Meningitis.pptx

Anatomy of the meninges
 The meninges are the membranes covering the brain and spinal cord.
 The Meninges consist of three membranes
1. Dura Mater
2. Arachnoid Mater
3. Pia Mater
Ref Last Anatomy

Dura Mater
 The dura mater consists of an outer endosteal layer, and an
inner meningeal layer.
 The outer layer is the periosteum which invests the surface of
any bone, and blood vessels pass through it to supply the bone
 The inner layer consists of a dense, strong fibrous membrane,
which is really the dura mater proper
 Folds of the inner layer project into the cranial cavity. Ex. Falx
Cerebri.
Last Anatomy Page 671

Arachnoid Mater
 The arachnoid mater consists of an impermeable delicate
membrane that everywhere is supported by the inner surface of
the inner layer of the dura mater with only a thin film of tissue
fluid between them in the subdural space
 Arachnoid herniates through little holes in the dura mater into
the venous sinuses. Such herniae are the arachnoid villi;
through their walls the cerebrospinal fluid ‘oozes’ back into the
blood
Last Anatomy Pg 670

Pia Mater
 The pia mater invests the brain and spinal cord.
 it contains blood vessels.
 It is made of thin vascular fibrous tissue and can be stripped away from the
brain surface.
 it is invaginated into the substance of the brain by the entering cerebral
arteries.
 The region between the pia and the arachnoid is the subarachnoid space,
filled with cerebrospinal fluid.
Last Anatomy Pg 670

What is Meningitis? Etiologies?
 Meningitis is the inflammation of the Meninges
 Most Common are Acute Bacterial meningitis ,
Partially Treated Bacterial Meningitis ,Viral meningitis
or Meningoencephalitis
 Uncommon forms of meningitis ,TB Meningitis ,
Fungal Meningitis ,Syphilis (acute) and Leptospirosis,
Amebic (Naegleria) meningoencephalitis
Page
2937 Nelsons 20th edition

Routes of Transmission
 Transmitted from person to person through
droplets of respiratory or throat secretions
 Close and prolonged contact
 Incubation period ranges from between 2 to 10
days

Routes of infection
 Nasopharynx
 Blood stream
 Direct spread (Skull fracture , menigo and
encepholocele)
 Middle Ear Infections
 Infected VP Shunts
 Congential Defects
 Sinusitis

Acute Bacterial(Pyogenic) Meningitis
 occurring in infants and older children.
 associated with a high rate of acute complications and risk of
long-term morbidity.
 The incidence of bacterial meningitis is high in febrile infants
that it should be included in the differential diagnosis of those
with altered mental status and other evidence of neurologic
dysfunction
Page

Common Causes of Acute Bacterial
Meningtis
 Streptococcus pneumoniae
 Neisseria meningitidis
 Haemophilus influenzae Type B
Page

Epidemiology
 A major risk factor for meningitis is the lack of immunity to specific pathogens associated with
young age.
 close contact , crowding, poverty, black or Native American race, and male gender.
 The mode of transmission is probably person-to-person contact through respiratory tract
secretions or droplets.
 The risk of meningitis is increased among infants and young children with occult bacteremia;
 CSF shunt infections increase the risk of meningitis caused by staphylococci.
 Defects of the complement system (C5-C8) are associated with recurrent meningococcal
infection.
 Splenic dysfunction (sickle cell anemia) or asplenia (caused by trauma or congenital defect) is
associated with an increased risk of pneumococcal, H. influenzae type b (to some extent), and,
rarely, meningococcal sepsis and meningitis.
 T-lymphocyte defects (congenital or acquired by chemotherapy, AIDS, or malignancy) are
associated with an increased risk of L. monocytogenes infections of the CNS

S.Pneumonia causig Acute Bacterial
Meningtis
 The vaccine led to a dramatic decrease in rates of invasive pneumococcal
disease.
 Additional risk factors for contracting pneumococcal meningitis include otitis
media, sinusitis, pneumonia, CSF otorrhea or rhinorrhea, the presence of a
cochlear implant, and chronic graft-versus-host disease following bone marrow
transplantation
Page

N.Meningitis causing Acute Bacterial
Meningitis
 Five serogroups of meningococcus—A, B, C, Y, and W-135—are responsible
for disease. Meningococcal meningitis may be sporadic or may occur in
epidemics.
 Nasopharyngeal carriage of N. meningitidis occurs in 1-15% of adults.
 Colonization may last weeks to months; recent colonization places nonimmune
younger children at greatest risk for meningitis.
 Most infections of children are acquired from a contact in a daycare facility, a
colonized adult family member, or an ill patient with meningococcal disease.
 Children younger than 5 yr have the highest rates of meningococcal infection.
 A second peak in incidence occurs in persons between 15 and 24 yr of age.
Page

Neisseria Meningitis (Pg 1358 Nelsons)
The most common clinical manifestation of meningococcal infection
 Asymptomatic carriage of the organism in the nasopharynx.
 Focal infections in various sites (e.g., myocardium, joints, pericardium, bone,
eye, peritoneum, sinuses, and middle ear) are well recognized, and all may
progress to disseminated disease. Urethritis, cervicitis, vulvovaginitis, orchitis,
and proctitis may also occur.
 Acute meningococcal septicemia cannot be distinguished from other viral or
bacterial infections early after onset of symptoms.

Neisseria Meningitis cont . (Pg 1358
Nelsons)
 a nonblanching or petechial rash will develop in more than 80% of cases.
 In fulminant meningococcal septicemia, the disease progresses rapidly over
several hours from fever with nonspecific signs to septic shock characterized by
prominent petechiae and purpura (purpura fulminans) with poor peripheral
perfusion, tachycardia (to compensate for reduced blood volume resulting from
capillary leak), increased respiratory rate (to compensate for pulmonary
edema), hypotension (a late sign of shock in young children), confusion, and
coma (resulting from decreased cerebral perfusion). Coagulopathy, electrolyte
disturbance (especially hypokalemia), acidosis, adrenal hemorrhage, renal
failure, and myocardial failure, may all develop
 Meningitis may be present.

Nelsons)
 Meningococcal meningitis is indistinguishable from meningitis
caused by other bacteria.
 Children younger than 5 yr of age rarely report headache.
 clinical signs of meningeal irritation may develop but are unusual
in infants.
 Seizures and focal neurologic signs occur less frequently than in
patients with meningitis caused by Streptococcus pneumoniae or
Haemophilus influenzae type b.
 A meningoencephalitis-like picture can occur that is associated
with rapidly progressive cerebral edema and death from raised
intracranial pressure, which may be more common with
serogroup A infection

Nelsons)
 Occult meningococcal bacteremia manifests as
fever with or without associated symptoms that
suggest a minor viral infection.
 Resolution of bacteremia may occur without
antibiotics, but sustained bacteremia leads to
meningitis in approximately 60% of cases and to
distant infection of other tissues.

Nelsons)
 Chronic meningococcemia, which occurs rarely, is characterized by
fever, nontoxic appearance, arthralgia, headache, splenomegaly, and a
maculopapular or petechial rash.
 Symptoms are intermittent, with a mean duration of illness of 6-8 wk.
 Blood culture results are usually positive, but cultures may initially be
sterile.
 Chronic meningococcemia may spontaneously resolve, but meningitis
may develop in untreated cases. Some cases have been associated
with complement deficiency and others with sulfonamide therapy.
 One report indicates that up to 47% of isolates from patients with
chronic meningococcemia (compared with less than 10% in acute
cases) have a mutation in the lpxl 1 gene, leading to a reduced
inflammatory response and the milder course of infection.

