Neonatal Meningitis Clinical Presentation
- Author: David C Dredge, MD; Chief Editor: Amy Kao, MD more...
History and Physical Examination
Regardless of the specific pathogen involved, neonatal meningitis is most often caused by vertical transmission during labor and delivery. It occurs most frequently in the days following birth and is more common in premature infants than in term infants. It is closely associated with sepsis.
Risk factors for the development of meningitis include low birth weight (< 2500 g), preterm birth (< 37 weeks’ gestation), premature rupture of membranes, traumatic delivery, fetal hypoxia, and maternal peripartum infection (including chorioamnionitis).
In evaluating a neonate for meningitis, the following 3 key points should be kept in mind:
It is important to remain vigilant for maternal infection “setups” (eg, prolonged rupture of membranes, fever, and chorioamnionitis) while remembering that asymptomatic maternal infection is always a possibility even with screening
Early-onset and late-onset bacterial infections have distinctive clinical courses (see below)
In herpes simplex virus (HSV) infections, the presence of skin lesions in a meningitic neonate is the exception rather than the rule
Symptoms appearing in the first 48 hours of life are referable primarily to systemic illness rather than to meningitis. Such symptoms include temperature instability, episodes of apnea or bradycardia, hypotension, feeding difficulty, hepatic dysfunction, and irritability alternating with lethargy. Respiratory symptoms can become prominent within hours of birth in group B streptococcal (GBS) infection; however, the symptom complex also is seen with infection by E coli or Listeria species.
Late-onset bacterial meningitis (ie, symptom onset after 48 hours of life) is more likely to be associated with neurological symptoms. Most commonly seen are stupor and irritability, which Volpe describes in more than 75% of affected neonates. Between 25% and 50% of neonates will exhibit the following neurological signs:
Bulging anterior fontanel
Extensor posturing or opisthotonos
Focal cerebral signs including gaze deviation and hemiparesis
Cranial nerve palsies
Nuchal rigidity is the least common sign in neonatal bacterial meningitis, occurring in fewer than 25% of affected neonates.
Early features of HSV meningitis may mimic those associated with bacterial meningitis, including pallor, irritability, high-pitched cry, respiratory distress, fever, or jaundice, progressing to pneumonitis, seizures, hepatic dysfunction, and disseminated intravascular coagulopathy (DIC).
Regardless of etiology, meningitis in neonates can progress rapidly to serious complications, including cerebral edema, hydrocephalus, hemorrhage, ventriculitis (especially with bacterial infection), abscess formation, and cerebral infarction.
Cerebral edema, hydrocephalus, and hemorrhage each may cause increased intracranial pressure, with potential for secondary ischemic injury to the brain because of decreased brain perfusion:
Cerebral edema results from vasogenic changes, cytotoxic cell injury, and, at times, inappropriate antidiuretic hormone (ADH) secretion
Hydrocephalus results from debris obstructing the flow of cerebrospinal fluid (CSF) through the ventricular system or from dysfunction of arachnoid villi; it occurs in as many as 24% of neonates with bacterial meningitis 
Hemorrhage occurs in regions of infarction or necrosis and should be suspected in a neonate with new focal neurological findings or clinical deterioration
Ventriculitis results in sequestration of infection to areas that are poorly accessible to systemic antimicrobial drugs. Inflammation of the ependymal lining of ventricles often obstructs CSF flow. Thus, all of these complications are interactive, making effective management difficult. Ventriculitis occurs in as many as 20% of infected neonates. Failure to respond to appropriate antibiotic therapy and signs of elevated intracranial pressure (ICP) may suggest the diagnosis. Intraventricular administration of antibiotics may be necessary in cases of ventriculitis.
Cerebral abscess occurs in as many as 13% of neonates with meningitis. New seizures, signs of elevated ICP, or new focal neurological signs suggest the diagnosis. Brain imaging with contrast is essential for making the definitive diagnosis. Surgical intervention may be required.
Cerebral infarction, both focal (arterial) and diffuse (venous), may complicate recovery. Autopsy studies have found evidence of infarction in 30-50% of specimens studied. Imaging studies suggest that the actual incidence of infarction may be even higher. Meningitis has been shown to be associated with 1.6% of all cases of neonatal arterial stroke and 7.7% of venous infarcts.
Necrotizing lesions secondary to HSV meningitis can be deleterious to the developing brain.
Other, longer-term complications that may develop include residual epilepsy, cognitive impairment, hearing loss, visual impairment, spastic paresis, and microcephaly. Some of these disorders may be difficult to detect during infancy.
Hearing, for example, is difficult to evaluate without the child’s cooperation, and even then, assessment may be limited to behavioral response to sounds. Brainstem auditory evoked response (BAER) testing does not evaluate all dimensions of hearing, but this test, which can be performed reliably in sedated infants, only slightly overestimates hearing loss, which occurs in 30% of survivors of bacterial meningitis and 14% of survivors of nonbacterial meningitis. Subtle impairment of sound discrimination may not be readily apparent.
Similarly, cognitive impairment may not be evident until the child has started school or advanced into higher grades where more complex analysis of information is necessary. Careful screening for neurological, cognitive, and developmental deficits must be conducted as part of routine pediatric care over a period of many years, and the responsible physician should be attentive to possible problems with perception, learning, or behavior that may result from neonatal infection.
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