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Neonatal Meningitis
Introduction
Meningitis during the neonatal period is a potentially devastating condition with dire long-term consequences. Despite advances in preventive and critical care medicine, bacterial meningitis continues to have an adverse outcome rate of 20 to 60% among its survivors.[1] Although the incidence and mortality have declined over the past few decades, it remains challenging to diagnose due to pathogens varying with gestational age at birth, age at presentation, and geographic location, the often subtleness of clinical presentation, and inconsistent findings among infected individuals.[2] Additionally, the use of antibiotics before cerebrospinal fluid analysis can lead to ambiguous results, and specialized testing for viral causes is often unavailable. These factors have led experts to hypothesize that this condition's true incidence and prevalence are likely much higher.
The immature immune system of neonates, especially preterm, puts them at high risk for bacterial meningitis. Their exposure during the peripartum period puts them at risk for unique bacterial and viral pathogens. The major pathogens in industrialized countries are group B Streptococcus, gram-negative rods, with Escherichia coli being the most common, and Listeria monocytogenes.[1] However, fungal and viral causes must be considered to diagnose and treat the condition adequately. Some experts recommend that all infants with proven or suspected sepsis undergo a lumbar puncture to rule out neonatal meningitis, with the goal of early diagnosis and appropriate treatment.[1]
Etiology
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Etiology
Pathogens causing neonatal meningitis vary depending on the neonate's gestational age at birth, age at presentation, and geographic location. The disease is categorized as early-onset or late-onset, defined as clinical signs of infection at ≤72 hours and >72 hours of life, respectively.[2] Late-onset is predominantly seen in premature infants, with patients in the intensive care unit likely affected by pathogens that differ from those with community-acquired infections.
Bacterial and Fungal Etiologies
Well-known risk factors for bacterial meningitis in neonates are preterm birth, maternal group B Streptococcus (GBS) or S agalactiae colonization, premature or prolonged rupture of membranes, and very low birth weight (VLBW, less than 1500 grams).[2]
The incidence of early-onset meningitis has been greatly reduced by using intrapartum antibiotics for GBS infection. However, GBS remains the most common cause of meningitis and neonatal sepsis, responsible for more than 40% of all early-onset infections.[3][4][5] The next most common pathogen, Escherichia coli, accounts for approximately 30% of all early-onset neonatal meningitis and is documented as the most common cause of early-onset sepsis and meningitis among VLBW and preterm newborns.[2][6] Listeria monocytogenes, Enterococcus sp, and Streptococcus pneumoniae are the other major pathogens causing early-onset bacterial meningitis in neonates.[2][7]
In the late-onset group, the incidence is directly related to gestational age, birth weight, and the setting where the patient presents for care. For community-acquired late-onset sepsis and meningitis, GBS and E coli remain predominant.[5] In patients in the hospital/intensive care unit at the time of presentation, the most common pathogens are coagulase-negative staphylococci and Staphylococcus aureus, followed by E coli and Klebsiella pneumoniae.[2][5][8] Empiric antibiotic therapy for late-onset illness should cover additional organisms in the nosocomial environment, including Pseudomonas aeruginosa and methicillin-resistant S aureus. Late-onset meningitis is a more frequent complication of neonatal sepsis than during other periods.
Some epidemiologic studies have noted a shift from GBS as the most common cause of neonatal meningitis in the last few decades. A recent study in China reported the most common pathogen identified in neonatal meningitis was E. coli (39%), followed by GBS (22.1%). Gram-negative bacteria were more common in preterm infants, whereas GBS was more common in term infants.[9] Data from East Asian populations have revealed an increased frequency of multidrug-resistant (MDR) organisms causing neonatal sepsis and meningitis, especially carbapenem-resistant Acinetobacter baumannii. This study also reported a correlation between lower Apgar scores and the risk of MDR meningitis.[10] An additional nosocomial pathogen that has been associated with meningitis in the neonatal period is Candida sp.[11]
A special mention of the bacteria Cronobacter (Enterobacter) sakazakii is warranted. It has been predominantly associated with outbreaks of sepsis and meningitis during early infancy (67% neonates) who have been fed powdered infant formulas. Meningitis in these patients is often complicated by brain abscesses, subdural empyemas, and hydrocephalus, leading to a high mortality rate.[12] Occasional cases have been reported in infants being fed expressed breast milk that has been stored.[13]
Citrobacter sp are noted to cause invasive disease in neonates and young infants, often with no risk factors. These pathogens are associated with a very high rate of brain abscesses (up to 75%) in patients with meningitis and subsequent central nervous system-related morbidity and mortality.[14]
It is important to note that infants exposed to HIV, even uninfected, are at a higher risk of bacterial infections, including GBS-associated meningitis.[15] Also, neonates with invasive devices, such as indwelling vascular catheters, ventricular shunts and reservoirs, and endotracheal tubes, have a higher risk of meningitis following hematogenous and cerebrospinal fluid (CSF) bacterial spread.