H.Influenze type B causing Acute
bacterial menigitis
 Before universal H. influenzae type b vaccination, approximately 70% of cases
of bacterial meningitis occurring in the 1st 5 yr of life were caused by this
pathogen.
 Invasive infections occurred primarily in infants 2 mo to 2 yr of age; peak
incidence was at 6-9 mo of age, and 50% of cases occurred in the 1st yr of life.
 The risk to children was markedly increased among family or daycare center
contacts of patients with H. influenzae type b disease.
 Incompletely vaccinated individuals, those in underdeveloped countries who are
not vaccinated, and those with blunted immunologic responses to vaccine (such
as children with HIV infection) remain at risk for H. influenzae type b meningitis.
 Page

Pathogenesis (Page
2940 Nelsons 20th
edition)
 Hematogenous dissemination of microorganisms from a distant site of
infection(Bacteremia)
 Bacterial colonization of the nasopharynx with a pathogenic microorganism.
 N. meningitidis and H. influenzae type b attach to mucosal epithelial cell receptors
by pili.
 Bacteria breach the mucosa and enter the circulation.
 Bacterial survival in the bloodstream is enhanced by large bacterial capsules that interfere
with opsonization
 Bacteria gain entry to the CSF through the 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.
 Chemotactic factors then incite a local inflammatory response characterized by
polymorphonuclear cell infiltration.

Pathogenesis Continued
 The presence of bacterial cell wall lipopolysaccharide (endotoxin) of Gram-
negative bacteria (H. influenzae type b, N. meningitidis) and of pneumococcal
cell wall components (teichoic acid, peptidoglycan) stimulates a marked
inflammatory response, with local production of tumor necrosis factor,
interleukin 1, prostaglandin E, and other inflammatory mediators.
 The subsequent inflammatory response is characterized by neutrophilic
infiltration, increased vascular permeability, alterations of the blood–brain
barrier, and vascular thrombosis.
 Meningitis-associated brain injury is not simply caused by viable bacteria but
occurs as a consequence of the host reaction to the inflammatory cascade
initiated by bacterial components.
 Rarely, meningitis may follow bacterial invasion from a contiguous Focus of
infection such as paranasal sinusitis, otitis media, mastoiditis, orbital cellulitis,
or cranial or vertebral osteomyelitis or may occur after introduction of bacteria
via penetrating cranial trauma, dermal sinus tracts, or meningomyeloceles.

Consequences (Page
2939 Nelsons 20th
edition)
Cerebral infarction,
 resulting from vascular occlusion because of inflammation,
vasospasm, and thrombosis, is a frequent sequela. Infarct size
ranges from microscopic to involvement of an entire hemisphere.
 Inflammation of spinal nerves and roots produces meningeal
signs, and inflammation of the cranial nerves produces cranial
neuropathies of optic, oculomotor, facial, and auditory nerves.
Increased intracranial pressure (ICP) also produces oculomotor
nerve palsy because of the presence of temporal lobe
compression of the nerve during tentorial herniation.
 Abducens nerve palsy may be a nonlocalizing sign of elevated
ICP.

 Increased ICP is a result of cell death (cytotoxic cerebral edema), cytokine-
induced increased capillary vascular permeability (vasogenic cerebral edema),
and, possibly, increased hydrostatic pressure (interstitial cerebral edema) after
obstructed reabsorption of CSF in the arachnoid villus or obstruction of the flow
of fluid from the ventricles
 Hydrocephalus can occur as an acute complication of bacterial meningitis. It
most often takes the form of a communicating hydrocephalus caused by
adhesive thickening of the arachnoid villi around he cisterns at the base of the
brain. Thus, there is interference with the normal resorption of CSF. Less often,
obstructive hydrocephalus develops after fibrosis and gliosis of the aqueduct of
Sylvius or the foramina of Magendie and Luschka.
 Raised CSF protein levels are partly a result of increased vascular permeability
of the blood–brain barrier and the loss of albumin-rich fluid from the capillaries
and veins traversing the subdural space. Continued transudation may result in
subdural effusions, usually found in the later phase of acute bacterial meningitis.
 Hypoglycorrhachia (reduced CSF glucose levels) is attributable to decreased
glucose transport by the cerebral tissue.

Clinical Manifestations (Page
2940 Nelsons
20th edition)
 2 predominant patterns.
 The more dramatic and, fortunately, less common presentation is sudden onset
with rapidly progressive manifestations of shock, purpura, disseminated
intravascular coagulation, and reduced levels of consciousness often resulting
in progression to coma or death within 24 hr.
 More often, meningitis is preceded by several days of fever accompanied by
upper respiratory tract or gastrointestinal symptoms, followed by nonspecific
signs of CNS infection, such as increasing lethargy and irritability.
 The signs and symptoms of meningitis are related to the nonspecific findings
associated with a systemic infection and to manifestations of meningeal
irritation.

Non Specific Symptoms (Page
2940 Nelsons
20th edition)
 Nonspecific findings include fever, anorexia and
 poor feeding, headache, symptoms of upper respiratory tract infection,
 myalgias, arthralgias, tachycardia, hypotension, and various cutaneous
 signs, such as petechiae, purpura, or an erythematous macular rash

Meningeal irritation (Page
2940 Nelsons
20th edition)
 is manifested as nuchal rigidity, back 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 after passive flexion
of the neck while supine). In children,
 particularly in those younger than 12-18 mo, Kernig and Brudzinski signs are
not consistently present.
 Indeed fever, headache, and nuchal rigidity are present in only 40% of adults
with bacterial meningitis

Symptoms of Increased ICP (Page
2940
Nelsons 20th edition)
 Is suggested by 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 signs of herniation.
 Papilledema is uncommon in uncomplicated meningitis and should suggest a
more chronic process, such as the presence of an intracranial abscess,
subdural empyema, or occlusion of a dural venous sinus.
 Focal neurologic signs usually are a result of vascular occlusion.
 Cranial neuropathies of the ocular, oculomotor, abducens, facial, and auditory
nerves may also be the result of focal inflammation.
 Overall,v approximately 10-20% of children with bacterial meningitis have focal
neurologic signs.

Seizures (Page
2940 Nelsons 20th edition)
 Seizures (focal or generalized) caused by cerebritis, infarction, or electrolyte
disturbances occur in 20-30% of patients with meningitis.
 Seizures that occur on presentation or within the 1st 4 days of onset are usually
of no prognostic significance.
 Seizures that persist after the 4th day of illness and those that are difficult to
treat may be associated with a poor prognosis.

Alteration of Mental Status (Page
2940
Nelsons 20th edition)
 are common among patients with meningitis and may be the consequence of
increased ICP, cerebritis, or hypotension;
 manifestations include irritability, lethargy, stupor, obtundation, and coma.
 Comatose patients have a poor prognosis.
 Additional manifestations of meningitis include photophobia and tache
cérébrale, which is elicited by stroking the skin with a blunt object and
observing a raised red streak within 30-60 sec

Diagnosis (Page
 The diagnosis of acute pyogenic meningitis is confirmed by analysis of the CSF, which
typically reveals microorganisms on Gram stain and culture, a neutrophilic pleocytosis,
elevated protein, and reduced glucose concentrations.
 LP should be performed
 when bacterial meningitis is suspected Blood cultures should be performed in all patients
with suspected meningitis.
 Blood cultures reveal the responsible bacteria in up to 80-90% of cases of meningitis.
 Elevations of the C-reactive protein, erythrocyte sedimentation rate, and procalcitonin
have been used to differentiate bacterial (usually elevated) from viral causes of
meningitis.
 If an LP is delayed, empirical antibiotic therapy should be initiated.
 CT scanning for evidence of a brain abscess or increased ICP should not delay therapy.
 LP may be performed after increased ICP has beentreated or a brain abscess has been
excluded

(Page
Features of impending herniation,
1. Alteration in the respiratory pattern (e.g., hyperventilation; Cheyne-Stokes
respirations, ataxic respirations, respiratory arrest),
2. Abnormalities of pupil size and reactivity,
3. Loss of brainstem reflexes, and decorticate or decerebrate posturing.
4. The Cushing reflex is a physiological nervous system response to acute elevations
of intracranial pressure (ICP), resulting in the Cushing triad of widened pulse pressure
(increasing systolic, decreasing diastolic) bradycardia, and irregular respirations
If any of these signs are present or the child is so ill that the lumbar puncture might induce
cardiorespiratory arrest, blood cultures should be drawn and supportive care, including
antibiotics, should be initiated. Once the patient has stabilized, it may be possible to
perform a lumbar puncture safely

