onset of parotitis, but days after the onset of parotitis, but encephalitis occurs 7 – 10 days later with encephalitis occurs 7 – 10 days later with frequent convulsions and coma. Diagnosis frequent convulsions and coma. Diagnosis is confirmed by virus isolation, serological is confirmed by virus isolation, serological methods and fluorescent antibody methods and fluorescent antibody techniques techniques

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Lymphocytic Lymphocytic Choriomeningitis.Choriomeningitis.

This virus is thought to be transmitted to This virus is thought to be transmitted to man by the inhalation or ingestion of dried man by the inhalation or ingestion of dried mica excreta. After incubation period of 1 mica excreta. After incubation period of 1 week there is malaise, headache and week there is malaise, headache and myalgia usually lasting 1 – 2 weeks. It is myalgia usually lasting 1 – 2 weeks. It is followed by meningo-encephalitis. followed by meningo-encephalitis.

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Slow Viral Diseases Slow Viral Diseases

Slow Viral Diseases are manifested Slow Viral Diseases are manifested months to years after the viral infection. months to years after the viral infection. Slow CNS infection is due to prions (Small Slow CNS infection is due to prions (Small protein-aceous particles). There is protein-aceous particles). There is dementia, poor congnitive functions, and dementia, poor congnitive functions, and behavior changes. Most common viruses behavior changes. Most common viruses causing such type of disease are measles causing such type of disease are measles (subacute sclerosing panencephalitis or (subacute sclerosing panencephalitis or SSPE), rubella, HIV and HSV.SSPE), rubella, HIV and HSV.

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Diagnosis. Diagnosis.

Diagnosis is essentially clinical and by Diagnosis is essentially clinical and by exclusion of diseases such as exclusion of diseases such as

meningitis, cerebral malaria, meningitis, cerebral malaria,

brain tumor, heat stroke brain tumor, heat stroke

and lead encephalopathy. and lead encephalopathy.

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1- Lumber Puncture. 1- Lumber Puncture.

Cerebrospinal fluid should be examined to Cerebrospinal fluid should be examined to exclude bacterial and tuberculous meningitis. In exclude bacterial and tuberculous meningitis. In viral encephalitis CSF is generally clear. In viral viral encephalitis CSF is generally clear. In viral encephalitis CSF is generally clear, leukocyte encephalitis CSF is generally clear, leukocyte count varies from 10 – 5000 cells with count varies from 10 – 5000 cells with polymorph initially and lymphocytes later. There polymorph initially and lymphocytes later. There is moderate elevation of protein with normal is moderate elevation of protein with normal glucose. glucose.

2- Antibody titer.2- Antibody titer.

Serologic testing should be done twice 15 days Serologic testing should be done twice 15 days apart or demonstrate rising titer (4 fold or more)apart or demonstrate rising titer (4 fold or more)

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3- Virus Isolation.3- Virus Isolation.Viruses can be isolated from blood, CSF, faces Viruses can be isolated from blood, CSF, faces and throat swabs.and throat swabs.

4- Brain CT Scan/MRI brain.4- Brain CT Scan/MRI brain.These are helpful in localizing the process as in These are helpful in localizing the process as in focal necrotizing encephalitis (Herpes simplex).focal necrotizing encephalitis (Herpes simplex).

5- Brain Biopsy.5- Brain Biopsy.The diagnosis is established and confirmed by The diagnosis is established and confirmed by brain biopsy. It is only indicated in cases, which brain biopsy. It is only indicated in cases, which are suspected to be having herpes encephalitis are suspected to be having herpes encephalitis because specific antiviral chemotherapy is because specific antiviral chemotherapy is available. Virus is then identified by immuno-available. Virus is then identified by immuno-flouresecent technique from brain biopsy. flouresecent technique from brain biopsy.

