Results

During the 18 month study period, 133 children with a working diagnosis of acute bacterial meningitis were enrolled. Nine patients did not fulfil the inclusion criteria, so the results from 124 children are presented. We estimate that this represents 83% of eligible children admitted to the participating centres. The patients’ ages ranged from 0.1 to 15.6 years (median 2.1 years). There were no fatalities in this series.

Meningococcal meningitis was diagnosed in 92 children (74%). Fifty two of these children had Neisseria meningitidis isolated by microscopy or culture of cerebrospinal fluid. Twenty six patients had cerebrospinal fluid pleocytosis plus positive meningococcal blood cultures or petechiae, and 14 children who did not undergo lumbar puncture had meningism and evidence of meningococcal disease.Streptococcus pneumoniae was isolated from the cerebrospinal fluid of 18 patients (15%). There was one case each of meningitis due to Haemophilus influenzae type b,Listeria monocytogenes, and group B streptococcus. In the remaining 11 cases (8%), all of whom had a cerebrospinal fluid neutrophil pleocytosis, the pathogen was unknown. Thirty four children had received parenteral penicillin before admission. This included 24 of the 26 patients with cerebrospinal fluid pleocytosis and signs of meningococcal disease.

The first audiological tests were performed within six hours of diagnosis in 83 children (67%). All but five had the first test performed within 24 hours. Twenty one children (17%) had hearing impairments detected at the time of their first OAE recordings. No children developed hearing loss at a later stage. The 21 children with evidence of hearing loss will be described according to their audiological diagnosis at discharge.

Three children (2.4%, 95% CI 0.5 to 6.9%) have persistent sensorineural hearing loss. The absence of OAEs in these children indicates cochlear damage. Their histories are summarised in table 1. Child number 3 complained of hearing loss at presentation.

Thirteen children had evidence of hearing impairment at the time of their first assessments but normal auditory function at discharge (table 2). The incidence of reversible hearing loss is therefore 10.5% (95% CI 5.7 to 17.3%). All these children had absent OAEs and normal tympanograms, indicating cochlear dysfunction. In eight cases the hearing loss was bilateral. Nine children regained normal hearing within 48 hours of diagnosis. An example of this ‘fleeting’ hearing loss is shown in fig1.

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Figure 1

OAE recordings from a child with fleeting hearing loss. Left hand panel of each recording (‘response waveform’) is a visual representation of the soundwaves produced by the ear. Right hand panel (‘power analysis’) is a fast Fourier transformation of the response showing strength of signal (black) and an estimate of noise (hatched) across the auditory frequencies. In the upper recording, taken at two hours after diagnosis, there is no emission. Lower recording shows strong OAE at 42 hours.

The prevalence of potential risk factors for hearing impairment is shown in table 3. For the sake of clarity, the data presented are for permanent and reversible sensorineural hearing loss combined. Independent analysis of each type of impairment produced similar results. No definite risk factors for sensorineural hearing loss were identified as the 95% CI for each relative risk included 1.0. Nevertheless, there did appear to be a trend towards a higher incidence of deafness in children who had been ill for over 24 hours before diagnosis (relative risk 2.72; 95% CI 0.93 to 7.98). The relationship between duration of symptoms and audiological outcome is demonstrated further in fig 2.

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Figure 2

Duration of symptoms and number of children with normal hearing and permanent or reversible sensorineural hearing loss (SNHL).

Thirty nine children in this study received dexamethasone as part of their treatment. In 29 patients the drug was given before, or concurrently with, the first dose of antibiotics. Dexamethasone was given within four hours of the diagnosis in eight others. In this non-randomised study the use of dexamethasone did not appear to affect audiological outcome. The relative risk of permanent or transient sensorineural hearing loss after steroid treatment was 1.70 (95% CI 0.68 to 4.23).

Five children (4.0%, 95% CI 1.3 to 9.2%), had absent OAEs in association with otoscopic and tympanometric evidence of middle ear effusions. All had mild to moderate hearing loss confirmed by auditory brainstem responses. These conductive impairments have persisted in four of the five children.

All children with hearing loss at discharge were followed up for at least nine months. Follow up data is also available for 104 (90%) of the remaining 116 children. Three of these children have mild to moderate conductive defects that were not present in hospital. The others have normal hearing.

Discussion

This study provides further evidence that hearing loss develops early in the course of bacterial meningitis. All children with hearing impairment had absent OAEs at the time of their first assessment. In most cases this was within six hours of diagnosis. Furthermore, three children actually complained of deafness at presentation. These findings extend the work of others who have detected sensorineural hearing loss within 24 to 48 hours of admission to hospital.5-7 As most children with hearing loss had been unwell for between 24 and 48 hours, our data suggest that hearing loss commences during the first two days of the illness.

Until now, the cause of postmeningitic hearing loss has been uncertain. Lesions of the cochlea, auditory nerves, brainstem, and higher centres have all been proposed.2 3 8-12 In our study, all children with sensorineural hearing loss failed to produce OAEs. Because the production of emissions is independent of the nervous system,14 this observation suggests that the cochlea is the site of the lesion in postmeningitic deafness.