Contraindications for an immediate LP
(Page
1. Evidence of increased ICP (other than a bulging fontanel) If disc edema or
focal findings suggest a mass lesion, a head CT should be obtained before
proceeding with lumbar puncture to prevent uncal or cerebellar herniation as
the CSF is removed
2. Severe cardiopulmonary compromise requiring prompt resuscitative
measures for shock or in patients in whom positioning for the LP would
further compromise cardiopulmonary function; and
3. Infection of the skin overlying the site of the LP.
4. Thrombocytopenia is a relative contraindication for LP. a platelet count <20
× 109/L

Lumbar Puncture (Page
2799 Nelsons 20th
edition)
 The patient should be situated in a lateral decubitus or seated position with the neck and legs flexed to
enlarge the intervertebral spaces.
 As a rule, sick neonates should be maintained in a seated position to prevent problems with ventilation and
perfusion
 Once the patient is situated, the physician identifies the appropriate interspace by drawing an imaginary line
from the iliac crest downward perpendicular to the vertebral column.
 In adults, lumbar punctures are usually performed in the L3-L4 or L4-L5 interspaces
 Next, the physician dons a mask, gown, and sterile gloves.
 The skin is thoroughly prepared with a cleansing agent, and sterile drapes are applied.
 The skin and underlying tissues are anesthetized by injecting a local anesthetic (e.g., 1% lidocaine) at the time
of the procedure or by applying a eutectic mixture of lidocaine and prilocaine (EMLA) to the skin 30 minutes
before the procedure.
 A 22-gauge, 1.5-3.0 in, sharp, beveled spinal needle with a properly fitting stylet is introduced in the
midsagittal plane and directed slightly cephalad.
 The physician should pause frequently, emove the stylet, and assess for CSF flow.
 Although a pop can occur as the needle penetrates the dura, it is more common to experience a subtle
change in resistance

CSF (Page
White Blood Cells
 Normal CSF contains up to 5/mm3 white blood cells, and a
newborn can have as many as 15/mm3
 Polymorphonuclear cells are always abnormal in a child, but
1-2/mm3 may be present in a normal neonate
 An elevated polymorphonuclear count suggests bacterial
meningitis or the early phase of aseptic meningitis
 CSF lymphocytosis can be seen in aseptic, tuberculous, or
fungal meningitis; demyelinating diseases; brain or spinal cord
tumor; immunologic disorders, including collagen vascular
diseases; and chemical irritation (following myelogram,
intrathecal methotrexate)

RBC (Page
• Normal CSF contains no red blood cells
• Their presence indicates a traumatic tap or a subarachnoid hemorrhage.
• Progressive clearing of the blood between the first and last samples indicates a
traumatic tap. Bloody CSF should be centrifuged immediately.
• A clear supernatant is consistent with a bloody tap,
• whereas xanthochromia (yellow color that results from the degradation of
hemoglobin) suggests a subarachnoid hemorrhage.
• Xanthochromia may be absent in bleeds <12 hrs old, particularly when
laboratories rely on visual inspection rather than spectroscopy.
• Xanthochromia can also occur in the setting of hyperbilirubinemia, carotenemia,
and markedly elevated CSF protein

Protein (Page
 The normal CSF protein is 10-40 mg/dL in a child and as high as 120 mg/dL in a
neonate.
 The CSF protein falls to the normal childhood range by 3 mo of age.
 The CSF protein may be elevated in many processes, including infectious,
immunologic, vascular, and degenerative
 diseases, blockage of CSF flow, as well as tumors of the brain (primary CNS
tumors, systemic tumors metastatic to the CNS, infiltrative acute lymphoblastic
leukemia) and spinal cord.
 With a traumatic tap, the CSF protein is increased by approximately 1 mg/dL for
every 1,000 red blood cells/mm3.
 Elevation of CSF immunoglobulin G, which normally represents approximately 10%
of the total protein, is observed in subacute sclerosing panencephalitis, in
postinfectious encephalomyelitis, and in some cases of multiple sclerosis.
 If the diagnosis of multiple sclerosis is suspected, the CSF should be tested for the
presence of oligoclonal bands.

CSF Gluclose (Page
2799 Nelsons 20th
edition)
 The CSF glucose content is approximately 60% of the blood glucose in a
healthy child.
 To prevent a spuriously elevated blood:CSF glucose ratio in a case of
suspected meningitis, it is advisable to collect the blood glucose before the
lumbar puncture when the child is relatively calm.
 Hypoglycorrhachia is found in association with diffuse meningeal disease,
particularly bacterial and tubercular meningitis.
 Widespread neoplastic involvement of the meninges, subarachnoid
hemorrhage, disorders involving the glucose transporter protein type1, fungal
meningitis, and, occasionally, aseptic meningitis can produce low CSF glucose
as well.

Other Findings in CSF (Page
2800 Nelsons
20th edition)
 A Gram stain of the CSF is essential if there is a suspicion for bacterial
meningitis; an acid-fast stain and India ink preparation can be used to assess
for tuberculous and fungal meningitis, respectively.
 CSF is then plated on different culture media depending on the suspected
pathogen.
 When indicated by the clinical presentation, it can also be helpful to assess for
the presence of specific antigens (e.g., latex agglutination for Neisseria
meningitidis, Haemophilus influenzae type b, or Streptococcus pneumoniae) or
to obtain antibody or polymerase chain reaction studies (e.g., herpes simplex
virus-1 and -2, West Nile virus, enteroviruses).
 In noninfectious cases, levels of CSF metabolites, such as lactate, amino acids,
and enolase, can provide clues to the underlying metabolic disease.

Cerebrospinal Fluid Findings page 2937 Nelsons
Condition Pressure Leucocytes
( mm3 )
Protien
(mg/dl)
Glucose
(mg/dl)
Comments
Normal 50-80 <5 or > 75%
lymphocytes
20-45 >50(75% of
Serum Glucose)
Acute Bacterial
meningitis
Usually
elevated
(100-300)
100-10,000 or
more; usually
300-2,000;
PMNs
predominate
Usually
100-500
Decreased,
usually <40 (or
<50% serum
glucose)
Organisms
usually seen on
Gram stain and
recovered
by culture
Partially
treated
bacterial
meningitis
Normal or
elevated
5-10,000; PMNs
usual but
mononuclear
cells may
predominate if
pretreated
for extended
period of
time
Usually
100-500
Normal or
decreased
Organisms may
be seen on
Gram stain
Pretreatment
may render
CSF sterile.
Antigen may
be detected by
agglutination
test

( mm3 )
Protien
(mg/dl)
Glucose
(mg/dl)
Comments
Viral meningitis
or
meningoencepha
litis
Normal or
slightly
elevated
(80-150)
Rarely >1,000
cells.
Usually 50-200 Generally
normal;
may be
decreased to
<40 in some
viral diseases,
particularly
mumps (15-20%
of cases)
HSV encephalitis
is
suggested by
focal seizures
or by focal
findings on CT
or MRI scans or
EEG.
Enteroviruses
and HSV
infrequently
recovered
from CSF. HSV
and
enteroviruses
may be
detected by PCR
of CSF

( mm3 )
Protien
(mg/dl)
Glucose
(mg/dl)
Comments
Tuberculous
meningitis
Usually elevated 10-500; PMNs
early, but
lymphocytes
predominate
through most of
the
course
100-3,000; may
be higher in
presence of
block
<50 in most
cases;
decreases with
time if
treatment is not
provided
Acid-fast
organisms almost
never seen on
smear.
Mycobacterium
tuberculosis may
be
detected by PCR
of CSF
Fungal
meningitis
Usually elevated 5-500; PMNs
early but
mononuclear
cells
predominate
through
most of the
course.
25-500 <50; decreases
with time if
treatment is not
provided
Budding yeast
may be seen.
Organisms may
be
recovered in
culture.
Cryptococcal
antigen (CSF
and serum) may
be positive
in cryptococcal
infection

