cns infection in chidren

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Page 1: Cns infection in chidren
Page 2: Cns infection in chidren

Acute CNS infection

Page 3: Cns infection in chidren

• What is it?

• What causes it?

• What happens in the system?

• How to recognize it?

• How to prove it?

• How to treat it?

• How to prevent?

Page 4: Cns infection in chidren

Significance

• Significant morbidity & mortality in children [1.2m cases worldwide]

• Diagnosis, challenging in young children

• High incidence of sequalae

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• Fever with altered sensorium

• Virus > bacteria > fungi & parasite

• Meningitis

• Meningoencephalitis

• Brain abscess

• Common symptoms

photophobia, neckpain/rigidity, fits, stupor

• Diagnosis by CSF

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Pyogenic meningitis

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Etiology

• < 2months• Maternal flora, NICU/PNW flora;

• GBS, GDS, gram-ve, listeria, HIB,

• 2m-12m• Pneumococci, meningococci, HIB[now less]

• Pseudomonos, staph.aureus, CONS.

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Reasons for infection

• Less immunity

• Contact with people with invasive disease

• Occult bacteremia [infants]

• Immunodeficiency

• Splenic dysfunction

• CSF leak , Meningomyelocele

• CSF shunt infection

Page 10: Cns infection in chidren

Risk of infection

• Pneumococci OM, sinusitis, pneumonia, CSF rhinorrhea.

• Meningococci contact with adults, nasopharyngeal carriage

• HIBContact in daycare center

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Pathogenesis

• Colonisation of nasopharynx

• Prior/concurrent viral URTI

• Bacteremia

• Hematogenous dissemination

• Contiguous spread from sinus, otitis, orbit

vertebral trauma, meningocele.

Page 12: Cns infection in chidren

Why few only get meningitis?

• Defective opsonic phagocytosis– Developmental defects– Absent preformed anticapsular antibodies– Deficient complement/properdin system– Splenic dysfunction

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Pathogenesis • Bacteria enter through choroid plexus of LV• Circulate to extra cerebral CSF & subarachnoid space• Rapidly multiply in CSF• Release of inflammatory mediators• Neutrophilic infiltrates• Increase vascular permeability• Altered BBB• Vascular thrombosis

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Pathology

• Thick exudate covering all areas

• Ventriculitis, arteritis, thrombosis

• Vascular occlusion, sinus occlusion.

• Cortical necrosis, cerebral infarct

• Subarachnoid hemorrhage

• Hydrocephalus

• ICT, inflammation of spinal nerves

Page 15: Cns infection in chidren

Clinical features • Nonspecific

– Fever,anorexia,myalgia,arthralgia,headache,– Purpura , petechiae, rash, photophobia.

• Meningeal signs– Neck rigidity, backache.– Kernig sign– Brudzinski sign– Crossed leg sign

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ICT signs

Headache, vomiting, drowsy, Fits Ptosis, squint, AF bulge, widened sutures Hypertension, bradycardia Stupor, coma Abnormal posturing Papilloedema [only in chronic ICT]

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• Focal neurological deficit

• Cranial neuropathy– 3rd nerve– 6th nerve– 7th nerve– 8th nerve

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Diagnosis

• LP & CSF analysis– Gram stain– Culture– Cell count– Glucose, protein– [Contraindications for LP]

• Blood culture

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CSF analysis• Cell count

– Normal• NB >30/mm3

• Child >5/mm3

– Meningitis >1000/mm3• Turbid 200-400/mm3

• Early; lymphocytic predominance

• Later; neutrophilic predominance

• low in severe sepsis

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CSF analysis in prior antibiotic therapy

• Culture, gramstain altered

• Pleocytosis, protein, glucose unaltered

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Traumatic LP

• Cell count, protein level altered

• Glucose, bacteriology unaltered.

Page 31: Cns infection in chidren

Condition Pressure mm-h2o

Cell count/mm3 Glucose mg/dl

Protein mg/dl

microbiology

Normal 50-80 <5,lymphocyte >50, 75% of blood level

20-40mg

Bacterial meningitis

100-300 100-1000, >75% neutrophils

<40mg 100-500 Gram stain+ve

Partially treated meningitis

N / elevated

5-1000,Lymphocytes?

