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7. Meningitis

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ACUTE BACTERIAL

MENINGITIS
Yafet Solomon, MD
OUTLINE

Introduction
Etiologies and risk factors
Clinical presentation
Diagnosis
Complications
Treatment
Prognosis
Prevention
INTRODUCTION

Viruses > bacteria > fungi > parasites (inorder


of frequency in causing CNS infections)

Meningitis
Encephalitis
Brain abscess
Myelitis
Subdural empyema/abscess
Epidural empyema/abscess etc
Common bacterial etiologies of meningitis and
risk factors
Streptococcus Age less than 2 years,
Pneumoniae Sickle cell disease,
immune-compromised
children, children with
cochlear implants,
unvaccinated
Neisseria Viral upper respiratory
meningitidis infetions like influenza,
smoke exposure
Hemophilus Sickle cell disease,
influenzae immune-compromised
children, asplenia,
parental smoking, short
duration of breast feeding,
EPIDEMIOLOGY

Age distribution
 H. influenzae, peak age 6months

 N. meningitidis, children 5-14 years

 S. pneumoniae children<1 year, and adults


EPIDEMIOLOGY, CONTD.
Epidemic meningococcal disease in
African
Meningitis Belt
 Epidemics occur every 5- 10 years
 Epidemics occur in dry season
 Peak age group 5-14 years
 Epidemic thresholds

15 cases/100,000 population/wk
(Population>30,000)
5 cases/wk (Population<30,000)
OTHER RISK FACTORS
Lack of immunity associated with young
age.

Male gender.

Infants & young children with occult


bacteremia

Defects of the complement system (C5-


C8) and
OTHER RISK FACTORS
T-lymphocyte defects (L. monocytogenes)

Congenital or acquired CSF leak


(pneumococcus)

Lumbosacral dermal sinus and


meningomyelocele
(staphylococcal & gram-negative enteric
bacteria)
PATHOGENESIS
The mode of transmission is probably person-
to-person contact through respiratory tract
secretions or droplets.

Bacteria gain entry to the CSF through choroid


plexus of the lateral ventricles and the meninges
and then circulate to the extracerebral CSF and
subarachnoid space. Bacteria rapidly multiply
because
the CSF concentrations of complement and antibody
are inadequate to contain bacterial proliferation.
PATHOGENESIS
A meningeal purulent exudate may be
distributed around the cerebral veins, venous
sinuses, convexity of the brain, & cerebellum &
in the sulci, sylvian fissures, basal cisterns, and
spinal cord.

Inflammation of spinal nerves and roots


produces meningeal signs,
CLINICAL MANIFESTATIONS
Initially - Nonspecific SSx & Signs (fever, URT or GI
SSx,
lethargy, irritability, tachycardia, hypotension,

cutaneous signs - petechiae)

Meningeal irritation
nuchal rigidity + pain,
Kernig sign (flexion of the hip 90 degrees with
subsequent
pain with extension of the leg), and
Brudzinski sign (involuntary flexion of the knees
and hips
CLINICAL
MANIFESTATIONS
Increased ICP

headache, emesis
bulging fontanel or diastasis (widening) of the
sutures
oculomotor (anisocoria, ptosis) or abducens
nerve
paralysis,
hypertension with bradycardia, apnea or
hyperventilation,
decorticate or decerebrate posturing, stupor,
coma, or
CLINICAL
MANIFESTATIONS
Focal neurologic signs

Cranial neuropathies of CN 2, 3, 6, 7 & 8

Seizures (focal or generalized)