( mm3 )
Protien
(mg/dl)
Glucose
(mg/dl)
Comments
Syphilis (acute) and
leptospirosis
Usually
elevated
50-500;
lymphocytes
predominate
50-200 Usually normal Positive CSF
serology.
Spirochetes not
demonstrable by
usual
techniques of
smear or
culture; dark-
field
examination may
be
positive
Amebic (Naegleria)
meningoencephalitis
Elevated 1,000-10,000 or
more; PMNs
predominate
50-500 Normal or slightly
decreased
Mobile amebas
may be seen
by hanging-drop
examination of
CSF at
room
temperature

Partially Treated Bacterial Meningitis
(Nelsons page 2940)
 A diagnostic conundrum in the evaluation of children with suspected bacterial
meningitis is the analysis of CSF obtained from children already receiving antibiotic
(usually oral) therapy
 This is an important issue, because 25-50% of children being evaluated for bacterial
meningitis are receiving oral antibiotics when their CSF is obtained. CSF obtained
from children with bacterial meningitis, after the initiation of antibiotics, may be
negative on Gram stain and culture
 Pleocytosis with a predominance of neutrophils, elevated protein level, and a
reduced concentration of CSF glucose usually persist for several days after the
administration of appropriate intravenous antibiotics. Therefore, despite negative
cultures, the presumptive diagnosis of bacterial meningitis can be made.
 Some clinicians test CSF for the presence of bacterial antigens if the child has been
pretreated with antibiotics and the diagnosis of bacterial meningitis is in doubt
 Polymerase chain reactions using broad-based bacterial 16S ribosomal RNA gene
patterns may be useful in diagnosing the cause of culture-negative meningitis
because of prior antibiotic therapy or the presence of a nonculturable fastidious
pathogen.

Traumatic LP (Page 2941 Nelsons)
 A traumatic LP may complicate the diagnosis of meningitis.
 Repeat LP at a higher interspace may produce less hemorrhagic fluid, but this
fluid usually also contains red blood cells.
 Interpretation of CSF leukocytes and protein concentration are affected by LPs
that are traumatic, although the Gram stain, culture, and glucose level may not
be influenced.
 Although methods for correcting for the presence of red blood cells have been
proposed, it is prudent to rely on the bacteriologic results rather than attempt to
interpret the CSF leukocyte and protein results of a traumatic LP.

Treatment (Page 2941 Nelsons)
 The therapeutic approach to patients with presumed bacterial meningitis
depends on the nature of the initial manifestations of the illness.
 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.
 Increased ICP should be treated simultaneously.
 Immediate treatment of associated multiple organ system failure, shock and
acute respiratory distress syndrome.

Treatment cont. (Page 2941 Nelsons)
 Patients who have a more protracted subacute course and become ill over a 4-
7 day period should also be evaluated for signs of increased ICP and focal
neurologic deficits.
 Unilateral headache, papilledema and other signs of increased ICP suggest a
focal lesion, such as a brain or epidural abscess, or subdural empyema.
 Under these circumstances, antibiotic therapy should be initiated before LP and
CT scanning.
 If signs of increased ICP and/or focal neurologic signs are present, CT scanning
should be performed first to determine the safety of performing an LP.

Initial Antibiotic Therapy (Page 2941
Nelsons)
 The initial (empirical) choice of therapy for meningitis in immunocompetent
infants and children is primarily influenced by the antibiotic susceptibilities of S.
pneumoniae. Selected antibiotics should achieve bactericidal levels in the CSF.
 S. pneumoniae are currently resistant to penicillin; relative resistance.
 Resistance to cefotaxime and ceftriaxone is also evident in up to 25% of
isolates.
 In contrast, most strains of N. meningitidis are sensitive to penicillin and
cephalosporins, although rare resistant isolates have been reported.
 Approximately 30-40% of isolates of H. influenzae type b produce β-lactamases
and, therefore, are resistant to ampicillin.
 These β-lactamase–producing strains are sensitive to the extended-spectrum
cephalosporins.

Nelsons)
 Based on the substantial rate of resistance of S. pneumoniae to β-
lactam drugs, vancomycin (60 mg/kg/24 hr, given every 6 hr) is
recommended as part of initial empirical therapy.
 Because of the efficacy of third-generation cephalosporins in the
therapy of meningitis caused by sensitive S. pneumoniae, N.
meningitidis, and H. influenzae type b, cefotaxime (300 mg/kg/24 hr,
given every 6 hr) or ceftriaxone (100 mg/ kg/24 hr administered
once per day or 50 mg/kg/dose, given every 12 hr) should also be
used in initial empirical therapy.
 Patients allergic to β-lactam antibiotics and >1 mo of age can be
treated with chloramphenicol, 100 mg/kg/24 hr, given every 6 hr.
 Another option for patients with allergy to β-lactam antibiotics is a
combination of vancomycin and rifampin.
 Alternatively, patients can be desensitized to the antibiotic

Nelsons)
 If L. monocytogenes infection is suspected, as in young infants or those with
a T-lymphocyte deficiency, ampicillin (200 mg/kg/24 hr, given every 6 hr)
also should also be given because cephalosporins are inactive against L.
monocytogenes.
 Intravenous trimethoprimsulfamethoxazole is an alternative treatment for L.
monocytogenes.
 If a patient is immunocompromised and Gram-negative bacterial meningitis is
suspected, initial therapy might include ceftazidime and an aminoglycoside or
meropenem.

Duration of antibiotic therapy (Pg 2941
Nelsons)
 Therapy for uncomplicated penicillin-sensitive S. pneumoniae meningitis should
be for 10-14 days with a third-generation cephalosporin or intravenous penicillin
(400,000 units/kg/24 hr, given every 4-6 hr).
 If the isolate is resistant to penicillin and the third-generation cephalosporin,
therapy should be completed with vancomycin.
 Intravenous penicillin (300,000 units/kg/24 hr) for 5-7 days is the treatment of
choice for uncomplicated N. meningitidis meningitis.
 Uncomplicated H. influenzae type b meningitis should be treated for 7-10 days.
 Patients who receive intravenous or oral antibiotics before LP and who do not
have an identifiable pathogen, but do have evidence of an acute bacterial
infection on the basis of their CSF profile, should continue to receive therapy
with ceftriaxone or cefotaxime for 7-10 days.
 If focal signs are present or the child does not respond to treatment, a
parameningeal focus may be present and a CT or MRI scan should be
performed.

Nelsons)
 A routine repeat LP is not indicated in all patients
with uncomplicated meningitis caused by antibiotic-
sensitive S. pneumoniae, N. meningitidis, or H.
influenzae type b.
 Repeat examination of CSF is indicated in some
neonates, in all patients with Gram-negative bacillary
meningitis, or in infection caused by a β-lactam–
resistant S. pneumoniae.
 The CSF should be sterile within 24-48 hr of initiation
of appropriate antibiotic therapy.

Nelsons)
 Meningitis caused by Escherichia coli or P.
aeruginosa requires therapy with a third-generation
cephalosporin active against the isolate in vitro.
 Most isolates of E. coli are sensitive to cefotaxime or
ceftriaxone, and most isolates of P. aeruginosa are
sensitive to ceftazidime.
 Gram-negative bacillary meningitis should be treated
for 3 wk or for at least 2 wk after CSF sterilization,
which may occur after 2-10 days of treatment.