Bacterial and Fungal Etiologies of Neonatal Meningitis
(most common pathogens are in bold)
| Early-Onset Meningitis |
Late-Onset Meningitis (community-acquired) |
Late-Onset Meningitis (nosocomial) |
| Streptococcus agalactiae (GBS) | Escherichia coli |
Coagulase-negative Staphylococcus |
| Escherichia coli | Streptococcus agalactiae (GBS) | Staphylococcus aureus |
| Listeria monocytogenes | Listeria monocytogenes |
Escherichia coli |
| Enterococcus species | Streptococcus pneumoniae | Streptococcus agalactiae (GBS) |
| Gram-negative enteric bacteria | Nieserria meningitidis | Candida species |
| Streptococcus pneumoniae | Enterococcus species | Gram-negative enteric bacteria |
| Gram-negative enteric bacteria | Enterococcus species |
Viral Etiologies
Neonates who do not test positive for bacterial etiologies but have abnormal CSF profiles are often presumed to have viral meningitis. Enterovirus infection is a common cause of neonatal meningitis, and human parechovirus type 3 has been identified as an emerging cause of meningoencephalitis.[16][17][18][19][20]
Neonatal infection with herpes simplex virus (HSV) is rare and, as such, a rare cause of neonatal meningitis. In a multicenter retrospective review of more than 26,000 infants undergoing evaluation for meningitis, HSV infection was identified in only 0.42% of reported cases, with the highest frequency of central nervous system (CNS) infection in the second week of life.[21] The global estimate of neonatal herpes infection is 10 per 100,000 live births, most commonly presenting between 7 and 21 days of life.[22]
Arboviruses such as West Nile virus and Chikungunya have been reported as extremely rare causes of neonatal meningitis and meningoencephalitis.[23]
Epidemiology
According to studies in the United Kingdom, the annual incidence of bacterial meningitis is 0.38 per 1000 live births, and that of viral meningitis is 0.83 per 1000 live births.[24][25][26] This is consistent with other reports that culture-proven neonatal bacterial meningitis is estimated at 0.3 per 1000 live births, but this is likely underestimated because only 30 to 50% of those in the neonatal intensive care unit (NICU) who are evaluated for sepsis have a lumbar puncture done, and 75% of the time, it occurs after the initiation of broad-spectrum antibiotics.[2] Consequently, the culture results may be falsely negative.
One study from Canada reported rates of neonatal meningitis ranging between 2.2 and 3.5/1000 NICU admissions over a 7-year period.[27]
In developing countries, the incidence is higher, at 0.8 to 6.1 per 1000 live births, with a mortality rate of up to 58%. The true incidence is likely higher as the epidemiology is limited in many rural, developing settings.[2][28]
Pathophysiology
Neonates are susceptible to invasive infections due to their "inexperienced" immune system and lack of maternal antibodies if born preterm. The most common mechanism is primary bloodstream infection seeding the CNS. Early-onset infection is mainly maternal in origin because pregnancy and delivery expose the fetus/neonate to many pathogens that can be transmitted through the vagina to ruptured amniotic membranes or via contact with the neonate's skin during passage through the birth canal. Organisms such as L. monocytogenes can be transmitted through the placenta. Late-onset infection is mainly nosocomial, with foreign devices such as endotracheal tubes, catheters, and feeding tubes, increasing the risk of infection.[2][29]
History and Physical
Classical findings such as seizure, bulging fontanelle, coma, and neck stiffness were found in 28%, 22%, 6%, and 3% of cases in one review from the United Kingdom.[4] Nonspecific findings of temperature instability (fever or hypothermia), lethargy, feeding intolerance, and poor perfusion (hypotension) have been reported as the most common presenting signs.[4][30]
The clinical presentation may vary based on the birthweight and gestational age at birth. For example, the most common signs in neonates weighing over 2500 grams include fever, irritability, seizures, and bulging fontanelle. In contrast, apnea, jaundice, and abdominal distention are most common in those weighing less than 2500 grams.[30] A physically demonstrable Brudzinski sign indicates meningitis, with passive neck flexion resulting in bilateral flexion at the hip joint.