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6-6- EEG.EEG.

infection of the brain causes very infection of the brain causes very marked disorganization of the EEG with marked disorganization of the EEG with the development of large amplitude, slow the development of large amplitude, slow waves. In herpes encephalitis there are waves. In herpes encephalitis there are large amplitude, slow waves at rate of large amplitude, slow waves at rate of 2 – 4 / Sec and these waves recur after 2 – 4 / Sec and these waves recur after every 2 sec on a background of very slow every 2 sec on a background of very slow activity in the temporal region. activity in the temporal region.

7- Blood Counts.7- Blood Counts.

these are done as routine to rule out these are done as routine to rule out bacterial infections. bacterial infections.

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Complications.Complications.

Early.Early. Hemiplegia.Hemiplegia. Squints.Squints. Deafness.Deafness. Intractable convulsions.Intractable convulsions. Bed Sores.Bed Sores. Aspirational Pneumonia, and Aspirational Pneumonia, and Urinary Tract infection from catheterization.Urinary Tract infection from catheterization.

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Late.Late. Mental Retardation.Mental Retardation. Hydrocephalus.Hydrocephalus. Epilepsy.Epilepsy. Learning Disabilities, and Learning Disabilities, and Behavior Disorders. Behavior Disorders.

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Management. Management. 1- Nursing Care.1- Nursing Care.

Nursing a comatose child Nursing a comatose child monitoring vital functions, monitoring vital functions, frequent suctioning of airways, frequent suctioning of airways, change of posture every ½-1 hours to avoid pressure sores change of posture every ½-1 hours to avoid pressure sores

and positional deformity. and positional deformity. Attention should be paid to oral hygiene, eye care, and Attention should be paid to oral hygiene, eye care, and

abdominal distension from bladder enlargement (urinary abdominal distension from bladder enlargement (urinary retention) and bowel care (ileus or severe constipation). retention) and bowel care (ileus or severe constipation).

2-2- Anticonvulsants.Anticonvulsants.Inj. Diazepam 0.2mg/kg I/V orInj. Diazepam 0.2mg/kg I/V orInj. Paraldehyde 0.15ml/kg PR.Inj. Paraldehyde 0.15ml/kg PR.Once convulsions are controlled give phenobarbitone 5-8 Once convulsions are controlled give phenobarbitone 5-8 mg/kg/day orally to prevent further convulsions.mg/kg/day orally to prevent further convulsions.

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3-3- Cerebral Edema:Cerebral Edema:

Raised intra-cranial pressure and cerebral Raised intra-cranial pressure and cerebral edema is present in most cases even edema is present in most cases even without any evidence of papilledema and without any evidence of papilledema and should be treated.should be treated.

(i).(i). dexamethasone.dexamethasone.

(ii).(ii). Mannitol Mannitol

4.4. Antiviral Drugs.Antiviral Drugs.

For herpes simplex virus infections, For herpes simplex virus infections, acyclovir is the treatment of choice. acyclovir is the treatment of choice.

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5-Intravenous Fluids.5-Intravenous Fluids.Maintain fluid and electrolyte balance. Maintain fluid and electrolyte balance. Fluids should be restricted to 60% of the Fluids should be restricted to 60% of the daily requirement and do not give dextrose daily requirement and do not give dextrose water or 0.18% saline which results in water or 0.18% saline which results in cerebral edema.cerebral edema.

6-Nutrition.6-Nutrition.Calories required are given through Calories required are given through nasogastric tube in the from of liquid and nasogastric tube in the from of liquid and semisolid diets e.g. milk, juices, soup, egg, semisolid diets e.g. milk, juices, soup, egg, etc. etc.

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7-Antibiotics. 7-Antibiotics.

Should be given until bacterial etiology is ruled Should be given until bacterial etiology is ruled out by blood and CSF examination.out by blood and CSF examination.

8-Antipyretics.8-Antipyretics.

High fever should be controlled by antipyretics High fever should be controlled by antipyretics or tepid water sponging. or tepid water sponging.

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Progonsis. Progonsis.

Most patients survive and some may have Most patients survive and some may have residual focal defects. residual focal defects.