Side Effects of Antibiotic therapy (Pg
2943 Nelsons)
 Side effects of antibiotic therapy of meningitis
include phlebitis, drug fever, rash, emesis,
oral candidiasis, and diarrhea.
 Ceftriaxone may cause reversible gallbladder
pseudolithiasis, detectable by abdominal
ultrasonography.
 This is usually asymptomatic but may be
associated with emesis and upper right
quadrant pain

Antibiotics used for the treatment of
Bacterial Meningitis
Neonates
Drugs 0-7 days 8-28 days Infants and Children
Amikacin 15-20 divided q12h 30 divided q8h 20-30 divided q8h
Ampicillin 150 divided q8h 200 divided q6h or q8h 300 divided q6h
Cefotaxime 100-150 divided q8h or
q12h
150-200 divided q6h or
q8h
q8h
Ceftriaxone - - 100 divided q12h or
q24h
Ceftazidime 100-150 divided q8h or
q12h
150 divided q8h 150 divided q8h
Gentamicin 5 divided q12h 7.5 divided q8h 7.5 divided q8h
Meropenem - - 120 divided q8h
Nafcillin 75 divided q8h or q12h 100-150 divided q6h or
q8h
200 divided q6h
Penicillin G 150,000 divided q8h or
q12h
200,000 divided q6h or
q8h
300,000 divided q4h or
q6h

Neonates
Drugs 0-7 days 8-28 days Infants and Children
Rifampin - 10-20 divided q12h 10-20 divided q12h or
q24h
Tobramycin 5 divided q12h 7.5 divided q8h 7.5 divided q8h
Vancomycin 20-30 divided q8h or
q12h
q8h
60 divided q6h

Corticosteriods in Management (Pg 2943
Nelsons)
 Rapid killing of bacteria in the CSF effectively sterilizes the meningeal infection
but releases toxic cell products after cell lysis (cell wall endotoxin) that
precipitate the cytokine-mediated inflammatory cascade.
 The resultant edema formation and neutrophilic infiltration may produce
additional neurologic injury with worsening of CNS signs and symptoms.
 Therefore, agents that limit production of inflammatory mediators may be of
benefit to patients with bacterial meningitis

Corticosteroids in Management (Pg 2943
Nelsons)
 Data support the use of intravenous dexamethasone, 0.15 mg/kg/ dose given every 6 hr for 2
days, in the treatment of children older than 6 wk with acute bacterial meningitis caused by H.
influenzae type b.
 Among children with meningitis caused by H. influenzae type b, corticosteroid recipients have a
shorter duration of fever, lower CSF protein and lactate levels, and a reduction in sensorineural
hearing loss.
 Data in children regarding benefits, if any, of corticosteroids in the treatment of meningitis
caused by other bacteria are inconclusive.
 Early steroid treatment of adults with bacterial meningitis, especially those with pneumococcal
meningitis, results in improved outcome.
 Corticosteroids appear to have maximum benefit if given 1-2 hr before antibiotics are initiated.
 They also may be effective if given concurrently with or soon after the first dose of antibiotics.
 Complications of corticosteroids include gastrointestinal bleeding, hypertension, hyperglycemia,
leukocytosis, and rebound fever after the last dose

Supportive Care (Pg 2943 Nelsons)
 Repeated medical and neurologic assessments of patients with
bacterial meningitis are essential to identify early signs of
cardiovascular, CNS, and metabolic complications
 Pulse rate, blood pressure, and respiratory rate should be monitored
frequently.
 Neurologic assessment, including pupillary reflexes, level of
consciousness, motor strength, cranial nerve signs, and evaluation for
seizures, should be made frequently in the 1st 72 hr, when the risk of
neurologic complications is greatest.
 Important laboratory studies include an assessment of blood urea
nitrogen; serum sodium, chloride, potassium, and bicarbonate levels;
urine output and specific gravity; complete blood and platelet counts;
and, in the presence of petechiae, purpura, or abnormal bleeding,
measures of coagulation function (fibrinogen, prothrombin, and partial

 Fluid administration may be returned to normal (1,500-1,700 mL/m2/24 hr) when
serum sodium levels are normal.
 Fluid restriction is not appropriate in the presence of systemic hypotension because
reduced blood pressure may result in reduced cerebral perfusion pressure and CNS
ischemia.
 Therefore, shock must be treated aggressively to prevent brain and other organ
dysfunction (acute tubular necrosis, acute respiratory distress syndrome).
 Patients with shock, a markedly elevated ICP, coma, and refractory seizures require
intensive monitoring with central arterial and venous access and frequent vital signs,
necessitating admission to a pediatric intensive care unit.
 Patients with septic shock may require fluid resuscitation and therapy with
vasoactive agents such as dopamine and epinephrine.
 The goal of such therapy in patients with meningitis is to avoid excessive increases
in ICP without compromising blood flow and oxygen delivery to vital organs.

 Neurologic complications include increased ICP with subsequent herniation,
seizures, and an enlarging head circumference because of a subdural effusion or
hydrocephalus.
 Signs of increased ICP should be treated emergently with endotracheal intubation
and hyperventilation (to maintain the pCO2 at approximately 25 mm Hg).
 In addition, intravenous furosemide (Lasix, 1 mg/kg) and mannitol (0.5-1.0 g/kg)
osmotherapy may reduce ICP (see Chapter 68).
 Furosemide reduces brain swelling by venodilation and diuresis without increasing
intracranial blood volume,
 whereas mannitol produces an osmolar gradient between the brain and plasma,
thus shifting fluid from the CNS to the plasma, with subsequent excretion during an
osmotic diuresis.
 Another approach to treating reductions of cerebral perfusion pressure caused by
elevations of intracranial pressure is to increase systemic blood

 Seizures are common during the course of bacterial meningitis. Immediate
therapy for seizures includes intravenous diazepam (0.1- 0.2 mg/kg/dose) or
lorazepam (0.05-0.10 mg/kg/dose), and careful attention paid to the risk of
respiratory suppression.
 Serum glucose, calcium, and sodium levels should be monitored.
 After immediate management of seizures, patients should receive phenytoin
(15-20 mg kg loading dose, 5 mg/kg/24 hr maintenance) to reduce the
likelihood of recurrence.
 Phenytoin is preferred to phenobarbital because it produces less CNS
depression and permits assessment of a patient’s level of consciousness.
 Serum phenytoin levels should be monitored to maintain them in the
therapeutic range (10-20 μg/mL).

Complications (Pg 2944 -2945) Nelsons)
 During the treatment of meningitis, acute CNS complications
 can include seizures, increased ICP, cranial nerve palsies, stroke cerebral or cerebellar
herniation, and thrombosis of the dural venous sinuses,
 Collections of fluid in the subdural space develop in 10-30% of patients with meningitis and are
asymptomatic in 85-90% of patients. Subdural effusions are especially common in infants.
 Symptomatic subdural effusions may result in a bulging fontanel, diastasis of sutures, enlarging
head circumference, emesis, seizures, fever, and abnormal results of cranial transillumination.
 CT or MRI scanning confirms the presence of a subdural effusion. In the presence of increased
ICP or a depressed level of consciousness, symptomatic subdural effusion should be treated by
aspiration through the open fontanel (see Chapters 68 and 590).
 Fever alone is not an indication for aspiration.
 SIADH occurs in some patients with meningitis, resulting in hyponatremia and reduced serum
osmolality.
 This may exacerbate cerebral edema or result in hyponatremic seizures (see Chapter 55).

 Fever associated with bacterial meningitis usually resolves within 5-7 days of the
onset of therapy.
 Prolonged fever (>10 days) is noted in approximately 10% of patients.
 Prolonged fever is usually caused by intercurrent viral infection, nosocomial or
secondary bacterial infection,
 thrombophlebitis, or drug reaction. Secondary fever refers to the recrudescence of
elevated temperature after an afebrile interval. Nosocomial infections are especially
important to consider in the evaluation of these patients.
 Pericarditis or arthritis may occur in patients being treated for meningitis, especially
that caused by N. meningitidis.
 Involvement of these sites may result either from bacterial dissemination or from
immune complex deposition.
 In general, infectious pericarditis or arthritis occurs earlier in the course of treatment
than does immune-mediated disease

 Thrombocytosis, eosinophilia, and anemia may develop during therapy for
meningitis.
 Anemia may be a result of hemolysis or bone marrow suppression.
 Disseminated intravascular coagulation is most often associated with the
rapidly progressive pattern of presentation and is noted most commonly in
patients with shock and purpura.
 The combination of endotoxemia and severe hypotension initiates the
coagulation cascade; the coexistence of ongoing thrombosis may produce
symmetric peripheral gangrene.