| Early Signs of Meningitis | Late Signs of Meningitis |
|
Temperature instability (fever or hypothermia) |
Seizures |
| Lethargy | Bulging fontanelle |
| Feeding intolerance | Nuchal rigidity |
| Bradycardia | |
| Hypotension |
Evaluation
Neonatal meningitis can be difficult to diagnose due to pathogens varying with gestational age at birth, age at presentation, geographic location, the often subtleness of clinical presentation, and inconsistent findings among infected individuals. Well-appearing febrile neonates can become toxic quickly and are at high risk for meningitis due to their immature immune systems. Lumbar puncture (LP) with cultures plus or minus molecular diagnostics of the CSF continues to be the gold standard for diagnosing neonatal meningitis. The current recommendation is to perform an LP on all neonates with confirmed or suspected sepsis.[2][6] Although LP and CSF cultures are essential for diagnosing neonatal meningitis, data shows that 30% of patients with early-onset sepsis and 70% with late-onset sepsis do not have LPs when evaluated.[31][32]
Select recommendations from the American Academy of Pediatrics Clinical Practice Guidelines for the Evaluation of Febrile Infants 8 to 60 Days Old are listed below:[33]
- Obtain CSF for analysis and bacterial culture in the workup of a febrile infant 8 to 21 days old.
- Enterovirus polymerase chain reaction (PCR) should be sent if pleocytosis is present on CSF testing during periods of increased local enterovirus prevalence.
- In infants at high risk for HSV, PCR testing should be obtained.
- High-risk patients for HSV include infants born to mothers with genital HSV lesions, maternal fever 48 hours before or within 48 hours of delivery, or if the infant has CSF pleocytosis in the absence of a positive Gram stain.
- Obtain CSF analysis for infants 22 to 28 days if inflammatory markers are abnormal and/or no other source of infection or fever is identified.
- Urinalysis and workup for urinary tract infections are universally recommended in evaluating patients with a fever in this age group.
CSF Indices By Infant Age
(upper limits of normal)[34][35][36][37]
|
Kestenbaum et al or Shah et al |
Byington et al | Thompson et al | |
|
White blood cells/mm3 <28 days of age |
15 | 18 | 15 |
|
White blood cells/mm3 29-60 days of age |
5 | 9 | 9 |
|
Protein (mg/dL) <28 days of age |
115 | 131 | 118 |
|
Protein (mg/dL) 29-60 days of age |
89 | 106 | 91 |
|
Glucose (mg/dL) <28 days of age |
30 | 25 | |
|
Glucose (mg/dL) 29-60 days of age |
30.5 | 27 |
A multicenter study from 2019 reported that most infants less than 60 days old with bacterial meningitis either have positive Gram stain results or corrected CSF pleocytosis (80.3% sensitivity). The bacterial meningitis score was noted to have poor specificity in this study; therefore, the authors recommend not using this prediction tool in infants less than 60 days old. The authors also noted that infants who did not have pleocytosis or abnormal Gram stain but were later proved to have bacterial meningitis either had peripheral leukocytosis or bandemia on presentation. Notably, correcting the CSF leukocyte count for red blood cells (RBCs) decreased the sensitivity of pleocytosis for meningitis in this population.[38] Results from a recent study suggest that for a traumatic LP subtracting one white blood cell (WBC) for every 400 RBCs in the CSF or using a complex calculation comparing the peripheral WBC to the CSF WBC counts may decrease the number of infants inaccurately diagnosed with meningitis.[39]
Monitoring in a hospitalized setting is required until culture results are obtained. The time to pathogen detection may vary based on the underlying pathogen and the clinical presentation. A multicenter study from 2018 reported that in infants under 60 days old with an underlying invasive bacterial infection (either bacteremia or meningitis), 88% of the pathogens were detected in blood, and 89% were detected in CSF cultures and/or Gram stain within 24 hours. In "well-appearing infants," the detection rate was 85% at 24 hours. They reported that in all "non–ill-appearing febrile infants," only 0.3% will have a pathogen detected after 24 hours, most commonly S. aureus.[40]
Polymerase Chain Reaction