Mortality varies from 10-50%. Mortality varies from 10-50%. The outcome is particularly poor in herpes The outcome is particularly poor in herpes

simplex encephalitis (mortality rate > 70%) simplex encephalitis (mortality rate > 70%) while better in enteroviral encephalitis. while better in enteroviral encephalitis. Encephalitis is usually severe in children > Encephalitis is usually severe in children > 1 year of age and in those presenting with 1 year of age and in those presenting with coma.coma.

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Cerebral Cerebral MalariaMalaria

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DefinitionDefinition It is a severe form of malaria It is a severe form of malaria

caused by Plasmodium caused by Plasmodium falciparum, manifesting asfalciparum, manifesting as

coma (GCS <11) coma (GCS <11) convulsions, and/orconvulsions, and/or hemoglobinuria.hemoglobinuria. OROR Malaria with coma persisting Malaria with coma persisting

for >30 min after a seizure. for >30 min after a seizure.

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EtiologyEtiology

Plasmodium falciparum is Plasmodium falciparum is transmitted from:transmitted from:

1.1. Bites of previously infected Bites of previously infected female anopheles mosquitoes.female anopheles mosquitoes.

2.2. Transfusion of infected blood.Transfusion of infected blood.

3.3. Organ transplant and by Organ transplant and by hypodermic needles. hypodermic needles.

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EpidemiologyEpidemiology The infection is usually much more The infection is usually much more

severe in young children. severe in young children. A and B blood groups are more A and B blood groups are more

protective than O groups.protective than O groups. Hemoglobin E and C are also more Hemoglobin E and C are also more

protective. protective. Fetal hemoglobin, sickle cell trait Fetal hemoglobin, sickle cell trait

and G6PD deficiency have lesser and G6PD deficiency have lesser tendency of plasmodium falciparum tendency of plasmodium falciparum infection.infection.

Malnutrition is protective as Malnutrition is protective as immunity is decreased.immunity is decreased.

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PathophysiologyPathophysiology First the Plasmodium falciparum enters the First the Plasmodium falciparum enters the

red blood cells. red blood cells. After 8 – 18 hours, these cells become After 8 – 18 hours, these cells become

increasingly sticky and tend to adhere to the increasingly sticky and tend to adhere to the endothelial lining of blood sinuses and endothelial lining of blood sinuses and vessels especially when the circulation is vessels especially when the circulation is slow. The fixed cells are unable to come slow. The fixed cells are unable to come back to the general circulation.back to the general circulation.

As more cells adhere, flow within the vessels As more cells adhere, flow within the vessels is progressively impeded and occlusion or is progressively impeded and occlusion or even rupture may occur. even rupture may occur.

The symptoms depend on the site and extent The symptoms depend on the site and extent of the occlusion of the blood vessels. The of the occlusion of the blood vessels. The lungs, brain and intestinal tract are usually lungs, brain and intestinal tract are usually more affected.more affected.

The parasites keep maturing in the infected The parasites keep maturing in the infected cells even when they are fixed to the cells even when they are fixed to the endothelium or sinuses.endothelium or sinuses.

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The release of merozoites, where The release of merozoites, where the circulation is slowed, facilitates the circulation is slowed, facilitates the invasion of nearby red blood the invasion of nearby red blood cells.cells.

Plasmodium falciparum invades all Plasmodium falciparum invades all erythrocytes irrespective of age and erythrocytes irrespective of age and so parasitemia in a non-immune so parasitemia in a non-immune child may be very heavy.child may be very heavy.

One schizont yields 8 – 32 One schizont yields 8 – 32 merozoites, the highest of all the merozoites, the highest of all the species.species.

Its incubation period is 10 – 13 daysIts incubation period is 10 – 13 days

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PathologyPathology When the parasitized red blood cells When the parasitized red blood cells

attach to the endothelium of venules and attach to the endothelium of venules and capillaries, the inflammatory process capillaries, the inflammatory process start around them. There is hemorrhage start around them. There is hemorrhage and necrosis around these vessels.and necrosis around these vessels.

