Acute bacterial meningitis during the first month of life is said to be more frequent than in any subsequent 30-day period of life. It poses a number of special problems. Infants, of course, cannot complain of headache, stiff neck may be absent, and one has only the nonspecific signs of a systemic illness: fever, irritability, drowsiness, vomiting, convulsions, and a bulging fontanel to suggest the presence of meningeal infection. Signs of meningeal irritation do occur, but only late in the course of the illness. A high index of suspicion and liberal use of the lumbar puncture are the keys to early diagnosis. Lumbar puncture is ideally performed before any antibiotics are administered for other neonatal infections or, at a minimum, blood cultures should be obtained before treatment. An antibiotic regimen sufficient to control a septicemia may allow a meningeal infection to smolder and to flare up after antibiotic therapy for the systemic infection has been discontinued.
A number of other facts about the natural history of neonatal meningitis are noteworthy. It is more common in males than in females. Obstetric abnormalities in the third trimester (premature birth, prolonged labor, premature rupture of fetal membranes) occur frequently in mothers of infants who develop meningitis in the first weeks of life. The most significant factor in the pathogenesis of the meningitis is maternal infection (usually a urinary tract infection or puerperal fever of unknown cause). The infection in both mother and infant is most often caused by gram-negative enterobacteria, particularly E. coli, and group B streptococci, and less often to Pseudomonas, Listeria, S. aureus, or Staphylococcus epidermidis (formerly albus), and group A streptococci. Analysis of postmortem material indicates that in most cases infection occurs at or near the time of birth, although clinical signs of meningitis may not become evident until several days or a week later.
In infants with meningitis, one should be prepared to find a unilateral or bilateral “sympathetic” subdural effusion regardless of bacterial type. Young age, rapid evolution of the illness, low polymorphonuclear cell count, and markedly elevated protein in the CSF correlate to some extent with the formation of effusions, according to Snedeker and coworkers. Also, these attributes greatly increase the likelihood of the meningitis being associated with neurologic signs. Transillumination of the skull is the simplest method of demonstrating the presence of an effusion, but CT and MRI are the definitive diagnostic tests. When aspirated, most of the effusions prove to be sterile. If recovery is delayed and neurologic signs persist, a succession of aspirations is required. Children in whom meningitis is complicated by subdural effusions are no more likely, according to authorative sources, to have residual neurologic signs and seizures than are those without effusions.
As already indicated, the lumbar puncture is an indispensable part of the examination of patients with the symptoms and signs of meningitis or of any patient in whom this diagnosis is suspected. Bacteremia is not a contraindication to lumbar puncture. The dilemma concerning the risk of promoting transtentorial or cerebellar herniation by lumbar puncture, even without a cerebral mass, as indicated in Chaps. 2 and 16, has been settled in favor of performing the tap if there is a reasonable suspicion of meningitis.