AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Despite advances in antimicrobial and general supportive therapies, central nervous system (CNS) infections remain a significant cause of morbidity and mortality in children. As classical signs and symptoms often are not present, especially in the younger children, diagnosing CNS infections is a challenge to the emergency physician. Also, even for children who have had prompt diagnosis and treatment, a high frequency of neurologic sequelae remains. This often leads to legal action against the emergency physician. The emergency physician is faced with the daunting task of separating out those few children with CNS infections from the vast majority of children who come to the ED with less serious infections.

Pathophysiology

To develop bacterial meningitis, the invading organism must gain access to the subarachnoid space. This is usually via hematogenous spread from the upper respiratory tract where the initial colonization has occurred. Less frequently, there is direct spread from a contiguous focus (eg, sinusitis, mastoiditis, otitis media) or through an injury, such as a skull fracture.

The most common causative organisms in the first month of life are Escherichia coli and group B streptococci. Listeria monocytogenes infection also occurs in patients in this age range and accounts for 5-10% of cases. Neisseria meningitidis infections occurring in the first month of life have been reported. From 30-60 days, group B streptococcal infection occurs frequently, and the gram-negative enterics decline in frequency. Streptococcus pneumoniae, Haemophilus influenzae, and N meningitidis occur rarely in this age group. In those older than 2 months, S pneumoniae and N meningitidis currently cause the majority of the cases of bacterial meningitis. H influenzae may still occur, especially in children who have not received the Hib vaccine.

The most common causative organisms (eg, N meningitidis, S pneumoniae, H influenzae) contain a polysaccharide capsule that allows them to colonize the nasopharynx of healthy children without any systemic or local reaction. A concurrent viral infection may facilitate the penetration of the nasopharyngeal epithelium by the bacteria. Once in the bloodstream, the polysaccharide capsule allows the bacteria to resist opsonization by the classical complement pathway and, thus, inhibit phagocytosis.

Unusual bacteria occasionally cause meningitis. Pasteurella multocida is known to cause skin infections from cat or dog bites. A recent case described a 7-week-old infant with P multocida meningitis after exposure to dog saliva with no wound, emphasizing the need to protect young children from this pathogen. This infection, while rare, is associated with significant morbidity and mortality.

Salmonella meningitis should be suspected in any child with this organism grown at any other site in an unwell child or one younger than 6 months. Mothers known to be infected with Salmonella during pregnancy may put their child at risk. As therapy is different for Salmonella meningitis, while rare, it must be considered in the above situations.

The bacteremic phase allows penetration of the cerebrospinal fluid (CSF) through the choroid plexus. The CSF is poorly equipped to control infection because type-specific antibodies do not penetrate the blood brain barrier well and complement components are absent or in low concentrations.

The cell walls of both gram-positive and gram-negative bacteria contain potent triggers of the inflammatory response. In the gram-positive bacteria, teichoic acid is considered the major pathogenic component. In gram-negative bacteria, lipopolysaccharide or endotoxin is the major pathogenic component. These components are released in the CSF during bacterial growth and especially with the lysis of bacterial cells. Antibiotic therapy causes a significant release of the mediators of the inflammatory response.

The mediators of the inflammatory response include cytokines (tumor necrosis factor, interleukin 1, 6, 8, 10), platelet activating factor, nitric oxide, prostaglandins, and leukotrienes. These mediators cause disruption of the blood brain barrier, vasodilation, neuronal toxicity, meningeal inflammation, platelet aggregation, and activation of leukocytes. The capillary endothelial cell is the main site of injury in bacterial meningitis; thus, it is a vasculitis, which results in destruction of vascular integrity. The ultimate consequences are damage to the blood brain barrier, brain edema, impaired cerebral blood flow, and neuronal injury.

Because of the damage done by the body's response to the infection, various anti-inflammatory agents have been used in an attempt to decrease the morbidity and mortality of bacterial meningitis. Only dexamethasone occasionally has been proven effective.

