Acute CNS infection

• 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?

Significance

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

• Diagnosis, challenging in young children• High incidence of sequalae

• Fever with altered sensorium• Virus > bacteria > fungi & parasite• Meningitis• Meningoencephalitis• Brain abscess• Common symptoms

photophobia,neckpain/rigidity,stupor,fits• Diagnosis by CSF

Pyogenic meningitis

Etiology

• < 2months• Maternal flora; NICU/PNW flora;• GBS, GDS, gram-ve, listeria, HIB,

• 2m-12m• Pneumococci, meningococci, HIB[now less]• Pseudomonos, staph.aureus, CONS.

Reasons for infection

• Less immunity• Contact with people with invasive disease• Occult bacteremia [infants]• Immunodeficiency• Splenic dysfunction• CSF leak ,Meningomyelocele• CSF shunt infection

Risk of infection

• Pneumococci OM, sinusitis, pneumonia, CSF rhinorrhea.

• Meningococci contact with adults, nasopharyngeal carriage

• HIBContact in daycare centre

Pathogenesis

• Colonisation of nasopharynx• Prior/concurrent viral URTI• Bacteremia

• Hematogenous dissemination• Contiguous spread from sinus, otitis, orbit

vertebral trauma, meningocele.

Why few only get meningitis?

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

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• Inc.vascular permeability• Altered BBB• Vascular thrombosis

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

Clinical features • Nonspecific

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

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

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

• Focal neurological deficit• Cranial neuropathy

– 3rd nerve– 6th nerve– 7th nerve– 8th nerve

Diagnosis

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

• Blood culture

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

CSF analysis in prior antibiotic therapy

• Culture, gramstain altered• Pleocytosis, protein, glucose unaltered

Traumatic LP

• Cell count,protein level altered• Glucose, bacteriology unaltered.

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

Treatment • Rapidly progressive [ ~24h]

LP antibioticsICT , FND CTbrain & antibioticsManage shock, ARDS

• Subacute course [4-7d]• Assess for ICT, FND• Antibiotics CT LP

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

Antibiotic therapy• Vancomycin & cefataxime/ceftrioxone

– Pneumococci,meningococci,HIB.• Ampicillin / cotrimaxazole I.V

– Listeria • Ceftazidime & aminoglycoside

– Immunocompromised

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.

Repeat LP

• After 48h• For ; resistant pneumococci,

gram-ve meningitis

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.

Complications • ICT, Herniation• Fits, Cranial N palsy• Dural V sinus thrombosis• Subdural effusion• SIADH• Pericarditis, Arthritis• Anemia, DIC

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,

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

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.

• Brainstem affected• Cranial N dysfunction• Hydrocephalus • Infarcts • Cerebral edema• SIADH• Dyselectrolytemia

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

Diagnosis • Contact with adult TB• Mx nonreactive 50%• CSF – lymphocytes• Glucose <40mg/dl• Protein high: 400-5000mg/dl• AFB +ve 30%

Thank you

Meningoencephalitis

• Acute inflammation of meninges & brain tissue

• CSF – pleocytosis• Gram stain & culture negative• Mostly self limiting

Etiology

• Enterovirus• Arbovirus• Herpes virus

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

Structures affected

• HSV; temporal lobe• Arbovirus; entire brain• Rabies; basal parts

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]

DD

• Meningitis of various organisms

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

Treatment

• Acyclovir for HSV• Non aspirin analgesic• Nurse in a quiet room