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Neonatal Meningitis

Neonatal Meningitis. Atman Shah (4 th Year). Introduction. Epidemiology Etiology Pathophysiology Clinical Presentation Diagnosis Management. Epidemiology- Neonatal Meningitis. 0.6 – 1.3 cases/1000 live births Etiology Group B Streptococcus Escherichia coli Listeria monocytogenes

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Neonatal Meningitis

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  1. Neonatal Meningitis Atman Shah(4th Year)

  2. Introduction • Epidemiology • Etiology • Pathophysiology • Clinical Presentation • Diagnosis • Management

  3. Epidemiology- Neonatal Meningitis • 0.6 – 1.3 cases/1000 live births • Etiology • Group B Streptococcus • Escherichia coli • Listeria monocytogenes • Incidence essentially unchanged in the past 20 years

  4. Morbidity/Mortality • In developed countries, the rate of mortality from bacterial meningitis among neonates has declined from almost 50% in the 1970s to less than 10% in the late 1990s. Morbidities found in a Study: • In a prospective sample of more than 1500 neonates surviving until age 5 years, the prevalence of neuromotor disabilities including cerebral palsy was 8.1%, learning disability 7.5%, seizures 7.3%, and hearing problems 25.8% (Bedford, 2001). • No problems were reported in 65% of babies who survived group B streptococcal (GBS) meningitis and in 41.5% of those who survived Escherichia coli meningitis.

  5. Pathophysiology • Hematogenous spread • blood to subarachnoid space • Mechanical disruption • Fracture of the base of the skull • Direct extension from ear, mastoid air cells, sinuses, orbit or other adjacent structure

  6. Pathogenic Event Host Defense Bacterial Evasion Mechanism Colonization and mucosal invasion, 1. Secretory IgA 2. Cellular cilia activity 3. Mucosal epithelium IgA protease secretion Ciliostasis Adhesive pili Survival in the blood stream Activation of Complement Pathways Blockage of Alternative Compliment Pathway by Mechanisms on the cell surface Crossing the blood-brain barrier Cerebral endothelium Passage through tight junctions between cells, mechanism unknown Survival within the CSF Poor opsonic activity Rapid bacterial replication

  7. Pathophysiology (cont.) • Pathologic changes of meningitis • Directly due to infection • Indirectly due to infection via the response of the immune system to infection

  8. Presentation • Classic Signs • Headache • Photophobia • Stiff neck • Change in mental status • Bulging fontanelle • Nausea • Vomiting

  9. Bulging fontanel

  10. Presentation (cont.) • Signs of Meningeal Irritation • Brudzinski Sign: when the inflamed meninges are stretched with neck flexion, the hips and knees involuntarily flex. • Kernig Sign: when the hip is flexed to 900 , examiner is unable to passively extend the leg fully. • Children with meningeal irritation often resist walking or being carried • Absence does not rule out intracranial infection • Not useful in neonates and young infants

  11. Presentation (Neonates) • Less obvious signs and symptoms • Poor Feeding • Irritability • Inconsolability • Listlessness

  12. Presentation: Disease Progression • Insidious (90%) • High likelihood of early presentation with non-specific illness • Typical of pneumococcal illness • Fulminant (10%) • Typical of meningococcal illness • May progress rapidly to petechiae, purpura fulminans, cardiovascular collapse

  13. Differential Diagnosis (Early Stage) • Gastroenteritis • Upper respiratory infection • Pneumonia • Otitis media • Viral syndrome

  14. Differential Diagnosis (Late Stage) • Encephalitis • Subarachnoid/Subdural Hemorrhage • Cerebral Abscess • Reye’s Syndrome • Toxic Ingestions • Seizure Disorders • DKA or other altered metabolic states • Hypothyroidism • Intussusception

  15. Management: Unstable Patient • Always assure stability of vital functions before attempting diagnostic procedures • Withhold lumbar puncture until after stabilization and antibiotic administration • Shock: rapid intravenous or intraosseous infusion of crystalloid solution • Limit fluids to maintenance rate after stabilized • Fluid overload can lead to worsening of cerebral edema

  16. Management: Elevated Intracranial Pres. • Recognition: worsening mental status, papilledema, bulging fontanelle, widening of sutures • Treatment • Elevate head of bed to 300 • Controlled ventilation to keep PCO2 between 30 and 35 mmHg • Mannitol, 0.25 – 1 g/kg

  17. Management: Stable Patient • Phlebotomy for diagnostic studies • Complete Blood Count • Serum Electrolytes • Blood Glucose • Renal Functions • Blood Culture • Lumbar Puncture for Cerebrospinal Fluid Analysis • CT Scan

  18. Meningitis with frontal subdural enhancing effusions

  19. Normal Values CSF in Infants/Neonates • Cell count: 0-7 wbc/mm3 (0% PMNs) • Glucose: 40-80 mg/dL (> 50% of Blood Sugar) • Protein: 5-40 mg/dL

  20. CSF Analysis Interpretation • Bacterial Etiology • Elevated wbc count • Predominantly polymorphonuclear leukocytes • Low glucose • High protein • Viral Etiology • Low wbc count • Predominantly mononuclear cell type • Normal glucose • Normal protein

  21. INITIAL ANTIBIOTIC TREATMENT • Ampicillin, 100 mg/kg AND • Aminoglycoside • Gentamicin, 2.5 mg/kg • Cephalosporin active against gram negative bacilli may be used instead of an aminoglycoside • Cefotaxime, 50 mg/kg

  22. Antibiotic Treatment(Known/Suspected Pneumococcal Infection) • Penicillin and cephalosporin resistance is possible • Vancomycin is the only antibiotic to which all strains of pneumococci are susceptible • Add Vancomycin, 15 mg/kg

  23. Corticosteroid Treatment • Dexamethasone, 0.15 mg/kg IV administered prior to or along with the initial antibiotics has been shown to decrease ICP, cerebral edema & CSF lactate. • Significantly decreases neurologic sequelae, including deafness

  24. The End

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