Viral meningitis is the most common infection of the CNS. It most frequently occurs in children younger than 1 year. Enterovirus is the most common causative agent and is a frequent cause of febrile illnesses in children. Other viral pathogens include paramyxoviruses, herpes, influenza, rubella, and adenovirus. Meningitis may occur in up to half of children younger than 3 months with enteroviral infection. Enteroviral infection can occur any time during the year but is associated with epidemics in the summer and fall. Viral infection causes an inflammatory response but to a lesser degree than bacterial infection. Damage from viral meningitis may be due to an associated encephalitis and increased intracranial pressure.

Although tuberculosis is the most common cause of death from a single agent in children worldwide, it is a rare infection in children in developed countries. The emergency physician must suspect this infection in children who are recent immigrants from underdeveloped countries, who are infected or are exposed to persons infected with HIV, or are from poor urban centers. Tuberculous meningitis and encephalitis are 2 of the more serious complications of tuberculosis. In its early stages, it is difficult to diagnose and, untreated, is usually fatal. Meningitis occurs 3-6 months after the primary infection.

Fungal meningitis is rare but may occur in immunocompromised patients; children with cancer, previous neurosurgery, or cranial trauma; or premature infants with low birth rates. Most cases are in children who are receiving antibiotic therapy and, thus, usually are inpatients.

The etiology of aseptic meningitis caused by drugs is not well understood. This form of meningitis is infrequent in the pediatric population.

Encephalitis is a similar disease of the central nervous system. This disease is an inflammation of brain parenchyma. Often, a viral agent is responsible. Viral entry occurs through hematogenous or neuronal routes.

The more common form of encephalitis is transmitted by bites of mosquitoes and ticks, infected with the virus. The virus comes from the Togavirus, Flavivirus, and Bunyavirus families.

The more common types of encephalitis in the United States are La Crosse virus, eastern equine encephalitis virus, and St Louis virus. Often, these causes of encephalitis cause similar signs and symptoms. Confirmation and differentiation come from laboratory testing. However, its utility is limited to a number of identifiable pathogens.

West Nile virus is becoming a leading cause of encephalitis, caused by the arbovirus from the Flaviviridae family. Mosquitoes, spreading virus between its natural hosts, migrating birds, transmit it. Mosquitoes bite humans, who become infected with the virus. However, human hosts are dead-end hosts for the virus.

Most humans do not develop the disease. Approximately 1 symptomatic infection develops for every 120-160 asymptomatic ones. The young and old are at risk of developing symptomatic disease.

It has become a greater public health issue, given that spread occurs with migratory birds. The first cases were identified in New York City in 1999, with additional cases being identified in the following years across the United States.

Encephalitis can be transmitted by other means. Herpetic encephalitis and rabies are two examples, where transmission occurs by direct contact and mammalian bites, respectively. In the case of herpetic encephalitis, there is evidence of virus reactivation and subsequent intraneuronal transmission, leading to encephalitis.

Frequency

United States

In 1995, 5755 cases of bacterial meningitis were reported. This is a dramatic decrease from the 12,920 cases reported in 1986. This is attributed to the decrease in H influenzae type B meningitis since the introduction of the Hib vaccine. The occurrences by infectious agent in 1995 are as follows:

• S pneumoniae: 1.1 per 100,000
• N meningitidis: 0.6 per 100,000
• Group B Streptococcus: 0.3 per 100,000
• L monocytogenes: 0.2 per 100,000
• H influenzae: 0.2 per 100,000

The advent of vaccine has changed the incidence of disease. The incidence of disease caused by H influenzae, S pneumoniae, and N meningitidis has decreased.

The advent of universal Hib vaccination in developed countries has lead to the reduction of more than 99% of invasive disease. The vaccine is directed against the H influenzae type b strain. This protection continues even when Hib is coadministered with other vaccines. Just as important, the vaccine continues to confer immunity into later childhood.

A similar effect occurs with the advent of pneumonococcal vaccine. This is true for the pneumococcal polysaccharide vaccines conjugated to various proteins. Given at ages 2, 4, and 6 months, this vaccine has reduced invasive disease more than 90%. Age groups most affected are those younger than age 2 years and those aged 2-5 years. This was proven in a surveillance study in Louisville, Kentucky.¹

However, vaccine for Neisseria has not been efficacious in younger children. This is due to poor immunogenic response. Current recommendation targets immunization for children older than age 2 years and high-risk patients with asplenic and terminal complement deficiencies. In addition, young adults living in close quarters, such as dormitories or military barracks, will benefit.

