The most common causes of bacterial meningitis
in the U.S. are Streptococcuspneumoniae (61%), Neisseria
meningitidis (16%), group B streptococcus (14%), Haemophilus
influenzae (7%), and Listeria monocytogenes (2%).
The median age of illness has risen to 39 years of age, and the
incidence of bacterial meningitis has declined.1 Changes
in epidemiology have mirrored vaccination practices in adults and
children against H. influenzae, S. pneumoniae,
and N. meningitidis. The incidence of penicillin-resistant S.
pneumoniae has increased, so that in some areas it accounts
for approximately one third of cases.1 These facts
are important because they affect the ED selection of empiric antibiotics
for presumptive bacterial meningitis.
S. pneumoniae, H. influenzae type
b, and N. meningitidis are encapsulated organisms
that invade the host through the upper airway, survive dissemination
through the blood stream, and then gain access to the subarachnoid
space. The subcapsular constituents of these organisms trigger inflammatory
cascades. The brain and meninges, encased in the fixed-volume skull,
become edematous. Cerebrospinal fluid (CSF) drainage is reduced
by interference with flow and absorption by the arachnoid granulations.
Intracranial blood vessels initially expand, increasing the volume
occupied by that compartment. The brain itself swells by several
mechanisms. Disruption of the blood–brain barrier allows
entry of protein and ultimately water (vasogenic edema), while hydrocephalus
forces CSF into the periventricular parenchyma (interstitial edema).
Eventually, cell membrane homeostasis may be compromised, leading
to increased intracellular water (cytotoxic edema).
The sum of these expanded volumes overwhelms the compensatory
displacement of CSF into the more compliant spinal compartment,
and intracranial pressure rises as a result. Because brain perfusion
depends on arterial pressure exceeding intracranial pressure, ischemia
Organisms can also gain entry to the CSF by direct contiguous
spread. Such direct spread may be from infected parameningeal structures
(e.g., brain abscess, otitis media, and sinusitis), traumatic or
congenital communications with the exterior, or neurosurgical procedures.
The bacteriologic characteristics of these infections may vary.
Immunologic deficiency states are increasingly common and predispose
to yet other organisms. The clinical and pathophysiologic effects
of organisms other than S. pneumoniae and N.
meningitidis depend on their capacity to stimulate the
host’s immune response. Important risk factors for bacterial
meningitis are listed in Table 168-1.
Table 168-1 Important
Risk Factors for Bacterial Meningitis
| Save Table
Table 168-1 Important
Risk Factors for Bacterial Meningitis
|Acute or chronic otitis media|
|Cerebrospinal fluid leak|
|Neurosurgical procedure/head injury|
|Indwelling neurosurgical device/cochlear implant|
|Liver disease |
|Unvaccinated to Haemophilus influenzae type
b, Neisseria meningitidis, or Streptococcus
Certain historic data should increase the suspicion of meningitis
and suggest specific pathogens. Several areas deserve special attention:
living conditions, trauma, immunocompetence, immunization history,
and antibiotic use. Military barracks and college dormitories are
typical environments in which clusters of cases due to N.
meningitidis occur. Day care centers historically have
been a source for multiple cases due to H. influenzae type
b. A history of head trauma (S. pneumoniae) or
neurosurgery (staphylococcal species or gram-negative rods) may
be significant. Meningococcal meningitis is still a common cause
of meningitis in sub-Saharan Africa.2 Conditions
that affect immunocompetence (e.g., history of surgical or functional
splenectomy, cancer chemotherapy, glucocorticoid therapy, or human
immunodeficiency virus) should be sought. Sinusitis or otitis can
result in meningitis from direct extension of infection.3 A
history of immunization to H. influenzae type b
makes meningitis due to this organism unlikely. Rates of pneumococcal
meningitis have also decreased in adults since the introduction
of pneumococcal vaccine.4 Recent exposure to antibiotics
may influence the clinical course and CSF findings.
Definitive diagnosis is based on demonstrating
bacterial organisms and a corresponding inflammatory response in
the CSF. The classic signs and symptoms are fever, neck stiffness,
headache, and altered mental status, and are probably present in
most cases of bacterial meningitis.5 However, the
absence of fever, neck stiffness, and altered mental status does not
exclude meningitis in adults.6,7 Seizures have
been reported in nearly a quarter7 of cases of
bacterial meningitis, and focal neurologic signs, usually cranial nerve palsies, are also reported.7 However,
among patients with altered mental status alone, the likelihood
of bacterial meningitis is low.8
Examination should include assessment for meningeal irritation
with resistance to passive neck flexion, Brudzinski sign (flexion
of hips and knees in response to passive neck flexion), and Kernig
sign (contraction of hamstrings in response to knee extension while
hip is flexed). Examine the skin for the purpura of meningococcemia,
streptococcemia, or rickettsial infection. Cutaneous stigmata suggesting
microembolization (e.g., petechiae, splinter hemorrhages, and pustular
lesions) can be aspirated when possible for Gram stain and culture.
Percuss the paranasal sinuses and examine the ears for evidence
of primary infection. Examine fundi for papilledema or absence of
venous pulsation, indicating increased intracranial pressure. Neurologic
examination should seek evidence of focal neurologic dysfunction,
such as disordered eye movements, homonymous visual field deficits,
facial asymmetry, and hemiparesis.7
When bacterial meningitis is suspected, treatment should precede
methods for diagnosis. Decision making involves prioritizing empiric
antibiotic administration, performing lumbar puncture, and diagnostic
for Presumptive Bacterial Meningitis
While addressing airway, oxygenation, and volume resuscitation,
the first priority is the administration of an antibiotic that gains
rapid entry to the subarachnoid space. Antibiotic therapy
should be initiated in the ED as soon as possible for presumptive
bacterial meningitis and should not be delayed ...