Neonatal Meningitis

Atman Shah (4th 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

Incidence essentially unchanged in the past 20 years

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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.
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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

Pathogenic Event
Colonization and mucosal invasion,

Host Defense
1. Secretory IgA 2. Cellular cilia activity 3. Mucosal epithelium

Bacterial Evasion Mechanism

IgA protease secretion Ciliostasis Adhesive pili Blockage of Alternative Compliment Pathway by Mechanisms on the cell surface Passage through tight junctions between cells, mechanism unknown Rapid bacterial replication

Survival in the blood stream

Activation of Complement Pathways

Crossing the blood-brain barrier

Cerebral endothelium

Survival within the CSF

Poor opsonic activity

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

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Presentation
Classic Signs
Headache Photophobia Stiff neck Change in mental status Bulging fontanelle Nausea Vomiting
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Bulging fontanel

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

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Presentation: Disease Progression

Insidious (90%)
High likelihood of early presentation with nonspecific illness Typical of pneumococcal illness

Fulminant (10%)
Typical of meningococcal illness May progress rapidly to petechiae, purpura fulminans, cardiovascular collapse
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Differential Diagnosis (Early Stage)

Gastroenteritis Upper respiratory infection Pneumonia Otitis media Viral syndrome

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Differential Diagnosis (Late Stage)

Encephalitis Subarachnoid/Subdural Hemorrhage Cerebral Abscess Reyes Syndrome Toxic Ingestions Seizure Disorders DKA or other altered metabolic states Hypothyroidism Intussusception
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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

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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
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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

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Meningitis with frontal subdural enhancing effusions

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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

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CSF Analysis Interpretation

Bacterial Etiology
Elevated wbc count Predominantly polymorphonuclear leukocytes Low glucose High protein Low wbc count Predominantly mononuclear cell type Normal glucose Normal protein
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Viral Etiology

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
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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

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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

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The End

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