The incidence of neonatal meningitis has shown no significant change in the last 25 years. Viral meningitis is the most common form of aseptic meningitis and, since the introduction of mumps vaccine, is caused by enteroviruses in up to 85% of cases. Incidence of encephalitis is more difficult to estimate because of difficulty in establishing the diagnosis. One report estimates an incidence of 1 in 500-1000 in the first 6 months of life.

International

The World Health Organization estimates that bacterial meningitis strikes 426,000 children younger than 5 years annually, with 85,000 deaths. The incidence of bacterial meningitis depends on the use of the Hib vaccine. A report from Japan shows an overall rate of 2.32 per 100,000 population with the rate in children younger than 4 years of 7.22.² The most common organisms in this same study were H influenzae, S pneumoniae, group B Streptococcus, and E coli, in that order.² In Finland, where the Hib vaccine is widely used, there was a decrease from 30 cases of meningitis due to H influenzae in children younger than 4 years in 1986 to no cases in 1991.³

The incidence of encephalitis is related to the extent of childhood vaccination. In a report from Japan, the overall incidence of meningoencephalitis was 3.3 per 100,000 population with an incidence of 6.6 per 100,000 in children younger than 4 years. The most frequent causative agents were measles, herpes, and rubella.

Mortality/Morbidity

Morbidity and mortality rates depend on the infectious agent, age of the child, general health, and prompt diagnosis and treatment. Despite improvement in antibiotic and supportive therapy, a significant mortality and morbidity rate remains.

• The overall mortality for bacterial meningitis is 5-10% and varies with causative organism and age. Neonatal meningitis has a mortality rate of 15-20%. In older children, the mortality rate is 3-10%. Meningitis from S pneumoniae has the highest mortality rate (26.3-30%); H influenzae type B has a 7.7-10.3% mortality rate; N meningitidis has the lowest mortality rate of the most common organisms, at 3.5-10.3%.
• • Up to 30% of children have neurological sequelae. This varies by organism, with S pneumoniae having the highest rate of complications.
  • Several studies indicate that the complication rate from S pneumoniae meningitis did not vary if the infection was from a penicillin sensitive or resistant strain. These studies showed that dexamethasone did not improve outcomes.
  • Another study showed a low (<5%) incidence of hearing loss in children diagnosed with meningococcal meningitis. Sensorineural hearing loss is one of the most frequent problems. Children at greatest risk for hearing loss include those with evidence of increased intracranial pressure, abnormal findings on CT scan, male sex, low glucose levels in CSF, infection by S pneumoniae, and nuchal rigidity.
  • As many of the children affected are very young and cognitive and motor skills are immature, some of the sequelae may not be recognized for years. A recent study followed children who recovered from meningitis for 5-10 years. They found 1 in 4 school-aged meningitis survivors had either serious and disabling sequelae or a functionally important behavior disorder or neuropsychiatric or auditory dysfunction that impaired their performance in school.
• Viral meningoencephalitis: Enteroviral infection usually has few complications. Herpes simplex and arbovirus infections, in addition to viral infections in AIDS patients, can result in severe neurological disease.
• Tuberculous meningitis: Morbidity and mortality rates are related to the stage of the disease. Stage I has a 30% significant morbidity, stage II 56%, and stage III 94%.

Race

Bacterial meningitis more frequently occurs in black and Hispanic children. This is thought to be related to socioeconomic rather than racial factors.

Sex

Prevalence of bacterial meningitis is higher in males. A recent report from Finland showed males more often had mumps and varicella encephalitis, whereas females had adenoviral and Mycoplasma encephalitis more often.