Alterations of mental status


TESTING FOR
MENINGEAL IRRITATION
DIAGNOSIS
LAB DIAGNOSIS
CSF analysis
Peripheral WBC count + differential
Blood & CSF cultures
Bacterial antigen testing
PCR of CSF & blood
CT scan (for dx of complications)
CSF EXAMINATION
CSF parameter Typical finding
Opening pressure 200 - 500mmH2O
White blood cell count 1000 - 5000/mm3; %Neutrophils
>80%
Protein 100-500 mg/dl
Glucose <40 mg/dl; CSF:serum
glucose<0.4
Gram Stain Positive in 60-90%
Culture Positive in 70-85%
Detection of bacterial antigen;
PCR
Form of Opening Leukocytes Protein Glucose Comments
meningitis pressure
and
differential
Normal 50 - 80 < 5, >75% 20 - 45 > 50
values mm H2O lymphocytes mg/dl mg/dl
Acute Usually usually 300 Usually usually < Organisms
bacterial elevated –2,000; 100 – 500 40 usually seen
meningitis (100 – PMNs on Gram
300) predominate stain /
culture
Partially Normal or 5 – 10,000; Usually Normal or
treated elevated PMNs usual 100 – 500 decreased
bacterial
meningitis
Viral Normal or Rarely Usually Generally
meningitis slightly >1,000 50 – 200 normal
elevated cells.
(80 – mononuclea
150) r cells
predominate
TB Usually 10 – 500; 100 – < 50 in Acid-fast
meningitis elevated lymphocytes 3,000 most organisms
LUMBAR PUNCTURE
INDICATIONS
To diagnose CNS infections
To drain CSF in communicating hydrocephalus
associated with intraventricular hemorrhage

To diagnose intracranial hemorrhage

To diagnose CNS involvement with leukemia

To inject chemotherapeutic agents

To instill contrast material for myelography


CONTRAINDICATIONS

Increased intracranial pressure (ICP)

Uncorrected thrombocytopenia/bleeding diathesis

Infection in skin or underlying tissue at/near


puncture site

Lumbosacral anomalies

Cardiorespiratory instability, which may be


PROCEDURE

Have an assistant restrain the infant in the lateral


decubitus
or sitting position, with spine flexed. Avoid flexion
of the
neck, as this increases the chance of airway
compromise.

Palpate inter-space that falls immediately above


or
below an imaginary line drawn between iliac
crests

Clean the lumbar area with antiseptic.


Drape, leaving puncture site & infant's face
exposed

Insert the needle in the midline into desired


interspace.

Aim slightly cephalad (on a plane with


the umbilicus) to avoid the vertebral bodies.

Advance the needle slowly to a depth of approx-


imately 1 to1.5 cm in a term infant, less in a
preterm
infant, until the epidermis and dermis are
traversed.
COMPLICATIONS of procedure
Post-LP headache * Infection * Hypoxemia

Intraspinal epidermoid tumor

Contamination of CSF sample with blood (traumatic


tap)

Aspiration, bleeding, CN 6 palsy, Cardiopulmonary


arrest

Intracranial decompression with cerebral herniation


Spinal cord puncture and nerve damage, deformity
of
COMPLICATIONS
Brain abscess
Seizure
Raised ICP
Hydrocephalus (usually
communicating)
CN Palsy
Subdural effusion
SIADH
Stroke
Cerebral and cerebellar herniation
Developmental delay
PRINCIPLES OF
TREATMENT
Agent used must be bactericidal against infecting organism

IV drugs should be used to reach a sufficient CSF concentration

A child with rapidly progressing disease of less than 24 hr


duration, in the absence of increased ICP, should receive
antibiotics as soon as possible after an LP is performed

If there are signs of increased ICP or focal neurologic findings,


antibiotics should be given without performing an LP and before
obtaining a CT scan
TREATMENT – CHOICE
OF ANTIBIOTICS
S Pneum, H infl & N men – IV penicillin / cephalosporins

CAF – bacteriostatic for GN rods but


bactericidal for S Pneum, H infl, and N meningitis

If GN rods are noted on gram stain – add an


aminoglycoside

For Neonatal bacterial meningitis: IV ampicillin and IV


gentamicin
(based on the most common etiologic agents)
TREATMENT
Duration of treatment

N meningitis 5-7 days


H influenzae 7-10 days
S pneumoniae 10-14 days
L monocytogenes 14-21 days
Enteric GN rods 3 wks
PROGNOSIS
Poor prognostic factors

ÞPneumococcal meningitis
ÞAge younger than 6 months
ÞSeizures lasting > 4 days after start of
treatment
ÞComa at presentation
ÞFocal neurologic signs at presentation
ÞLow CSF glucose < 20 mg/dL
PREVENTION
Chemoprohylaxis for “close contacts”
 H.influenzae
 N.meningitidis

Immunization
 H.influenzae
 S Pneumoniae

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