Real-time PCR assays to detect multiple pathogens, including S pneumoniae, E coli, GBS, S aureus, and L monocytogenes, had a higher detection rate than traditional cultures (72% vs 48%), even if antibiotics had been started (58% vs 29%).[2] Multipathogen PCR films and arrays are now used to simultaneously detect viral and bacterial pathogens. A 2015 study used a PCR panel capable of detecting 14 pathogens in the CSF (E coli, Haemophilus influenzae, L monocytogenes, Neisseria meningitides, S agalactiae (GBS), Streptococcus pneumoniae, cytomegalovirus, enterovirus, Epstein-Barr virus, HSV types 1 and 2, human herpes virus 6, varicella zoster, human parechovirus, and Cryptococcus neoformans/gattii).[41] The study reported that the PCR panel could detect the causative agent in culture-positive and culture-negative meningitis with a 1 hour turn-around time. The authors highlighted the role of PCR panels as a reliable tool in detecting culture-negative CSF infections, especially in those infants who received antibiotics before an LP.[41] Additionally, it has been suggested that the rapid detection of a pathogen like an enterovirus with a more benign clinical course may help limit invasive interventions and antibiotic exposure in young infants with negative cultures.[42]
PCR testing for HSV is essential for diagnosing HSV CNS involvement. A large multicenter study noted significant variation in HSV testing across emergency departments in North America when evaluating neonates for meningitis. This variation did not correlate with local HSV incidence. The authors concluded, "Our data emphasize the need for improved management strategies focused on the early identification of infants at both high and low risk of HSV infection."[21] HSV should be suspected in all patients with neonatal meningitis, especially if there is CSF pleocytosis in the absence of Gram stain findings. HSV PCR should be promptly sent to the appropriate laboratory to ensure the diagnosis is not missed.
When to Defer Lumbar Punctures
The 2012 Committee on Fetus and Newborn recommend performing an LP for all infants with sepsis or bacteremia.[43] However, deferring the LP is appropriate in asymptomatic individuals. In other words, if the neonate is being considered for an LP solely because of maternal risk factors, the LP can be safely deferred in the absence of clinical signs suggestive of infection.[6] Similarly, patients with signs of respiratory distress were found to correlate poorly with CSF positivity; therefore, LP can be deferred in these patients in the absence of bacteremia and clinical improvement after antibiotic initiation for respiratory causes.[6] All patients with culture-confirmed bacteremia should have an LP performed, as up to 25% of these patients may have concurrent meningitis.[44]
Radiographic Evaluation
Expert opinion varies regarding the radiographic evaluation of neonates with meningitis. Some authors recommend a sonographic evaluation of every infant with evidence of meningitis, while some recommend sonography only if there is suspicion of neurologic complications.[45] Most experts recommend cranial sonography as the initial study, with repeat testing if there is evidence of neurologic complications. Magnetic resonance imaging (MRI) of the brain is the recommended follow-up study in stable patients.[45] This is to evaluate neurologic tissue and identify organic complications of the infection. Ventriculitis is a common complication of meningitis and is seen as an irregular and echogenic ependyma with intraventricular debris and stranding on cranial sonography.[45] Other radiographic findings with bacterial meningitis may include subdural empyema, intracranial abscesses, and parameningeal abscesses. Hydrocephalus is a common complication of meningitis that can be detected by neuroimaging.
Treatment / Management
Recommendations for empiric therapy vary by geographic region, local resistance patterns, and expert opinion. For most patients with suspected early-onset neonatal meningitis, ampicillin plus an aminoglycoside (eg, gentamicin) or an expanded spectrum cephalosporin (eg, cefotaxime, ceftazidime, or cefepime) should be started empirically.[2] According to an expert review from the United Kingdom, empiric therapy for meningitis in the first week of life should include ampicillin, cefotaxime, and gentamicin.[46]
One recent source citing World Health Organization standards indicated that ampicillin or penicillin plus gentamicin are recommended empiric therapy in developing countries, with cephalosporins reserved for second-line treatment.[47] It should be noted that all antimicrobials need to be dosed based on gestational and postnatal age recommendations and at meningeal dosing. This recommendation is due to the growing concern about ampicillin resistance in gram-negative organisms. A study from 2003 evaluated serious bacterial infection in infants less than 90 days old, reporting that 78% of the pathogens causing meningitis in this population were resistant to ampicillin.[48] However, ampicillin must remain part of the initial regimen to cover for GBS and L monocytogenes. Empiric antibiotic therapy for late-onset illness should cover additional organisms in the nosocomial environment, including Pseudomonas aeruginosa and methicillin-resistant S aureus.