Age

For both meningitis and encephalitis, the greatest occurrence is in children younger than 4 years with a peak incidence in those aged 3-8 months.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Bacterial meningitis
• • The younger the child, the less likely he or she is to exhibit the classic symptoms of fever, headache, and meningeal signs.
  • Meningitis in the neonatal period is associated with maternal infection or pyrexia at delivery. The child younger than 3 months may have very nonspecific symptoms, including hyperthermia or hypothermia, change in sleeping or eating habits, irritability or lethargy, vomiting, high pitched cry, or seizures.
  • Meningismus and a bulging fontanel may be observed but are not needed for diagnosis.
  • A child who is quiet at rest but who cries when moved or comforted may have meningeal irritation (paradoxical irritability).
  • After age 3 months, the child may display symptoms more often associated with bacterial meningitis, with fever, vomiting, irritability, lethargy, or any change in behavior.
  • After age 2-3 years, children may complain of headache, stiff neck, and photophobia.
  • The clinical course may be brief and fulminant with rapid progression of symptoms or may follow a more gradual course with several days of upper respiratory infection progressing to more severe symptoms. The fulminant course is more often associated with N meningitidis infection.
• Viral meningitis
• • In areas with widespread vaccination of children, enteroviruses are the most common causes of viral meningitis. The onset is variable and may have several days of fever, anorexia, and general malaise. It also may present as a rather abrupt onset of fever, nausea, vomiting, and headache.
  • Additional symptoms are shared with enteroviral infections, such as pharyngitis, conjunctivitis, and myositis.
  • Other causes of viral meningitis also may be associated with encephalitis. Arboviral infections frequently have associated encephalitis and seizures.
  • Adenoviral, mumps, and varicella-zoster infections tend to be more severe than enteroviral infections, and often evidence of encephalitis is present.
  • In areas with low vaccination rates, mumps virus is often the most frequent cause of meningitis.
• Tuberculous meningitis: Occurring 3-6 months after primary infection, this may present suddenly or insidiously and usually has 3 clinical stages.
• • The first stage consists of 1-2 weeks of fever, headache, malaise, and irritability.
  • The second stage may occur suddenly and consists of more typical meningeal signs.
  • The final stage consists of worsening neurological condition, coma, and death.
• Fungal meningitis occurs in immunocompromised patients and has a variable presentation.
• Aseptic meningitis may be caused by drugs, usually nonsteroidal anti-inflammatory drugs (NSAIDs), IVIG, and antibiotics. A recent report was of a pediatric patient with a trimethoprim-sulfamethoxazole–induced meningitis. Symptoms were similar to those of viral meningitis. Symptoms may occur within minutes of ingestion of the drug.
• Encephalitis
  • Diagnosis for the causative viral agent is aided by historical facts. Information such as season of year, travel, activities, and exposure to animals helps with diagnosis.
  • A distinction between viral encephalitis and postinfectious encephalomyelitis is important because management and prognosis are different. With postinfectious encephalomyelitis, the usual presentation is a nonspecific respiratory viral syndrome.

Physical

Physical examination findings are widely variable based on age and infecting organism. It is important to remember that the younger the child, the less specific the symptoms.

• In the young infant findings that definitely point to meningitis are rare.
• • The infant may be febrile or hypothermic.
  • Bulging of the fontanel, diastasis of the sutures, and nuchal rigidity point to meningitis but are usually late findings.
• As the child grows older, the physical examination becomes more reliable.
• • Meningeal signs (eg, headache, nuchal rigidity, positive Kernig and Brudzinski signs) should be sought, and their presence or absence recorded.
  • Focal neurological signs may be present in up to 15% of patients and are associated with a worse prognosis.
  • Seizures occur in up to 30% of children with bacterial meningitis.
  • Obtundation and coma occur in 15-20% of patients and are more frequent with pneumococcal meningitis.
  • Encephalitis may present like meningitis or the symptoms of the systemic viral infection may predominate.
• Encephalitis
• • Physical findings for encephalitis are fever, headache, and decreased neurological function. Decreased neurological functions include altered mental status, focal neurological function, and seizure activities. These findings can help identify the virus type and prognosis.
  • In West Nile virus, the signs and symptoms are nonspecific and include fever, malaise, periocular pain, lymphadenopathy, and myalgia.
  • West Nile virus has some unique physical findings including fine, maculopapular, erythematous rash; proximal muscle weakness; and flaccid paralysis. This rash is commonly found in children.
  • Critically ill patients have neurological dysfunction, such as altered mental status and cranial nerve dysfunction, as the major physical finding.