N /decreased 100-500 Gramstain ,c/s maybe -veAntigens +ve

Viral meningitis

Normal Less cells,lymphocytes

N, less in mumps

<200

TBM More <500,lymphocytes

<40 100-3000 Stain –veCulture ± ve

Fungal More 5-500 N More? Culture

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Treatment • Rapidly progressive [ ~24h]

LP antibiotics

ICT , FND CTbrain & antibiotics

Manage shock, ARDS

• Subacute course [4-7d]

• Assess for ICT, FND

• Antibiotics CT LP

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Supportive care• Monitoring

– Vitals– BUN,electrolytes,HCO3,IO, CBC,Platelets,Ca– Periodic neurologic assessment

• PR,sensorium,power,cranial N ex, head circ,

• Supportive care– IVF restrict for ICT,SIADH, more for shock – ICT ETI & ventilation,frusemide,mannitol– Seizures diazepam,phenytoin

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Antibiotic therapy• Vancomycin & cefataxime/ceftrioxone

– Pneumococci,meningococci,HIB.

• Ampicillin / cotrimaxazole I.V– Listeria

• Ceftazidime & aminoglycoside– Immunocompromised

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Duration of therapy

Pneumococci : 7-10 days Menigococci: 5-7 days HIB; 7-10 days E.coli,Pseudomonos ; 3 weeks Antibiotics started before LP [partially

treated meningitis] ; ceftrioxone 7-10 days.

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Repeat LP

• After 48h

• For ; resistant pneumococci, gram-ve meningitis

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Corticosteroids

• Rapid bacterial killing

• Cell lysis

• Release of inflammatory mediators

• Edema

• Neutrophilic infiltration

• 1-2h before antibiotics

• Dexamathasone q6h for 2 days.

• Less fever, less deafness.

Page 38: Cns infection in chidren

Complications • ICT, Herniation

• Fits, Cranial N palsy

• Dural Vein sinus thrombosis

• Subdural effusion

• SIADH

• Pericarditis, Arthritis

• Anemia, DIC

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Prognosis

• Mortality >10% [more in pneumococci]

• Prognosis poor in– Infants– Fits >4days– Coma, FND on presentation

• Neurological sequalae 20%– Behavior changes 50%– Deafness [pneumo,HIB], visual loss– MR,fits,

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Prevention

• Meningococci– Rifampacin for close contacts [10mg/kg/day q12h for 2days]– Quadrivalent vaccine for high risk children

• HIB– Rifampacin for contacts for 4days– Conjugate vaccine

• Pneumococci – Heptavalent conjugate vaccine

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Thank you

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TBM

• Subacute / ?chronic meningitis

• From lymphohematogenous dissemination

• Caseous lesion in cortex / meninges

• Discharge of TB bacilli in CSF

• Thick exudate infiltrate blood vessels

• Inflammation,obstruction,infarct.

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• Brainstem affected

• Cranial N dysfunction

• Hydrocephalus

• Infarcts

• Cerebral edema

• SIADH

• Dyselectrolytemia

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Features • 6m-4yrs

• 3 stages

• Prodrome stage; 1-2 wks, nonspecific symptoms, stagnant development

• Abrupt stage;lethargy,fits,meningeal signs focal ND,cranial neuropathy,hydrocephalus.

Encephalitic picture

• Coma stage; posturing,hemi/paraplegia,poor vital signs

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Diagnosis • Contact with adult TB

• Mx nonreactive 50%

• CSF – lymphocytes

• Glucose <40mg/dl

• Protein high: 400-5000mg/dl

• AFB +ve 30%

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Thank you

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Meningoencephalitis

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• Acute inflammation of meninges & brain tissue

• CSF – pleocytosis

• Gram stain & culture negative

• Mostly self limiting

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Etiology

• Enterovirus

• Arbovirus

• Herpes virus

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Pathogenesis

• Direct invasion & destruction by virus• Host reaction to viral antigens• Meningeal congestion• Mononuclear infiltration• Neuronal disruption• Neuronophagia• Demyelination

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Structures affected

• HSV; temporal lobe

• Arbovirus; entire brain

• Rabies; basal parts

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Clinical features• Depends on parenchymal involvement• Preceding mild febrile illness & exantheme• Acute onset of high fever, headache,

irritability,lethargy,nausea,myalgia• Convulsions,stupor,coma• Fluctuating FND,emotional outburst• Ant.horn cell injuryflaccid paralysis [west

nile,entero virus]

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DD

• Meningitis of various organisms

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Diagnosis • CSF: lymphocytic predominance

– Protein: normal,high in HSV– Glucose: normal,low in mumps– Culture of organism [entero V]– Viral antigen by PCR– Culture from NPswab,feces,urine

• EEG: focal seizures [temporal];HSV• CT/MRI: swollen brain parenchyma

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Treatment

• Acyclovir for HSV

• Non aspirin analgesic

• Nursing in a quiet room