In late-onset meningitis, vancomycin should be added to the above empiric regimen when the suspicion of nosocomial pathogens is high.[2] Some experts recommend a carbapenem instead of the expanded-spectrum cephalosporin when late-onset meningitis is suspected in infants with prolonged hospitalization, especially if the CSF Gram stain or the blood culture is suggestive of gram-negative infection.[3]
It is important to remember that not all late-onset meningitis patients warrant nosocomial organism coverage. If the infant is discharged home after birth and presents in the late-onset period, they will be considered to have late-onset community-acquired neonatal meningitis. In this case, the empiric coverage may be the same as that of early-onset meningitis.
An LP should be repeated in 24 to 48 hours if the patient does not demonstrate clinical improvement. According to some experts, repeating the LP to show CSF clearance is unnecessary if there is clinical improvement.[2] Others recommend ensuring CSF pathogen clearance after 2 to 3 weeks of continued antibiotic therapy.[46]
Definitive therapy should be instituted when the causative organism and its susceptibilities have been determined. GBS therapy can be modified to ampicillin or penicillin monotherapy once repeat LP notes sterility and response to therapy. E. coli and other gram-negative pathogens are typically treated with a combination of a third-generation cephalosporin plus an aminoglycoside until sterility and response to therapy can be confirmed. At that time, the aminoglycoside is usually stopped. L. monocytogenes infection is commonly treated with ampicillin monotherapy following repeat CSF sampling.
There is no data to help determine the duration of antibiotic therapy for neonatal meningitis. The minimum acceptable duration by European guidelines is 14 days for GBS and L. monocytogenes infections and 21 days for gram-negative organisms.[46] Delayed CSF clearance and/or abnormalities on neuroimaging warrant prolonged therapy.[46] Persistently positive CSF cultures suggest ventriculitis, hemorrhage, or abscess formation. In the United States, the recommended duration of treatment for uncomplicated meningitis is 14 days for GBS, L. monocytogenes, and S. pneumoniae infections and 21 days for Pseudomonas and gram-negative enteric bacteria.[2]
There are no clear guidelines on when to suspect and initiate empiric therapy for HSV meningitis. According to some infectious disease experts, empiric evaluation and treatment for neonatal HSV are warranted if there are clear signs of HSV infection (skin vesicles, seizures, or liver inflammation or failure) or CSF pleocytosis is found outside of the enteroviral season.[49] They also recommend considering HSV in neonates with CSF pleocytosis regardless of the season if the infant is febrile and without another clear diagnosis of infection. In advocating empiric acyclovir therapy in these patients, this expert identified no risk of adverse effects of acyclovir. This outcome required adequate attention to hydration and rapid viral diagnostic testing, ensuring less than 48 hours of acyclovir therapy in patients who did not have HSV infection.[49]
Intraventricular antibiotics, dexamethasone, intravenous immunoglobulins, granulocyte or granulocyte-macrophage colony-stimulating factor, and oral glycerol are not recommended in routine practice.[2]
Differential Diagnosis
The differential diagnosis includes all noninfectious causes of the typical signs and symptoms associated with neonatal meningitis, such as seizures, irritability, poor feeding, and fever. If CNS bacterial and viral infection have been ruled out, the following should be considered:
- Neonatal seizure disorders
- Inborn errors of metabolism
- Intracranial hemorrhage
- Cerebral aneurysm
- Central venous thrombosis
- Sepsis from non-neurologic foci
Prognosis
Despite the decrease in mortality, neonatal meningitis continues to have high morbidity. Global mortality estimates are approximately 190,000 cases per year.[50] In Western countries, the mortality rate is about 10 to 15%, with the highest rates in preterm neonates.[2] In low-income countries, the mortality rate is as high as 58%, with moderate to severe neurodevelopmental impairment in approximately 23% of survivors.[51] In high-income countries, the rate of neurological sequelae is 20 to 50%.[50][52] A meta-analysis of neurodevelopmental outcomes in children with GBS meningitis noted that 32% had neurodevelopmental impairment at 18 months, including 18% with moderate to severe impairment.[53] Furthermore, compared to the general population, the risk of death remains higher five years after the acute illness.[50][54]
A study from Tunisia revealed a neurologic complication rate of 21.6%. Respiratory distress, low birth weight, shock, and pleocytosis of fewer than 500 cells/mm3 were indicators of a worse prognosis. Adding ofloxacin to the antibiotic regimen was associated with decreased neurological sequelae in survivors.[55] Another study noted that infant feeding difficulties and concomitant pneumonia were prognostic predictors of poor outcomes.[56] Also, high CSF protein, both during and after acute illness, has been linked to poorer outcomes.[56][57]