Causes

• Risk factors for bacterial meningitis
• • Age
  • Low family income
  • Attendance at day care
  • Head trauma
  • Splenectomy
  • Chronic disease
  • Children with facial cellulitis, periorbital cellulitis, sinusitis, and septic arthritis have an increased risk of meningitis.
  • Maternal infection and pyrexia at the time of delivery are associated with neonatal meningitis.
• Use of the Hib vaccine decreases likelihood of infection from that agent.
• Viral meningoencephalitis
• • Immunizations for measles, mumps, and rubella decrease the risk of infection from those agents.
  • It is unclear why some patients with systemic viral illnesses develop meningitis or encephalitis.
• Fungal meningitis occurs in immunocompromised patients.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Children who have partially treated meningitis or develop it while on antibiotics have modified signs and symptoms, and the diagnosis is usually delayed.

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Complete blood count (CBC) with differential
• Blood cultures
• Coagulation studies
• Serum glucose
• Electrolytes
• Bacterial antigen studies can be performed on urine and serum; they can be useful in cases of pretreated meningitis. However, a negative bacterial antigen study result does not rule out meningitis.

Imaging Studies

• Imaging studies rarely are required in the initial management of meningitis or encephalitis when the clinical presentation is typical. Exceptions include the need to rule out other pathology before performing an LP or when focal neurologic signs are present.
• Imaging may be useful to check for abscesses, subdural effusions, empyema, or hydrocephalus.
• Normal CT scan findings do not rule out increased intracranial pressure (ICP).

Procedures

• The most important laboratory study is examination of CSF. The lumbar puncture (LP) should include opening and closing pressure in the cooperative patient.
• • Cell count
  • Gram stain
  • Culture and sensitivity
  • Glucose
  • Protein and antigen
  • Acid-fast bacillus
  • Fungal stains
• Bacterial meningitis
• • White blood cell (WBC) counts over 1000/mm³ usually are caused by bacterial infections. Counts of 500-1000/mm³ may be bacterial or viral and need further evaluation. Lower counts are usually associated with viral infections. The total WBC count cannot definitely distinguish between bacterial and other causes. It was generally believed that a predominance of polymorphonucleocytes (PMNs) pointed to bacterial meningitis, but this has been unreliable.
  • Gram stain may aid in diagnosis, but the diagnosis may be missed in up to 30% of cases of culture-proven disease.
  • The protein concentration usually is elevated in bacterial meningitis, but it also is elevated by a traumatic tap. The glucose is usually reduced in bacterial meningitis. Normal CSF glucose should be greater than two-thirds that of the serum glucose. levels less than 50% of serum are suggestive of bacterial meningitis.
  • Ancillary tests, such as total protein concentration, glucose concentration, and percent of neutrophils in CSF, are not helpful to for diagnosis, when the cell counts are low (less than 30/mm³). Its utility is useful only when they are highly abnormal. 
  • Latex agglutination tests are available to test for S pneumoniae, H influenzae, group B Streptococcus, and N meningitidis. A negative result, however, does not rule out bacterial infection.
  • Even with normal CSF results, the fluid should be sent for culture. N meningitidis and S pneumoniae are known to give normal CSF results.
  • In cases where antibiotic administration leads to CSF sterilization, polymerase chain reaction (PCR) may have a role in identifying the pathogen. PCR is able to identify the pathogen quickly and accurately. The sample does not need to have a high number of organisms. However, this test needs further validation.
• Clinical decision rule
• • There is an interest to differentiate bacterial meningitis and aseptic meningitis. To date, there are 5 clinical decision rules. These clinical decision rules identify low-risk patients by scoring or modeling clinical variables, blood variable, and CSF variables. With any clinical decision rule, they are used to identify patients at risk of meningitis. Those who are at low risk can avoid parenteral antibiotic and hospitalization.
  • The clinical decision rule by Nigrovic et al⁴ has shown high accuracy and simplicity of use. Comparison among the 5 clinical decision rules has not been performed. In addition, general applicability of these rules has not been validated.
• Viral meningitis
• • The WBC count in viral meningitis is usually below 500/mm³, with greater than 50% lymphocytes.
  • The protein may be elevated.
  • The glucose level may be normal or low.
  • Gram stain results are negative.
• Encephalitis
• • In addition to the studies for meningitis, an EEG, CT scan, and MRI have been used for evaluation.
  • More recently, PCR has been used for diagnosis.
  • CSF analysis shows pleocytosis (predominantly mononuclear cells) and high levels of protein. A small percentage (3-5%) of samples have normal CSF. Identification of viral antigen or nucleic acid may provide some diagnostic help.
  • Serial antibody analysis is helpful for prognostic purposes. Routine measurements do not aid in the treatment during the acute phase. New ELISA and PCR assays are available for diagnosis.
  • In cases of West Nile virus, CSF shows pleocytosis and moderately elevated protein levels. CT shows no abnormalities. MRI may show enhancement of meninges and periventricular regions. Diagnosis test is WNV ELISA. However, this test has cross reactivities to other flaviviruses.
• Traumatic LP
• • If bleeding occurs during the procedure and the CSF is contaminated with blood, the interpretation becomes more difficult.
  • The use of corrected WBC:RBC ratio (1:500) and percent of neutrophils to “normalize” the cell count was shown to have limited utility in predicting those with meningitis. The “corrected CSF” was shown to underestimate the true white blood cell count, causing clinicians to underdiagnosis borderline meningitis cases. 
  • In any situation when a traumatic LP occurs and the interpretation is difficult, it is better to treat and wait for the results of the CSF culture.
  • In very bloody LPs, a drop of the fluid on the sterile dressing usually will produce a double ring if there is CSF fluid present.
  • When in doubt, treat and attempt the LP later.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Prehospital Care