Prognosis Complications (Pg2945)
Nelsons)
 Appropriate antibiotic therapy and supportive care have reduced the mortality of
bacterial meningitis after the neonatal period to <10%.
 The highest mortality rates are observed with pneumococcal meningitis.
 Severe neurodevelopmental sequelae may occur in 10-20% of patients
recovering from bacterial meningitis, and as many as 50% have some, albeit
subtle, neurobehavioral morbidity.
 The prognosis is poorest among infants younger than 6 mo and in those with
high concentrations of bacteria/bacterial products in their CSF.
 Those with seizures occurring more than 4 days into therapy or with coma or
focal neurologic signs on presentation have an increased risk of long-term
sequelae.
 There does not appear to be a correlation between duration of symptoms
before diagnosis of meningitis and outcome.

Prognosis Complications (Pg2945)
Nelsons)
 The most common neurologic sequelae include hearing loss, cognitive impairment,
recurrent seizures, delay in acquisition of language, visual impairment, and
behavioral problems.
 Sensorineural hearing loss is the most common sequela of bacterial meningitis
and, usually, is already present at the time of initial presentation.
 It is a result of cochlear infection and occurs in as many as 30% of patients with
pneumococcal meningitis, 10% with meningococcal, and 5-20% of those with H.
influenzae type b meningitis.
 Hearing loss may also be caused by direct inflammation of the auditory nerve.
 All patients with bacterial meningitis should undergo careful audiologic assessment
before or soon after discharge from the hospital.
 Frequent reassessment on an outpatient basis is indicated for patients who have a
hearing deficit.

Prevention (Pg2946) Nelsons)
 N.Menigitidis :- Chemoprophlaxis of rifampin 10
mg/kg/dose every 12 hr (maximum dose of 600 mg) for
2 days as soon as possible after identification of a
case of suspected meningococcal meningitis or sepsis.
 Exposed contacts should be treated immediately on
suspicion
 Two quadrivalent (A, C, Y, W-135), conjugated
vaccines (MCV-4; Menactra and Menveo) are licensed
by the FDA.
 This vaccine is licensed for use in children ages 6 wk
through 18 months.

 H.influenze B:- Rifampin prophylaxis should be given to all
household contacts of patients with invasive disease
caused by H. influenzae type b.
 The dose of rifampin is 20 mg/kg/24 hr (maximum dose of
600 mg) given once each day for 4 days.
 Rifampin colors the urine and perspiration red-orange,
stains contact lenses, and reduces the serum
concentrations of some drugs, including oral
contraceptives.
 Rifampin is contraindicated during pregnancy.

 Routine administration of conjugate vaccine against S.
pneumoniae is recommended for children younger than 5
yr of age.
 The initial dose is given at about 2 mo of age.
 Children who are at high risk of invasive pneumococcal
infections, including those with functional or anatomic
asplenia and those with underlying immunodeficiency

Viral Meningoencephalitis (Pg 2946
Nelsons)
 Viral meningoencephalitis is an acute inflammatory
process involving the meninges and, to a variable
degree, brain tissue.
 These infections are relatively common and caused by a
number of different agents.
 The CSF is characterized by pleocytosis and the
absence of microorganisms on Gram stain and routine
bacterial culture.
 In most instances, the infections are self-limited.
 In some cases, substantial morbidity and mortality occur.

Etiology (Pg 2946 Nelsons)
 Enteroviruses are the most common cause of viral meningoencephalitis.
 The severity of ranges from mild, self-limited illness with primarily meningeal
involvement to severe encephalitis resulting in death or significant sequelae.
 Human enterovirus 68 has been associated with neurologic symptoms
including flaccid paralysis. Parechoviruses may be an important cause of
aseptic meningitis or encephalitis in infants.
 The clinical manifestations are similar to that of the enteroviruses with the
exception of more severe MRI lesions of the cerebral cortex and at times an
absence of a CSF pleocytosis.

 Arboviruses are arthropod-borne agents, responsible for some cases of
meningoencephalitis during summer months.
 Mosquitoes and ticks are the most common vectors, spreading disease to
humans and other vertebrates, such as horses, after biting infected birds or
small animals.
 The most common arboviruses responsible for CNS infection in the United
States are West Nile virus (WNV)
 WNV may also be transmitted by blood transfusion, organ transplantation,
or vertically across the placenta.
 Most children with WNV are either asymptomatic or have a nonspecific
viral-like illness.
 Approximately 1% develop CNS disease; adults are more severely affected
than children.

 Herpes family
 Herpes simplex virus (HSV) type 1 is an important cause of severe, sporadic encephalitis in children and adults.
 Brain involvement usually is focal; progression to coma and death occurs in 70% of cases without antiviral therapy.
 Severe encephalitis with diffuse brain involvement is caused by HSV type 2 in neonates who usually contract the virus
from their mothers at delivery.
 A mild transient form of meningoencephalitis may accompany genital herpes infection in sexually active adolescents;
most of these infections are caused by HSV type 2.
 Varicella-zoster virus may cause CNS infection in close temporal relationship with chickenpox.
 The most common manifestation of CNS involvement is cerebellar ataxia, and the most severe is acute encephalitis.
 After primary infection, varicella-zoster virus becomes latent in spinal and cranial nerve roots and ganglia, expressing
itself later as herpes zoster, sometimes with accompanying mild meningoencephalitis.
 Cytomegalovirus infection of the CNS may be part of congenital infection or disseminated disease in
immunocompromised hosts, but it does not cause meningoencephalitis in normal infants and children.
 Epstein-Barr virus is associated with myriad CNS syndromes.
 Human herpes virus 6 can cause encephalitis, especially among immunocompromised hosts.

Mumps is a common pathogen in regions where mumps
vaccine is not widely used.
Mumps meningoencephalitis is mild, but deafness from
damage of the 8th cranial nerve may be a sequela.
 Meningoencephalitis is caused occasionally by
respiratory viruses (adenovirus, Influenza virus,
parainfluenza virus), rubeola, rubella, or rabies; it may
follow live virus vaccinations against polio, measles,

Epidemiology (Pg 2946 Nelsons)
 Infection with enteroviruses is spread directly from person to person, with a
usual incubation period of 4-6 days.
 Most cases in temperate climates occur in the summer and fall.
 Epidemiologic considerations in aseptic meningitis due to agents other than
enteroviruses also include season, geography (travel), climatic conditions,
animal exposures, mosquito or tick bites, and factors related to the specific
pathogen.

Pathogensis and Pathology (Pg 2947
Nelsons)
 Neurologic damage is caused by direct invasion and destruction of neural
tissues by actively multiplying viruses or by a host reaction to viral
antigens.
 Tissue sections of the brain generally are characterized by meningeal
congestion and mononuclear infiltration, perivascular cuffs of lymphocytes
and plasma cells, some perivascular tissue necrosis with myelin
breakdown, and neuronal disruption in various stages, including, ultimately,
neuronophagia and endothelial proliferation or necrosis.
 A marked degree of demyelination with preservation of neurons and their
axons is considered to represent predominantly “postinfectious” or an
autoimmune encephalitis.
 The cerebral cortex, especially the temporal lobe, is often severely affected
by HSV; the arboviruses tend to affect the entire brain; rabies has a
predilection for the basal structures. Involvement of the spinal cord, nerve
roots, and peripheral nerves is variable.

Clinical Manifestations (Pg 2947 Nelsons)
 The progression and severity of disease are determined by the relative
degree of meningeal and parenchymal involvement.
 Some children may appear to be mildly affected initially, only to lapse into
coma and die suddenly.
 In others, the illness may be ushered in by high fever, violent convulsions
interspersed with bizarre movements, and hallucinations alternating with
brief periods of clarity, followed by complete recovery.
 The onset of illness is generally acute.
 CNS signs and symptoms are often preceded by a nonspecific febrile
illness of a few days’ duration.
 The presenting manifestations in older children are headache and
hyperesthesia
 infants, irritability and lethargy.