All these lead to the blockage of vessels All these lead to the blockage of vessels by parasitized red blood cells. Fibrin by parasitized red blood cells. Fibrin thrombi may also form in the arterioles thrombi may also form in the arterioles and capillaries giving a picture of DIC. and capillaries giving a picture of DIC. The same process in the brain lead to the The same process in the brain lead to the cerebral edema. cerebral edema.

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The immunofourescence has shown the The immunofourescence has shown the deposition of plasmodium falciparum deposition of plasmodium falciparum antigen and antibody complex in antigen and antibody complex in capillaries. There are two suggested capillaries. There are two suggested ways to explain:ways to explain:

ICAM (Intercellular Adhesion Molecule) ICAM (Intercellular Adhesion Molecule) medicated increased adherence of medicated increased adherence of RBC’s to the endothelium of cerebral RBC’s to the endothelium of cerebral vessels.vessels.

NO (Nitric oxide) mediated increased NO (Nitric oxide) mediated increased fragility and destruction of cerebral fragility and destruction of cerebral matter. matter.

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Clinical FeaturesClinical Features The characteristic adult pattern of cerebral The characteristic adult pattern of cerebral

malaria is not present in children especially malaria is not present in children especially under 5 years of age.under 5 years of age.

The clinical signs and symptoms usually The clinical signs and symptoms usually start after 8-15 days of infection.start after 8-15 days of infection. Initially Initially there are behavior changes like anorexia, there are behavior changes like anorexia, fretfulness, unusual crying, drowsiness, or fretfulness, unusual crying, drowsiness, or disturbance of sleep.disturbance of sleep.

Fever may be absent or increase gradually for Fever may be absent or increase gradually for 1-2 days or the onset may be sudden with 1-2 days or the onset may be sudden with high-grade temperature with or without high-grade temperature with or without prodromal chill.prodromal chill.

The complaints include headache, nausea, The complaints include headache, nausea, generalized aching, particularly of the back. generalized aching, particularly of the back.

When the spleen has enlarged quickly and is When the spleen has enlarged quickly and is tender, there can be pain in the abdomen.tender, there can be pain in the abdomen.

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Cerebral symptomsCerebral symptoms are evidenced by are evidenced by convulsions or coma. The neurologic convulsions or coma. The neurologic signs in infants and children are those of signs in infants and children are those of increased intracranial pressure and increased intracranial pressure and symmetric upper motor neuron and symmetric upper motor neuron and brainstem disturbances such as brainstem disturbances such as disconjugate gaze and decerebrate and disconjugate gaze and decerebrate and decorticate postures.decorticate postures.

There is severe pallor and splenomegaly There is severe pallor and splenomegaly (or hepatosplenomegaly; liver may only (or hepatosplenomegaly; liver may only be enlarged at times).be enlarged at times).

The classic picture of a child with high-The classic picture of a child with high-grade fever who is unconscious and grade fever who is unconscious and convulsing cannot be mistaken.convulsing cannot be mistaken.

There is no neck rigidity (except There is no neck rigidity (except abnormal posturing).abnormal posturing).

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DiagnosisDiagnosis1.1. CBCCBC

Leucopenia is variable.Leucopenia is variable. Monocytosis is common.Monocytosis is common. AnemiaAnemia Reticulocyte count increasedReticulocyte count increased..

2.2. Thick and thin blood filmThick and thin blood film: (most specific : (most specific test)test)

Initially ring forms are seen and after 10 Initially ring forms are seen and after 10 days crescents (gametocytes) are seen.days crescents (gametocytes) are seen.

Up to 20 % of RBC’s may be infected. Up to 20 % of RBC’s may be infected. Negative if antimalarials are given.Negative if antimalarials are given.

3.3. CSFCSF:: Usually normal if no associated Usually normal if no associated

meningitismeningitis

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4.4. Serum electrolytesSerum electrolytes..5.5. Blood sugarBlood sugar: : hypoglycemia.hypoglycemia.6.6. Detection of parasitic antigen:Detection of parasitic antigen:

a.a. ICT – MalariaICT – Malariab.b. DNA / RNA are detected DNA / RNA are detected with with probes.probes.