• Prehospital care usually is confined to transporting children who are critically ill or have experienced a seizure from the meningitis or encephalitis.
• General supportive care is required depending on the child's condition.
• Subsequent diagnosis of a potentially transmissible disease must be communicated to prehospital care providers, especially with N meningitidis infections.

Emergency Department Care

• Immediate stabilization and support of the critically ill or seizing child is necessary.
• When meningitis or encephalitis is suspected, an LP is indicated.
• • If the child's condition is unstable or there is suspicion of increased intracranial pressure, the LP should be delayed.
  • It is very important that antibiotic therapy is immediately commenced in the ill child and not delayed until after the LP.
  • If prompt LP cannot be performed, administration of antibiotics should be initiated. However, sterilization of CSF will occur. It was previously thought that sterilization occurs within 2-3 hours. However, in a retrospective study, complete sterilization was found to occur within 2 hours for meningococcal meningitis. With pneumonococcal infections, sterilization occurred within 4 hours.
• If the child is hemodynamically stable, intravenous fluids should be administered at maintenance. Careful record of the patient's weight, urine specific gravity, and serum osmolarity will help guide further fluid therapy. Patients who present with dehydration need rehydration and should not have fluid restriction. Seizures should be treated promptly and should be expected at any time during the initial management.

Consultations

• Children with bacterial meningitis require hospitalization for intravenous antibiotics and appropriate support.
• • Depending on the child's condition, admission to a pediatric intensive care unit may be warranted.
  • Regardless, consultation with a pediatrician, infectious disease specialist, and/or a critical care specialist may be needed.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.

Drug Category: Antibiotics

IV antibiotics are required for bacterial meningitis. If the causative organism is unknown, antibiotics regimens can be based on the child's age.

Infants younger than 30 days, ampicillin and an aminoglycoside or a cephalosporin (cefotaxime) are recommended.

Children 30-60 days old, ampicillin and a cephalosporin (ceftriaxone or cefotaxime) can be used. Since S pneumoniae occasionally occurs in this age range, vancomycin should be considered instead of ampicillin.

In older children, a cephalosporin (eg, cefotaxime, ceftriaxone) or ampicillin plus chloramphenicol can be used.

Incidence of resistant S pneumoniae is increasing. If this is considered to be a potential pathogen, add vancomycin to the therapeutic regimen. Use of penicillin or ampicillin in the 3 months prior to illness is associated with increased risk of infection with resistant S pneumoniae.

Drug Category: Corticosteroids

Despite newer more effective antibiotic therapy, sequelae remain significant. Some damage may be due to release of cytokines when bacteria are killed. Dexamethasone inhibits the production of cytokines. Currently, it is indicated for children with suspected meningitis who are older than 6 weeks and is recommended for treatment of infants and children with H influenzae B meningitis.

It appears that dexamethasone is effective against other organisms as well. The use of corticosteroid, prior to or along with the first dose of antibiotic, has decreased morbidity and mortality. A decrease in patients with hearing loss, long-term neurological sequelae, and deaths were observed. These finding were applicable in high-income countries. 