The cochlea has also been identified as the site of the auditory lesion in animal experiments. In the guinea pig, appropriate bacterial toxins have been shown to damage the organ of Corti.19 In other experiments, bacteria and inflammatory cells have been seen in the cochlear aqueduct and the inner ear.20 21 The cochlear aqueduct, which links the scala tympani to the subarachnoid space, has also been proposed as a route of bacterial invasion in children.3 8 9 Indeed, the fact that the aqueduct is more likely to be patent in infancy than in adulthood22may explain the higher incidence of postmeningitic hearing loss in childhood.

The most striking finding of this study was that 10% of the subjects had a rapidly reversible hearing loss. All these children had evidence of hearing loss at admission but regained normal hearing within five days of diagnosis. Indeed, most cases had resolved within 48 hours. We do not believe that this ‘fleeting’ hearing loss has been reported before. Previous reports of reversible hearing loss have described children who have an impairment in hospital but then regain normal hearing over the following weeks or months.3 6-11

In our study, all children with reversible hearing loss had absent OAEs and normal tympanograms. This indicates cochlear dysfunction. We can only postulate as to the mechanism of this. It may result from the effects of bacterial toxins or inflammatory mediators on the hair cells of the organ of Corti.19 23 Alternatively, the endocochlear potential could be disrupted by the same mechanisms.24 Other possibilities include a metabolic defect secondary to low cerebrospinal fluid glucose,9 and the effect of changes in intracranial pressure transmitted through the cochlear aqueduct. The latter mechanism is supported by case reports of patients who have lost hearing after lumbar puncture.25However, this finding has only been reported in adults, most of whom have undergone invasive procedures such as myelography or spinal anaesthesia. The fluid shift after diagnostic lumbar puncture with a paediatric needle is likely to be much less. Furthermore, three of our patients had evidence of hearing loss before lumbar puncture and one did not undergo the procedure. We do not therefore believe that fleeting hearing loss is caused by lumbar puncture. This conclusion is supported by the recent finding that large changes in intracranial pressure do not abolish OAEs in children.26

It is tempting to propose that fleeting hearing loss would progress to permanent deafness if the meningitis had not been treated. This hypothesis is supported by the work of Bhatt et al who found that rabbits always showed signs of hearing loss 12 hours after the intrathecal injection of live pneumococci.21 Untreated animals progressed to permanent deafness whereas animals given antibiotics 12 hours after the induction of meningitis usually regained normal hearing.27

In a recent meta-analysis, the incidence of deafness in children surviving bacterial meningitis was reported to be 10.5% (95% CI 8.6 to 12.7%).1 The incidence of permanent deafness in our study, at 2.4%, was much less. We are confident that this figure is accurate because all our patients underwent thorough audiological testing and we studied over 80% of eligible patients in the study area. Our inclusion criteria could be criticised because 51 patients did not have a bacterium isolated from the cerebrospinal fluid. However, the exclusion of these children does not alter the incidence figures for permanent and reversible sensorineural hearing loss.

How, then, can we account for the low incidence of postmeningitic hearing loss in this study? In most previous studies, H influenzae type b was the leading cause of meningitis.1 After the introduction of H influenzaetype b vaccination, this form of meningitis is now rare. Consequently, nearly three quarters of our cases were caused by the meningococcus. However, this change in epidemiology is unlikely to explain the rarity of deafness in our study because the incidence of hearing loss after meningococcal meningitis (1.1%) was also much lower than expected. The use of steroids cannot explain the reduction in deafness either. Dexamethasone has been shown to significantly reduce the incidence of deafness in some studies,28 29 but in our population the children treated with steroids actually had a higher incidence of hearing loss (relative risk 1.70).

Another possibility is that the children in this study were less likely to become deaf because they were treated quickly. Half the children had been unwell for less than 24 hours before admission to hospital. In previous reports the average duration of symptoms has been around two days.5 7 28 The relationship between the duration of illness and complications of meningitis is controversial.30 Most prospective studies have not reported a significantly higher rate of deafness in children with long histories.3 5 6 31 However, this negative finding may be due to a lack of statistical power in these studies,32and it is interesting to note that some large prospective33 and retrospective9 34 studies have reported statistically significant results. In this study, the duration of symptoms was not identified as a definite risk factor for sensorineural hearing loss (see table 3). Nevertheless, hearing loss was nearly three times as common in children who had been ill for over 24 hours. There is therefore some evidence that deafness was uncommon because of early diagnosis and prompt treatment. This hypothesis is supported by our discovery of fleeting hearing loss. As we have already discussed, this phenomenon appears to represent a critical period, around the second day of the illness, during which hearing loss can be reversed.

In summary, we have shown that sensorineural hearing loss develops very early in meningitis. In our study, it was exclusively cochlear in origin. Ten per cent of our patients had a fleeting hearing loss caused by reversible cochlear dysfunction. It is possible that this transient hearing loss would have progressed to permanent deafness if the meningitis had not been treated promptly.