7.7. Serological tests: Serological tests: Not very Not very specific but species specific specific but species specific antibodies can be detected.antibodies can be detected.

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ManagementManagementSupportive treatmentSupportive treatmentAnemiaAnemia Give blood transfusion if hemoglobin <6 Give blood transfusion if hemoglobin <6

gm %. (Pack cells 10 mlkg).gm %. (Pack cells 10 mlkg).

HypoglycemiaHypoglycemia:: Give 50 % glucose bolus I/V stat and then Give 50 % glucose bolus I/V stat and then

regular glucose supplements with 10 % regular glucose supplements with 10 % dextrose water.dextrose water.

Renal FailureRenal Failure:: Increase hydration Increase hydration May require dialysis.May require dialysis. Decrease the dose of anti-malarial to 1/3Decrease the dose of anti-malarial to 1/3. .

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ConvulsionsConvulsions:: Diazepam 0.3 – 0.5 mg IV slow;Diazepam 0.3 – 0.5 mg IV slow; Phenobarbitone (10 mg/kg PO/NG tube stat, Phenobarbitone (10 mg/kg PO/NG tube stat,

then maintenance dose 5 mg/kg/day in 2 then maintenance dose 5 mg/kg/day in 2 divided doses).divided doses).

Paraldehyde (0. 15 ml/kg P/R).Paraldehyde (0. 15 ml/kg P/R).

Lowering of high temperature.Lowering of high temperature. Tepid sponging or paracetamol orally by N/G Tepid sponging or paracetamol orally by N/G

tube.tube.

FluidsFluids:: 5% dextrose saline 20-40ml/kg in 30 minutes or 5% dextrose saline 20-40ml/kg in 30 minutes or

dextran 75%.dextran 75%. Late shift to 5% dextrose 1/5 saline.Late shift to 5% dextrose 1/5 saline. Total fluid 100-150 ml/kg/day.Total fluid 100-150 ml/kg/day.

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Specific Treatment.Specific Treatment. Start IV Start IV anti-malarial anti-malarial and then shift to oral when and then shift to oral when

the patient becomes conscious.the patient becomes conscious.1 injection quinine dihydrochloride1 injection quinine dihydrochloride (300 mg/1 ml (300 mg/1 ml

vial).vial). 20 mg/kg IV stat, then 10 mg/kg IV-8 hourly for 7 20 mg/kg IV stat, then 10 mg/kg IV-8 hourly for 7

days (1 mg in 1 ml of 5% dextrose water over 2-4 days (1 mg in 1 ml of 5% dextrose water over 2-4 hours. hours.

8.3 mg quinine base = 10 mg quinine 8.3 mg quinine base = 10 mg quinine dihydrochloride.dihydrochloride.

Injection ArtemethrineInjection Artemethrine:: It is also use in these daysIt is also use in these days Dose 3.2 mg/kg IM stat then 1.6 mg/kg/day for 2 days.Dose 3.2 mg/kg IM stat then 1.6 mg/kg/day for 2 days.2 2 Injection Choloroquine dihydrochloride: (200 Injection Choloroquine dihydrochloride: (200

mg/5ml vial)mg/5ml vial) 5 mg/kg in 10 ml/kg of isotonic saline in 3-4 hours, 5 mg/kg in 10 ml/kg of isotonic saline in 3-4 hours,

then repeat same dose at 6 hours, then give 5mg/kg then repeat same dose at 6 hours, then give 5mg/kg daily for 3 days.daily for 3 days.