Most reviews report that infection severity correlates with outcomes, but there is no difference in outcome by pathogens.[46] The exception is an infection due to an MDR organism. A study evaluating the case fatality rate between neonatal MDR and non-MDR meningitis over a 29-year period reported a fatality rate of 58.8% in patients with MDR meningitis versus 9.5% in non-MDR meningitis.[10]
Seizures, irritability, bulging anterior fontanelle, and nuchal rigidity have been associated with poor outcomes. Other predictors of poor outcomes in survivors of neonatal bacterial meningitis include somnolence/coma, hypotension, and leukopenia.[2] Another source noted that seizures and the need for vasopressors predicted complications in patients with neonatal meningitis.[58]
The prognosis for neonates with enteroviral and parechovirus meningitis appears favorable. One study indicated that despite abnormal MRIs in 35% of neonates, all had normal neurodevelopmental, visual, and hearing exams at 12 months of life.[59]
Complications
Persistent bacteremia or CSF infection should raise concern for complications of meningitis, including obstructive ventriculitis, subdural empyema, multiple small vessel thrombi, intracranial abscesses, and parameningeal abscesses.[45][46] A long-term follow-up study from the United Kingdom reported ventriculitis, hydrocephalus, and convulsions as the most frequent complications of bacterial meningitis, occurring at a combined rate of 26%.[26] Ventriculitis is most often seen with gram-negative meningitis and can progress to chronic ventriculitis with septations.[45] Ventriculitis is more common in children with intraventricular hemorrhages associated with prematurity and infection.[57]
Infections caused by members of the Enterobacteriaceae family are the most common cause of brain abscess formation following CSF infection.[45] Hearing loss is a potential long-term consequence of neonatal meningitis. Some experts recommend studies evaluating the efficacy of adjuvant corticosteroids to reduce hearing loss and neurological complications of this disease.[50] Ischemic stroke is a possible complication of bacterial neonatal meningitis in general[60], and ischemic stroke and cerebral sinovenous thrombosis are possible complications of late-onset GBS meningitis in particular.[61]
Deterrence and Patient Education
Population awareness regarding the risk of bacterial transmission from mother to fetus is essential to decrease the incidence of this disease. World Meningitis Day on April 24 is intended to raise general awareness.[50] Adequate screening and prophylactic treatment are essential preventive measures against neonatal meningitis. Intrapartum prophylactic antibiotic therapy, versus risk factor-based management, is recommended for mothers colonized with GBS to prevent this disease. This practice has dramatically decreased the incidence of early-onset GBS infections, but the incidence of late-onset GBS remains unaffected.[62]
GBS vaccines are being developed to help prevent neonatal meningitis. Early phase 1 and 2 trial results testing GBS vaccines with maternal vaccination to prevent neonatal meningitis are underway.[50] Maternal vaccination against GBS and E coli can potentially decrease neonatal meningitis incidence by two-thirds.[46]
Enhancing Healthcare Team Outcomes
Neonates with suspected meningitis should optimally be in the care of a neonatologist in an intensive care setting. Consultations with a pediatric infectious diseases physician and pediatric neurologist may be warranted based on presenting symptoms. An experienced neuroradiologist may help assess for complications. An audiologist is needed when the neonate is stable to evaluate for hearing problems. Finally, a neurodevelopmental and/or developmental-behavioral pediatrician is recommended to assess and follow patients as they mature after hospital discharge. If complications develop, neurosurgical consultation may be necessary to assist with the management of patients with neonatal meningitis.
Neonatal meningitis requires diligent clinical assessment, with multiple diagnostic tests and early CSF assessment. The emergency medical provider is an essential team member, as they are tasked with performing an LP in all patients with suspected disease. The neonatal intensive care physicians, physician assistants, nurse practitioners, clinical nurse specialists, and nurses help monitor the neonate and will be the first to notice if any neurologic complications arise. Doing so can help address these complications early to minimize long-term consequences. The clinical pathologist must report Gram stain findings as soon as they are confirmed to ensure appropriate antibiotic therapy. The pharmacist will help with adequate dosing of gestational aged and weight-based antimicrobial agents required for treatment. Clinical audiologists are essential for assessing hearing impairment in patients with meningitis in both the inpatient and outpatient settings. A neurodevelopmental team consisting of physicians, nurses, physical therapists, occupational therapists, and social workers can facilitate early intervention and help to maximize positive outcomes in patients with neonatal meningitis. A well-integrated interprofessional team can better ensure timely assessment and management of this potentially devastating condition and help improve clinical outcomes.[Level 5]
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