Pediatric emergency medicine trisk 567

TABLE 94.3
ETIOLOGIES OF ACUTE BACTERIAL MENINGITIS CHILDREN
OUTSIDE THE NEONATAL PERIOD

Goals of Treatment
The goal of treatment is the rapid recognition and treatment of bacterial meningitis to decrease a child’s risk of
neurologic sequelae. The clinical team should consider neuroimaging prior to LP in the immunocompromised
child or the child with focal neurologic deficits. Clinical outcomes include time to appropriate parenteral
antibiotics, CSF sterility at 24 to 48 hours, and neurologic outcome.
Clinical Considerations
Clinical recognition: The most common signs and symptoms of bacterial meningitis are listed in Table 94.4 .
Before 2 months of age, the history is usually that of irritability, an altered sleep pattern, vomiting, and decreased
oral intake. In particular, paradoxical irritability points to the diagnosis of meningitis. Irritability in the infant
without inflammation of the meninges is generally alleviated by maternal fondling; however, in the child with
meningitis, any handling, even directed toward soothing the infant, may increase irritability by its effect on the
inflamed meninges. The amount of time spent sleeping may either increase because of obtundation or decrease
from irritability. Bulging of the fontanelle, an almost certain sign of meningitis in the febrile, ill-appearing infant,
is a late finding. Vomiting is a sensitive but nonspecific feature of infantile meningitis.
As the child ages past 2 months, the symptoms gradually become more specific for involvement of the central
nervous system (CNS). A change in the level of activity is almost always noticeable. However, it is only in the
child older than 2 years that meningitis manifests reliably with complaints of headache, neck stiffness, and
photophobia.


TABLE 94.4
SIGNS AND SYMPTOMS OF MENINGITIS
Signs
Age

Symptoms

Early

Late

0–3 mo

Paradoxical irritability

Lethargy

Bulging fontanelle

Altered sleep pattern

Irritability

Shock

Vomiting
Lethargy

Fever
Hypothermia (<1 mo)

Irritability

Fever

Nuchal rigidity

Altered sleep pattern

Irritability

Coma

4–24 mo

Lethargy
>2 yrs

Shock

Headache

Fever

Coma

Neck pain

Nuchal rigidity

Shock

Lethargy

Irritability

The physical examination in the young infant rarely provides specific corroboration, even when the history

suggests meningitis. Fever may be absent in these children, despite the presence of bacterial infection. Any child
younger than 2 months who is brought to the ED with a documented temperature of ≥100.4°F (38˚C) should be
considered at risk for meningitis. The physical signs are sufficiently elusive that many experts caution that one
should not rely exclusively on the examination to rule out meningeal infection. It is estimated that bacterial
meningitis occurs in 1% to 2% of febrile young infants (Chapter 31 Fever ).
After 2 months of age, increasing, but not absolute, reliance can be placed on the physical findings; fever is
typically noted. Specific evidence of meningeal irritation is often present, including nuchal rigidity and, less often,
Kernig (pain with extension of the leg on a flexed femur) and Brudzinski (involuntary lifting of the legs when the
head is raised while the child is lying supine) signs. When an LP fails to confirm the diagnosis of meningitis,
despite the presence of meningeal signs, other conditions must be pursued that can mimic the findings on physical
examination. Conditions capable of producing the findings typical of meningismus (irritation of the meninges
without pleocytosis in the CSF) include severe pharyngitis, retropharyngeal abscess (RTA), cervical adenitis,
arthritis or osteomyelitis of the cervical spine, upper lobe pneumonia, subarachnoid hemorrhage, pyelonephritis,
and tetanus.
Seizures are a presenting complaint for 20% of children with bacterial meningitis. Many of these are focal,
recurrent, or prolonged seizures. Most clinicians advise that children younger than 6 months with a first-time
febrile seizure should routinely have LP performed to discern the presence of CNS infection, unless there are
specific contraindications or an alternative diagnosis is readily apparent. Febrile seizures are reviewed in Chapter
72 Seizures .


TABLE 94.5
IMMEDIATE MANAGEMENT STEPS FOR CHILDREN WITH SUSPECTED OR CONFIRMED
BACTERIAL MENINGITIS
Immediate
evaluation

Initiate hemodynamic monitoring and support
Achieve venous access; use cardiorespiratory monitors

Laboratory
evaluation

Ensure adequate ventilation and cardiac function
CSF for cell count and differential; Gram stain and culture; glucose; protein
Consider holding CSF in the laboratory for enteroviral or HSV PCR, AFB culture,
cryptococcal, or arboviral studies
CBC, blood culture, electrolytes, serum glucose, BUN and creatinine, prothrombin time
and partial thromboplastin time

Medications

Fluid resuscitation for septic shock, if present
If Mycobacterium tuberculosis or H. influenzae type b is the suspected cause of
meningitis, consider dexamethasone (0.15 mg/kg) before or with the first dose of
antibiotics
Antibiotics (see Table 94.7 )
Glucose (if serum glucose <50 mg/dL) 0.25–1 g/kg
Treat acidosis and coagulopathy, if present.

