Mechanisms of brain damage in H. influenzae meningitis.

Abstract

In recent years H. injluenzae has become the most common cause of bacterial meningitis in infants in the United States of America (1, 2). Although, over the last two decades, with steady improvement in methods of treatment (2, 3) the mortality rate has declined from over 90 per cent to about 10 to 15 per cent, the sequelae in the survivors may be serious. As many as 10 to 20 per cent may be left with some degree of neurological deficit. The cause of this is still uncertain. Alexander (4) has suggested that arteritis with thrombosis, and cerebritis, are the causes of neuronal damage, and others (5, 6) have emphasized the importance of subdural effusions. It is claimed that such effusions become enclosed by membranes which lead to restriction of brain growth at a time when the latter is still rapid. The present study of 34 fatal cases examined at the Cincinnati General and Children's Hospitals between 1932 and 1958 is mainly oriented to this problem of the mechanism or mechanisms by which H. injluenzae meningitis sometimes results in significant permanent brain damage. Although this form of meningitis was recognized at the end of the 19th century (7), and numerom; cases were diagnosed soon after World War I (8), only one paper is known to us (9) in which detailed attention is given to the pathological lesions. This was based upon an analysis of 14 fatal cases from the Boston City and Massachusetts General Hospitals. It contains much valuable information about the evolution of the inflammatory process in the meninges, associated vascular lesions, and brain damage, as well as clinico-pathological correlations. However, the time of its publication, in 1948, was before complicating subdural effusions had received adequate recognition and this factor was not considered.