Clinical Manifestations (Pg 2947 Nelsons)
 Headache is most often frontal or generalized;
 adolescents frequently complain of retrobulbar pain.
 Fever, nausea and vomiting, photophobia, and pain in the neck, back, and legs are
common.
 As body temperature increases, there may be mental dullness, progressing to stupor in
combination with bizarre movements and convulsions.
 Focal neurologic signs may be stationary, progressive, or fluctuating.
 WNV and nonpolio enteroviruses may cause anterior horn cell injury and a flaccid
paralysis.
 For those reported with WNV, encephalitis is more common than aseptic meningitis.
 acute flaccid paralysis may be noted in approximately 5% of patients. Nonetheless,
many patients have a nonspecific febrile illness “West Nile fever” and may never seek
medical attention.
 Loss of bowel and bladder control and unprovoked emotional outbursts may occur.

Clinical Manifestation (Pg 2947 Nelsons)
 Exanthems often precede or accompany the CNS
signs, especially with echoviruses, coxsackieviruses,
varicella-zoster virus, measles, rubella, and,
occasionally, WNV.
 Examination often reveals nuchal rigidity without
significant localizing neurologic changes, at least at
the onset.
 Specific forms or complicating manifestations of CNS
viral infection include Guillain-Barré syndrome,
transverse myelitis, hemiplegia, and cerebellar
ataxia.

Diagnosis (Pg 2947 Nelsons)
 The diagnosis of viral encephalitis is usually made on the basis of the clinical
presentation of nonspecific prodrome followed by progressive CNS symptoms.
 The diagnosis is supported by examination of the CSF, which usually shows a
mild mononuclear predominance.
 Other tests of potential value in the evaluation of patients with suspected viral
meningoencephalitis include an electroencephalogram (EEG) and
neuroimaging studies.
 The EEG typically shows diffuse slow-wave activity, usually without focal
changes.
 Neuroimaging studies (CT or MRI) may show swelling of the brain parenchyma.
 Focal seizures or focal findings on EEG, CT, or MRI, especially involving the
temporal lobes, suggest HSV encephalitis.

Lab Findings (Pg 2947 Nelsons)
 The CSF contains from a few to several thousand cells per cubic millimeter.
 Early in the disease, the cells are often polymorphonuclear; later, mononuclear
cells predominate.
 This change in cellular type is often demonstrated in CSF samples obtained as
little as 8-12 hr apart.
 The protein concentration in CSF tends to be normal or slightly elevated, but
concentrations may be very high if brain destruction is extensive, such as that
accompanying HSV encephalitis.
 The glucose level is usually normal, although with certain viruses, for example,
mumps, a substantial depression of CSF glucose concentrations may be
observed.
 The CSF may be normal with parechovirus and in those who have encephalitis
in the absence of meningeal involvement

 The success of isolating viruses from the CSF of children with viral
meningoencephalitis is determined by the time in the clinical course that the
specimen is obtained, the specific etiologic agent, whether the infection is a
meningitic as opposed to a localized encephalitic process, and the skill of the
diagnostic laboratory staff.
 Isolating a virus is most likely early in the illness, and the enteroviruses tend to
be the easiest to isolate, although recovery of these agents from the CSF rarely
exceeds 70%.
 To increase the likelihood of identifying the putative viral pathogen, specimens
for culture should also be obtained from nasopharyngeal swabs, feces, and
urine.
 Although isolating a virus from 1 or more of these sites does not prove
causality, it is highly suggestive. Detection of viral DNA or RNA by polymerase
chain reaction is the test of choice in the diagnosis of CNS infection caused by
HSV, parechovirus and enteroviruses, respectively.
 CSF serology is the diagnostic test of choice for WNV

 A serum specimen should be obtained early in the course of illness and, if viral
cultures are not diagnostic, again 2-3 wk later for serologic studies.
 Serologic methods are not practical for diagnosing CNS infections caused by
the enteroviruses because there are too many serotypes.
 This approach may be useful, however, in confirming that a case is caused by a
known circulating serotype.
 Serologic tests may also be of value in determining the etiology of
nonenteroviral CNS infection, such as arboviral infection.

Treatment (Pg 2948 Nelsons)
 Acyclovir for HSV encephalitis
 Treatment of viral meningoencephalitis is supportive.
 Treatment of mild disease may require only symptomatic
relief.
 Headache and hyperesthesia are treated with rest, non–
aspirin containing analgesics, and a reduction in room light,
noise, and visitors.
 Acetaminophen is recommended for fever.
 Opioid agents and medications to reduce nausea may be
useful, but if possible, their use in children should be
minimized because they may induce misleading signs and

 It is important to monitor patients with severe encephalitis closely for convulsions,
cerebral edema, inadequate respiratory exchange, disturbed fluid and electrolyte
balance, aspiration and asphyxia, and cardiac or respiratory arrest of central origin.
 In patients with evidence of increased ICP, placement of a pressure transducer in
the epidural space may be indicated.
 The risks of cardiac and respiratory failure or arrest are high with severe disease.
 All fluids, electrolytes, and medications are initially given parenterally.
 In prolonged states of coma, parenteral alimentation is indicated.
 SIADH is common in acute CNS disorders; monitoring of serum sodium
concentrations is required for early detection.
 Normal blood levels of glucose, magnesium, and calcium must be maintained to
minimize the likelihood of convulsions.
 If cerebral edema or seizures become evident, vigorous treatment should be
instituted.

Prognosis (Pg 2948 Nelsons)
 Supportive and rehabilitative efforts are very important after patients recover
from the acute phase of illness.
 Motor incoordination, convulsive disorders, total or partial deafness, and
behavioral disturbances may follow viral CNS infections.
 Visual disturbances from chorioretinopathy and perceptual amblyopia may also
occur.
 Special facilities and, at times, institutional placement may become necessary.
 Some sequelae of infection may be very subtle. Therefore, neurodevelopmental
 and audiologic evaluations should be part of the routine follow-up
 of children who have recovered from viral meningoencephalitis.

 Most children completely recover from viral infections of the CNS, although
the prognosis depends on the severity of the clinical illness, the specific
causative organism, and the age of the child.
 If the clinical illness is severe and substantial parenchymal involvement is
evident, the prognosis is poor, with potential deficits being intellectual,
motor, psychiatric, epileptic, visual, or auditory in nature.
 Severe sequelae should also be anticipated in those with infection caused
by HSV.
 Although some literature suggests that infants who contract viral
meningoencephalitis have a poorer long-term outcome than older children,
most other data refute this observation.
 Approximately 10% of children younger than 2 yr of age with enteroviral
CNS infections suffer an acute complication such as seizures, increased
ICP, or coma. Almost all have favorable long-term neurologic outcomes.

Prevention (Pg 2948 Nelsons)
 Widespread use of effective viral vaccines for polio, measles, mumps, rubella,
and varicella has almost eliminated CNS complications.
 The availability of domestic animal vaccine programs against rabies has
reduced the frequency of rabies encephalitis.
 Control of insect vectors by suitable spraying methods and eradication of insect
breeding sites, however, reduces the incidence of these infections.
 Furthermore, minimizing mosquito bites through the application of N,N-diethyl-
3- methylbenzamide (DEET)-containing insect repellents on exposed skin and
wearing long-sleeved shirts, long pants, and socks when outdoors, especially at
dawn and dusk, reduces the risk of arboviral infection.

Esoniphilic Meningitis (Pg 2948 Nelsons)
 Eosinophilic meningitis is defined as 10 or more eosinophils/mm3 of CSF.
 The most common cause worldwide of eosinophilic pleocytosis is CNS infection
with helminthic parasites.

 Although any tissue-migrating helminth may cause eosinophilic meningitis, the
most common cause is human infection with the rat lungworm, Angiostrongylus
cantonensis
 Other parasites that can cause eosinophilic meningitis include Gnathostoma
spinigerum (dog and cat roundworm) Baylisascaris procyonis (raccoon
roundworm), Ascaris lumbricoides (human roundworm), Trichinella spiralis,
Toxocara canis, T. gondii, Paragonimus westermani, Echinococcus granulosus,
Schistosoma japonicum, Onchocerca volvulus, and Taenia solium.
 Eosinophilic meningitis may also occur as an unusual manifestation of more
common viral, bacterial, or fungal infections of the CNS.
 Noninfectious causes of eosinophilic meningitis include multiple sclerosis,
malignancy, hypereosinophilic syndrome, or a reaction to medications or a
ventriculoperitoneal shunt.

