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Acute CNS infection

Cnsinfection

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Page 1: Cnsinfection

Acute CNS infection

Page 2: Cnsinfection

• 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?

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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

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Risk of infection

• Pneumococci

OM, sinusitis, pneumonia, CSF rhinorrhea.

• Meningococci

contact with adults, nasopharyngeal carriage

• HIB

Contact 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.

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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

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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.

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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 -ve

Antigens +ve

Viral

meningitis

Normal Less cells,

lymphocytes

N, less in

mumps

<200

TBM More <500,

lymphocytes

<40 100-3000 Stain –ve

Culture ± 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.

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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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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