Version May 2024
INTRODUCTION — Bacterial meningitis is more common in the first month than at any other time of life [1]. Despite advances in infant intensive care, neonatal meningitis remains a devastating disease with considerable risk of mortality and morbidity.
The neurologic complications of bacterial meningitis in the neonate will be discussed here. The clinical features, diagnosis, and treatment of bacterial meningitis in neonates are discussed separately. (See "Bacterial meningitis in the neonate: Clinical features and diagnosis" and "Bacterial meningitis in the neonate: Treatment and outcome".)
ACUTE COMPLICATIONS — Acute complications of neonatal bacterial meningitis include cerebral edema (vasogenic and cytotoxic), increased intracranial pressure (ICP), ventriculitis, cerebritis, hydrocephalus, brain abscess, cerebral infarction, cerebral venous thrombosis, arterial stroke, and subdural effusion or empyema [2,3]. Development of these complications may necessitate additional evaluation, neurosurgical consultation, and/or lengthened duration of antimicrobial therapy.
Ventriculitis — Ventriculitis refers to inflammation of the ventricular fluid and lining of the ventricles and is sometimes associated with obstruction to cerebrospinal fluid (CSF) flow. Ventriculitis is a common complication of neonatal meningitis, occurring in up to 20 percent of cases [4]. It is diagnosed by neuroimaging and/or ventricular tap [4].
There are no reliable clinical signs of ventriculitis, although evidence of increased ICP usually is present [5]. It must be suspected on the basis of failure to respond clinically and bacteriologically to appropriate antimicrobial therapy; if ventriculitis results in obstruction to CSF flow, the access of systemic antibiotics to the ventricular CSF can be limited [3]. (See "Bacterial meningitis in the neonate: Treatment and outcome", section on 'Monitoring response to therapy'.)
Neuroimaging should be performed to make the diagnosis. Cranial sonography can demonstrate findings suggestive of ventriculitis or obstructed flow of CSF (intraventricular strands attached to ventricular surface, echogenic ependyma, dilated ventricles) and can be performed at the bedside [3,6]. Contrast-enhanced magnetic resonance imaging (MRI) can provide important structural information and will demonstrate enhancement of the lining of the ventricles, but it usually is not necessary for initial management.
Ventricular fluid aspiration should be performed for infants who have ventriculitis and are not responding to appropriate antibiotic therapy, either clinically or microbiologically. In this setting, cultures of CSF often remain positive for the infecting organism for several days or longer. In addition, ventricular fluid aspiration should be performed if there is evidence of an obstruction to the flow of CSF.
The management of infants with ventriculitis is best undertaken in consultation with specialists in pediatric infectious diseases and pediatric neurosurgery. Commonly, ventriculitis resolves in association with appropriate systemic antibiotic therapy. In very select cases, treatment can involve direct instillation of an antimicrobial into the ventricle. Uncommonly, the duration of antimicrobial therapy may extend several weeks longer than the time required to sterilize the ventricular CSF and can be as long as six to eight weeks.
Hydrocephalus — Hydrocephalus occurs in approximately 25 percent of infants with neonatal meningitis overall [7,8] and 30 to 44 percent of cases of gram-negative neonatal meningitis [4,9]. Hydrocephalus is more common in meningitis caused by group B streptococcus (GBS) type III than by other types of GBS and also in K1 Escherichia coli meningitis than in non-K1 E. coli meningitis [10].
Clinical findings of hydrocephalus include signs of increased ICP (bradycardia, hypertension, respiratory depression) and accelerated head growth [3]. However, these are late findings; significant dilatation of the ventricles can occur before head growth becomes abnormal.
Diagnosis is made with neuroimaging. In the neonate, cranial sonography is the preferred technique for the initial examination because it is portable and avoids ionizing radiation and/or anesthesia. Limited imaging using ultrafast MRI also does not typically require sedation and is increasingly used as an alternative to ultrasonography in the evaluation of hydrocephalus in infants. The evaluation and management of hydrocephalus are discussed in greater detail separately. (See "Hydrocephalus in children: Clinical features and diagnosis" and "Hydrocephalus in children: Management and prognosis".)