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Quinine SulphateQuinine Sulphate:: 10 mg/kg/dose – 8 hourly for 4-7 days 10 mg/kg/dose – 8 hourly for 4-7 days

PO.PO.Chloroquin phosphate / Chloroquin phosphate / hydrochlorosuin sulphate:hydrochlorosuin sulphate:

10 mg/kg stat10 mg/kg stat Then 10 mg/kg next dayThen 10 mg/kg next day Then 5 mg/kg next dayThen 5 mg/kg next day Injection chloroquin Injection chloroquin

dihydrochloride: (200 mg/5ml dihydrochloride: (200 mg/5ml vial)vial)

5 mg/kg in 10 ml/kg of isotonic saline 5 mg/kg in 10 ml/kg of isotonic saline in 3-4 hours, then repeat same dose in 3-4 hours, then repeat same dose at 6 hours, then give 5mg/kg daily for at 6 hours, then give 5mg/kg daily for 3 days.3 days.

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Differential Diagnosis.Differential Diagnosis. Febrile FitsFebrile Fits: Age 6 months – 6 years, patient : Age 6 months – 6 years, patient

is arousable, CSF clear.is arousable, CSF clear. Pyogenic meningitisPyogenic meningitis: Toxic ill patient. Signs : Toxic ill patient. Signs

of meningeal irritation positive. CSF is turbid of meningeal irritation positive. CSF is turbid and abnormal.and abnormal.

Viral encephalitisViral encephalitis: Anemia, coagulo-pathy : Anemia, coagulo-pathy and malarial parasite is absent. CSF may be and malarial parasite is absent. CSF may be normal with increased proteins and normal with increased proteins and pleocytosis.pleocytosis.

SOLSOL: Increased ICP evidenced by vomiting, : Increased ICP evidenced by vomiting, headache, diplopia and papill-edema.. headache, diplopia and papill-edema.. Localizing signs and cranial nerve palsies are Localizing signs and cranial nerve palsies are present. Malarial parasite is absent. MRI/CT present. Malarial parasite is absent. MRI/CT scan confirm.scan confirm.

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Hepatic comaHepatic coma: Deep jaundice and : Deep jaundice and less anemia. Liver is usually smaller. less anemia. Liver is usually smaller. LFT’s gross abnormality. Coagulation LFT’s gross abnormality. Coagulation defects. Decreased serum proteins defects. Decreased serum proteins and especially serum albumin. and especially serum albumin. Malarial parasite is negative.Malarial parasite is negative.

Hypoglycemic comaHypoglycemic coma: Afebrile, : Afebrile, cold and sweating. Jaundice, anemia, cold and sweating. Jaundice, anemia, bleeding and MP are absent. Serum bleeding and MP are absent. Serum sugar is <40 mg%.sugar is <40 mg%.

UremiaUremia: H/o preceding edema, : H/o preceding edema, diarrhea, and vomiting. Hematuria, diarrhea, and vomiting. Hematuria, dysuria and recurrent abdominal pain. dysuria and recurrent abdominal pain. H/O previous UTI or renal stones. H/O previous UTI or renal stones.

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Criteria for cerebral malaria Criteria for cerebral malaria diagnosisdiagnosis

CNSCNS:: Unarousable or coma > 6 hours.Unarousable or coma > 6 hours. Focal or generalized fits.Focal or generalized fits. Posture (opisthotonic, Posture (opisthotonic,

decerebrate, decorticate).decerebrate, decorticate). Conjugate deviation of the eyes. Conjugate deviation of the eyes. Retinal hemorrhages.Retinal hemorrhages.

RenalRenal:: Urine output < 400 ml/day.Urine output < 400 ml/day. Serum creatinine > 3 mg%.Serum creatinine > 3 mg%.

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PrognosisPrognosis Mortality of cerebral malaria ranges Mortality of cerebral malaria ranges

from 10-30 %.from 10-30 %. Death in most of the cases occur Death in most of the cases occur

within 24 hours of admission / within 24 hours of admission / treatment.treatment.

Some children have a rapid and Some children have a rapid and progressive recovery, but most of the progressive recovery, but most of the time duration of impaired time duration of impaired consciousness after treatment being consciousness after treatment being started ranges form few hours to started ranges form few hours to several days. several days.

Majority of the surviving children had Majority of the surviving children had a full recovery but about 10% have a a full recovery but about 10% have a permanent neurologic deficit.permanent neurologic deficit.

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Thank you