Concerns exists that selection for resistant pneumonococcal strains may occur with dexamethasone administration. Some evidence suggests that its use may impair antibiotic penetration through the blood-brain barrier, especially by vancomycin.

For a related CME activity, see Corticosteroids May Not Reduce Mortality in Children With Bacterial Meningitis.

Drug Category: Prophylactic antibiotic

Used prophylactically in contacts of children with H influenzae or N meningitidis, as described.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Children with suspected bacterial meningitis should be admitted to the hospital for intravenous antibiotic therapy.
• Adequate fluid administration is necessary to maintain perfusion, especially cerebral perfusion. Fluid restrictions (to prevent cerebral edema) may be more harmful because patients may be under resuscitated.

Further Outpatient Care

• Children with suspected viral meningitis who appear well may receive care as outpatients, provided follow-up care can be ensured.
• With continued pressure to decrease hospital stays, there are occasions when patients may be discharged from the hospital to continue parenteral antibiotics at home.

In/Out Patient Meds

• All children with suspected bacterial meningitis should be admitted.
• Well-appearing children with viral meningitis can be cared for as outpatients with only symptomatic treatment required.

Transfer

• Children with bacterial meningitis and encephalitis should be admitted to a hospital capable of managing critically ill children.
• This may require a transfer to a pediatric hospital or large general hospital.

Deterrence/Prevention

• Routine childhood immunizations have been shown to effectively decrease the incidence of certain types of meningitis and encephalitis.
• Antibiotic prophylaxis is recommended for all household contacts in those households with at least 1 unvaccinated child younger than 48 months in patients with H influenzae meningitis.
• • Treat all contacts in the household if any child is younger than 12 months.
  • Prophylaxis should be started as soon as possible.
  • Careful observation of any contacts and immediate evaluation is warranted if a fever develops.
• Prophylaxis is recommended for all persons in contact with oral secretions of patients with N meningitidis meningitis. This includes a health care worker who performed mouth-to-mouth resuscitation, intubation, or suctioning.
• • The use of rifampin, ceftriaxone, and ciprofloxacin has been effective prophylaxis. In a systematic review, ciprofloxacin and ceftriaxone are more effective up to 4 weeks of posttreatment against resistant strains of N meningitidis.

Complications

• Despite early aggressive management, the complications from bacterial meningitis remain significant.
• • In the neonatal period, the mortality rate is 15-25%.
  • After the neonatal period, the mortality rate drops to about 5% with appropriate care.
  • The morbidity rate is up to 40% depending on the causative organism and delay in therapy.
  • Hib meningitis has up to 15% rate of permanent neurological sequelae.
• Focal neurological sequelae may occur in 10-15% of patients. These problems are hemiparesis, facial palsy, visual field defects, hearing loss, and cranial nerve palsies.
• • Seizures may occur at any point of the patient's course. Seizures that continue after the fourth day of hospitalization are focal in nature or are difficult to control have a greater likelihood of neurological sequelae.
• Most children with enteroviral meningitis have an uncomplicated course.

Prognosis

• The prognosis for appropriately treated meningitis has improved, but there is still a 5% mortality rate and significant morbidity.
• The prognosis varies with the age of the child, clinical condition, and infecting organism.
• The prognosis from viral meningitis usually is very good.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Missed meningitis is one of the most frequent lawsuits in pediatrics against emergency physicians, leading to large claims. Therefore, a high index of suspicion is needed and accurate charting of pertinent positive and negative findings is crucial. Missed meningitis is second only to missed myocardial infarction in total damages per year. Many lawsuits are filed even though treatment was promptly instituted because of the frequency of neurologic sequelae.
• Partially treated meningitis is difficult to diagnose; therefore, children on antibiotics should be carefully evaluated. Because of the high incidence of sequelae, parents should be cautioned from the beginning that even with appropriate medical care, the child may have some complications.
• Delay in initiating antibiotic therapy has resulted in lawsuits. Even though morbidity is known to be associated with even the most prompt therapy, if there are sequelae and antibiotics were delayed, the physician will be at a disadvantage if legal action is taken.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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Article Last Updated: Jul 2, 2008