CSF, cerebrospinal fluid; HSV, herpes simplex virus; PCR, polymerase chain reaction; AFB, acid-fast bacilli; CBC, complete blood count.

Triage considerations: Children with fever and altered mental status or neck pain should be evaluated promptly
for meningitis. Associated tachycardia and hypotension can be seen in children with meningitis who are in
compensated or uncompensated shock, respectively. If meningococcus is suspected, providers should wear simple
face masks and utilize droplet precautions.
Clinical assessment: Initial considerations in the management of children with bacterial meningitis are listed in
Table 94.5 . Confirmation of meningitis is by sampling of the CSF. The most common CSF parameters associated
with various causes of meningitis are summarized in Table 94.6 . The CSF Gram stain will be positive for an
organism in approximately two-thirds (40% to 90%) of cases of bacterial meningitis and the results of Gram stain

should be used to add additional antimicrobial therapy when appropriate. It is prudent to await culture
confirmation before antibiotic coverage is narrowed. In certain patients, computed tomography (CT) should be
considered prior to LP. These criteria are not as well defined for pediatric patients, but in adult patients, they
include immunocompromised state; history of focal CNS disease; presence of papilledema; and focal neurologic
deficit.
Seizures occur in 20% of children with bacterial meningitis and, occasionally, in those with viral infections of
the CNS, such as meningoencephalitis due to HSV. One should always be suspicious of derangement of the
glucose or sodium as a cause of convulsive activity. However, most seizures are caused by irritation of the brain
from the infectious process. Subdural effusion and, less often, empyema occur in 20% to 40% of young children
with meningitis but usually appear later in the course.
Management: The optimal antibiotics for empiric treatment of acute bacterial meningitis would offer coverage
for the most common pathogens, be bactericidal, and cross the blood–brain barrier. Treatment options for
meningitis in normal hosts are described in Table 94.7 . Treatment of tuberculosis meningitis and HSV meningitis
is described elsewhere. Evaluation and treatment of meningitis in immunocompromised hosts (e.g., human
immunodeficiency virus [HIV]-infected children) should be undertaken with consultation with an ID specialist.
Consideration should be given to admitting children with suspected bacterial meningitis to an intensive care unit
setting for close initial monitoring. Standard precautions are indicated for most causes of bacterial meningitis,
except for meningococcus (droplet precautions) and tuberculosis meningitis (airborne precautions). Electrolyte
imbalances seen in bacterial meningitis and their treatment are discussed in Chapter 100 Renal and Electrolyte
Emergencies .


TABLE 94.6
USUAL RANGES FOR CEREBROSPINAL FLUID PARAMETERS

Herpes Simplex Virus, Neonatal
CLINICAL PEARLS AND PITFALLS
Most mothers of infants with HSV infection do not provide a history of HSV, as primary infection can
be asymptomatic and vesicular lesions deep in the female genitourinary tract cannot be visualized by
the mothers. Thus, a “negative” maternal history of herpes does not rule out herpes in an infant.

HSV has substantial overlap with bacterial causes of sepsis and meningitis.
The three main forms of neonatal disease are skin, eye, and mouth (SEM) disease, CNS disease,
and disseminated disease.
HSV should be considered in the differential diagnosis of any febrile neonate with a CSF pleocytosis
and in infants with elevated hepatic transaminases or coagulopathy.
Early recognition of HSV disease and prompt initiation of acyclovir can decrease the substantial
morbidity and mortality in infants.
Current Evidence
HSV has three major manifestations in the neonatal period. HSV genital lesions will be described in the section on
sexually transmitted infections (STIs). It is estimated that 45% of adults in the United States are seropositive for
HSV-1 and 16% for HSV-2. Both viruses can cause oral or genitourinary infection, but approximately 75% of
neonatal HSV disease is caused by HSV-2. In one study, 0.4% of 0- to 60-day-old infants in whom lumbar
punctures were performed had HSV infection, with a peak in the 2nd and 3rd weeks of life. Neonatal HSV is
thought to complicate 1 in 3,200 deliveries, resulting in approximately 1,500 cases/yr in the United States. Risk
factors for transmission to neonates include primary maternal infection; vaginal delivery; prolonged rupture of
membranes; HSV-2; and use of fetal scalp electrodes. The risk of neonatal HSV is highest during the primary
infection in the mother, as viremia is often higher than with recurrent infections, and an effective immune response
has yet to be mounted. However, 75% of mothers of HSV-infected neonates did not report a history of herpes, as
primary infection can be asymptomatic. As such, the lack of maternal history of HSV should not provide false
reassurance to the PEM clinician.