Brain abscess — Brain abscess occurs in approximately 10 percent of patients with neonatal meningitis [7] and in 11 to 19 percent of patients with gram-negative neonatal bacterial meningitis [4,9]. The risk of brain abscess is increased in neonates with meningitis caused by Citrobacter koseri [11,12], Serratia marcescens [13], Proteus mirabilis [2,14], and Cronobacter sakazakii (formerly known as Enterobacter) [15,16]. Brain abscess is a rare complication of neonatal meningitis caused by extended-spectrum beta-lactamase-producing Klebsiella pneumoniae [17].
Findings consistent with brain abscess(es) typically develop in the second week of illness [3]. The findings can be subtle and include vomiting, bulging fontanelle, increased head circumference, separation of the cranial sutures, hemiparesis, focal seizures, and increased peripheral white blood cell count [2,3]. Development of a brain abscess should be suspected in neonates with new-onset seizures, prominent focal cerebral signs, or poor clinical response to antibiotic therapy. Marked clinical deterioration can occur if an abscess ruptures into the lateral ventricle or subarachnoid space [3,18].
Findings on repeat lumbar puncture can include CSF pleocytosis of up to a few hundred cells, with a predominance of mononuclear cells, and elevated protein [18]. If the abscess has ruptured into the lateral ventricle or subarachnoid space, the CSF white blood cell count and protein can be increased and the CSF glucose can be decreased compared with those at the time of initial diagnosis [3].
If brain abscess is suspected, neuroimaging should be performed. The diagnosis is best made by contrast-enhanced MRI, which provides better resolution than other modalities, including computed tomography. Characteristic cranial MRI findings of a brain abscess include a variably circumscribed region of decreased attenuation and contrast enhancement of the rim. The area of decreased attenuation is often of greater extent than the abscess itself because of the presence of cerebritis with surrounding edema [3]. (See "Bacterial meningitis in the neonate: Treatment and outcome", section on 'Neuroimaging'.)
A pediatric neurosurgeon should be consulted regarding the need for surgical intervention (needle aspiration or excision). Ultrasound-guided aspiration may be of particular value for initial diagnosis and drainage and for determining antibiotic levels in the abscess cavity. Serial brain imaging at weekly or biweekly intervals should be performed to monitor the evolution of the lesion [3]. The duration of antibiotic therapy may need to be extended to six to eight weeks, depending on the clinical and radiographic response. The minimum duration of treatment for brain abscess-complicating GBS meningitis is 21 days and for brain abscess-complicating gram-negative meningitis is 21 days (or at least 14 days after sterilization of CSF is achieved).
The development of a brain abscess is associated with poor prognosis [3]. In one series of 30 cases of neonatal brain abscess (20 were associated with meningitis, 27 were caused by Proteus species), there were four deaths (three from the initial illness and one from a shunt complication) [2]. Among the 27 who survived the acute illness, 16 had seizures. Among the 17 survivors who were followed until two years of age, 13 (76 percent) had an intelligence quotient (IQ) or developmental quotient (DQ) less than 80.
Infarction — Neonatal meningitis can be complicated by severe cerebrovascular disease, including arterial ischemic stroke and cerebral sinovenous thrombosis [3,19]. Autopsy studies indicate that infarction occurs in 30 to 50 percent of cases of fatal neonatal meningitis [20,21]. When infarction develops, it tends to occur early in the disease process, most commonly within the first week after the diagnosis of meningitis [7,22]. Clinical manifestations may include focal seizures and hemiparesis. Thromboses more often arise in small than in major vessels and involve veins more often than arteries. Two distinct patterns of focal infarction have been identified in neonates with GBS meningitis: a deep perforator arterial stroke to the basal ganglia, thalamus, and periventricular white matter and a superficial injury with patchy, focal infarctions of the cortical surface [22]. Hemorrhagic infarction involving the basal ganglia and thalami has been described but is uncommon [23]. (See "Stroke in the newborn: Classification, manifestations, and diagnosis".)