Epidemiology (Pg 2948 Nelsons)
 A. cantonensis is found in Southeast Asia, the South Pacific, Japan, Taiwan,
Egypt, Ivory Coast, and Cuba. Infection is acquired by eating raw or
undercooked freshwater snails, slugs, prawns, or crabs containing infectious
3rd-stage larvae.
 Gnathostoma infections are found in Japan, China, India, Bangladesh, and
Southeast Asia.
 Gnathostomiasis is acquired by eating undercooked or raw fish, frog, bird, or
snake meat

Clinical manifestation (Pg 2948 Nelsons)
 When eosinophilic meningitis results from helminthic infestation, patients
become ill 1-3 wk after exposure.
 This reflects the transit time for parasites to migrate from the gastrointestinal
tract to the CNS.
 Common concomitant findings include fever, peripheral eosinophilia, vomiting,
abdominal pain, creeping skin eruptions, or pleurisy.
 Neurologic symptoms may include headache, meningismus, ataxia, cranial
nerve palsies, and paresthesias.
 Paraparesis or incontinence can result from radiculitis or myelitis.

Diagnosis (Pg 2948 Nelsons)
 The presumptive diagnosis of helminth-induced eosinophilic meningitis is most
often based on travel and exposure history in the presence of typical clinical
and laboratory findings.
 Direct visualization of helminths in CSF is affected by the relatively low
organism burden, resulting in limited diagnostic sensitivity.
 Serologic assays for helminthic infections are also of limited utility because they
are not readily available commercially and there is substantial cross-reactivity
between different helminth species.

 Treatment is supportive, because infection is
self-limited and anthelmintic drugs do not
appear to influence the outcome of infection.
 Analgesics should be given for headache and
radiculitis, and CSF removal or shunting should
be performed to relieve hydrocephalus, if
present.
 Steroids may decrease the duration of
headaches in adults with eosinophilic
meningitis.

 The prognosis is good; 70% of patients improve sufficiently
to leave the hospital in 1-2 wk.
 Mortality associated with eosinophilic meningitis is <1%.

TB Meningitis
 Tuberculous meningitis (TBM) is a manifestation of extrapulmonary TB,
developing in 1%–5% of the approximately 10 million cases of TB
worldwide.
 common cause of meningitis (and the most common cause of chronic
meningitis) in endemic areas worldwide, particularly among patients co-
infected with HIV.
 TBM is often difficult to diagnose, as initial symptoms are generally
subacute and often nonspecific (although occasionally may present
more acutely), and neck stiffness is typically not present in the early
course of the illness.
 Presenting symptoms may vary from 1 day to 9 months (generally, a
week to a month).
 Children Below 5 years are more prone
https://emedicine.medscape.com/article/1166190-
overview#a2

Etiology
 The causative organism of tuberculous meningitis (TBM) is Mycobacterium
tuberculosis.
 M. tuberculosis is an aerobic gram-positive rod that stains poorly with
hematoxylin and eosin (H&E) because of its thick cell wall that contains lipids,
peptidoglycans, and arabinomannans.
 The high lipid content in its wall makes the cells impervious to Gram staining.
 Ziehl-Neelsen stain forms a complex in the cell wall that prevents decolorization
by acid or alcohol, and the bacilli are stained a bright red, which stands out
clearly against a blue background.
overview#a4

Risk Factors
 Human migration plays a large role in the epidemiology of TB.
 HIV co-infection is the strongest risk factor for progression to active TB; the risk
has been estimated to be as great as 10% per year, compared with 5-10%
lifetime risk among persons with TB but not HIV infection.
 Patients infected with HIV, especially those with AIDS, are at very high risk of
developing active TB when exposed to a person with infectious drug-
susceptible or drug-resistant TB.
 They have a higher incidence of drug-resistant TB, in part due
to Mycobacterium avium-intracellulare, and have worse outcomes
overview#a4

Epidemiology
 Children aged 5–14 years often have been referred to as the favored age
because they have lower rates of TB than any other age group.
 Younger children are more likely to develop meningeal, disseminated, or
lymphatic TB, whereas adolescents more frequently present with pleural,
genitourinary, or peritoneal disease.
 Childhood TB has a limited influence on the immediate epidemiology of the
disease because children rarely are a source of infection to others.
 TBM is uncommon, however, in children younger than 6 months and extremely
rare in infants younger than 3 months, as the causative pathological sequelae
generally take at least 3 months to develop

Pathphysiology
 Mycobacterium tuberculosis bacilli enter the host by droplet inhalation, and initially
infect alveolar macrophages.
 Localized infection worsens in the lungs, and then disseminates to the regional
lymph nodes occurs, resulting in the primary complex.
 The bacilli may then seed to the central nervous system (CNS) and result in any of
three forms of CNS TB: tuberculous meningitis, intracranial tuberculoma, and spinal
tuberculous arachnoiditis.
 Tuberculous pneumonia may result in heavier and more prolonged tuberculous
bacteremia, which renders CNS dissemination more likely, particularly if miliary TB
develops.
 In the brain, the bacilli may form small subpial or subependymal foci of metastatic
caseous lesions, known as Rich foci, after the original pathologic studies of Rich
and McCordick.As the disease progresses, the Rich foci enlarge and may
eventually rupture into the subarachnoid space, resulting in meningitis.
overview#a3

Pathphysiology Cont.
 The location of the expanding tubercle (ie, Rich focus) determines the type of
CNS involvement. Tubercles rupturing into the subarachnoid space cause
meningitis, whereas those deeper in the brain parenchyma or in the spinal cord
cause tuberculomas or abscesses. While an abscess or tuberculoma may
rupture into the ventricle, a Rich focus does not.
 A thick gelatinous exudate may infiltrate the cortical or meningeal blood
vessels, producing inflammation, obstruction, or infarction. Unlike most forms of
bacterial meningitis, TBM tends to occur at the skull base (basal meningitis),
which accounts for the frequent dysfunction of cranial nerves (including III, VI,
and VII), and obstructive hydrocephalus from obstruction of basilar cisterns.
Subsequent neurological pathology is produced by three general processes:
adhesion formation, obliterative vasculitis, and encephalitis or myelitis.
overview#a3

Clinical Features
 Always secondary to primary tb
 First phase -> Vague Symptoms.
 Child does not play is irriatable , drowsy and or restless.
 Anorexia or Vomiting maybe present.
 Older Children may complain of a headache
 Second Phase
 Child is drowsy with neck stiffness and rigidity
 Kerneig and Brudniski sign maybe positive, anterior fontanelle maybe bulge.
 Twitching of muscles, convulsion and raised temperature
 Strabismus Nystagmus and papilodema maybe be present

Clinical Features
 Fundoscopy-> Choroidal TB maybe present.
 Terminal Phase
 Child is characteristically comatose with opisthotonos (spasm of the muscles
causing backward arching of the head, neck, and spine, as in severe
tetanus, some kinds of meningitis, and strychnine poisoning.) and
multiple focal paresis
 Cranial Nerve Palsies are present
 High grade fever often occurs terminally

Diagnosis
 Lumbar Puncture
 Presence of TB somewhere else in the body strong supportive focus
 CXR
 Tuberculin Test

Treatment
 AntiTB meds:- includes simultaneous administration of 4 drugs
1) Isoniazid
2) Rifampicin
3) Streptomycin
4) Pyranzimide
These 4 drugs for the 1st 3 months followed by 2 another for 15 months usually
Rifampicin and INH
Total Period 18 months

Treatment continued
 Steriod to reduce cerebral edema can be given also to reduce fibrosis and
subsequent obstruction of CSF
 2mg/kg for 24 hours of prednisolone for 6-8 weeks at the start of the
treatment starting 3 days after initiation of anti TB meds.

References
 Nelsons Text book
 Medscape
 Basis of Pediatrics

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