Subdural effusion — Subdural effusion occurs in approximately 11 percent of neonates with bacterial meningitis [8] and 7 to 13 percent of those with gram-negative meningitis [4,9]. However, clinically significant subdural effusion is uncommon in neonates with bacterial meningitis and subdural empyema is rare [3].
Clinical findings of subdural effusion are often subtle or absent. They can include a full or bulging fontanelle, accelerated head growth, or signs of increased ICP [3,8].
Most subdural effusions resolve spontaneously [3,24,25]. Indications for aspiration can include suspicion that the fluid is infected (eg, subdural empyema), imminent development of craniocerebral disproportion, focal neurologic findings, and/or evidence of increased ICP if the findings appear to be related to the effusion [3,24]. Subdural empyema is best managed by surgical drainage if the collection is large [24].
LONG-TERM COMPLICATIONS — Long-term complications of neonatal meningitis include hydrocephalus, multicystic encephalomalacia and porencephaly (the end of the continuum of multifocal parenchymal injury), and cerebral cortical and white matter atrophy [3]. The clinical manifestations of these complications include [4,7]:
●Developmental delay in approximately 25 to 50 percent
●Hydrocephalus in approximately 15 to 20 percent, with a higher incidence in gram-negative meningitis (see "Hydrocephalus in children: Clinical features and diagnosis")
●Late-onset seizures in approximately 10 to 20 percent (see "Seizures and epilepsy in children: Clinical and laboratory diagnosis")
●Cerebral palsy in approximately 15 to 20 percent (see "Cerebral palsy: Epidemiology, etiology, and prevention" and "Cerebral palsy: Classification and clinical features")
●Hearing loss (which occurs acutely) in approximately 5 to 10 percent (see "Hearing loss in children: Etiology" and "Hearing loss in children: Screening and evaluation")
●Cortical blindness in <10 percent
In a study of 43 survivors of neonatal group B streptococcal (GBS) meningitis who underwent standardized developmental assessment at a mean age of seven years (range 3 to 12 years), 44 percent had developmental delay, which was mild to moderate in 25 percent and severe in 19 percent [26].
Additional adverse outcomes that have been reported following neonatal meningitis include progressive myelopathy, chronic arachnoiditis, and infantile spasms in an infant who also had extensive sinus thrombosis [27,28].
The rate of long-term complications varies to some extent with the causative organism. (See "Bacterial meningitis in the neonate: Treatment and outcome", section on 'Outcome'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Bacterial meningitis in infants and children".)
SUMMARY
●Acute complications of neonatal bacterial meningitis include cerebral edema, increased intracranial pressure (ICP), ventriculitis, hydrocephalus, brain abscess, cerebral infarction, and subdural effusion or empyema. Neonates being treated for bacterial meningitis should be monitored for signs of acute complications throughout their course. Clinical manifestations may include:
•Failure to respond clinically and bacteriologically to appropriate antimicrobial therapy (see "Bacterial meningitis in the neonate: Treatment and outcome", section on 'Monitoring response to therapy')
•Signs of increased ICP (bradycardia, hypertension, respiratory depression, bulging fontanelle, accelerated head growth, separation of the cranial sutures) (see 'Hydrocephalus' above and 'Brain abscess' above and 'Subdural effusion' above)
•Hemiparesis (see 'Brain abscess' above and 'Infarction' above)
•Focal seizures or new-onset seizures (see 'Brain abscess' above and 'Infarction' above)
●Development of these complications may necessitate additional evaluation, neurosurgical consultation, and/or increased duration of antimicrobial therapy. (See 'Acute complications' above.)
●Long-term complications of neonatal meningitis include hydrocephalus, multicystic encephalomalacia and porencephaly (the end of the continuum of multifocal parenchymal injury), and cerebral cortical and white matter atrophy. The clinical manifestations of these complications include developmental delay, late-onset seizures, cerebral palsy, hearing loss, cortical blindness, and learning disabilities. (See 'Long-term complications' above.)
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