663 INCUBATOR NOISE AND HEARING-LOSS
Letters
to
the Editor
suggested that ambient noise in incubaof the sensory neural hearing-loss which has been reported to be prevalent among premature infants. Harris et al. expressed a similar concern after recording sound-pressure levels in incubators and head boxes. Exposure to increased levels of noise is as undesirable for the newborn immature infant as it is for any other individual, but, like Schulte and Stennert,3 we cannot accept that ambient noise in incubators is alone the cause of sensory neural hearing-loss among low-birth-weight survivors. These infants are at risk of hypoxia and hyperbilirubinaemia, both of which may cause sensory neural hearing-loss. They are also liable to bleed into the subependymal matrix of the brain and into the ventricles. Extension of these haemorrhages into the inner ear has been reported in infants who died after receiving ventilatory support for respiratory distress.4 All these factors, therefore, must be considered when attempting to evaluate the influence of ambient noise on the hearing of low-birth-weight infants nursed in incubators. We have examined the hearing of a group of 111 infants who weighed 1500 g at birth.5 These infants represented 86% of the surviving infants of this birth-weight who were cared for in the neonatal unit of University College Hospital in the years 1966-72. All these infants were nursed in commercially available incubators for periods ranging from 2 to 80 days (mean 37 days). None received continuous positive airway pressure from a head box. Sound-pressure levels at all octave frequencies in our incubators were similar to those reported by Harris et al .2 10 (9%) of these infants had sensory neural hearing-loss (mean 51 dB) when tested at a mean age of 6-5years. None of the audiograms of these 10 children showed notches at 4000 Hz, which are considered to be characteristic of damage to the cochlea due to long-term noise exposure. They all had either a gradual fall of threshold towards the high frequencies, or an abrupt loss at 8000 Hz only. The mean duration of incubator stay did not differ between the infants with sensory neural hearing-loss and those without. In contrast, perinatal illnesses, particularly those known or likely to have caused hypoxia in the newborn period, including apnoca, were significantly associated with sensory neural hearing-loss. Jaundice seemed to have an additive effect. We conclude that sensory neural hearing-loss in very-lowbirth weight infants is probably caused by hypoxia in the newborn period and is not due to the ambient noise in commerSIR,-Douek
tors
TREATMENT OF PURULENT MENINGITIS IN INFANTS
SIR,-When treated with intravenous antibiotics purulent meningitis in infants less than 2 months of age has a high fatality-rate (40-70%’,2). This is explained by the low concentration of the antibiotics in cerebrospinal fluid (c.s.F.). For example, ampicillin, given at a dosage as high as 400 mg/kg/day results in c.s.F. levels lower than 4 mg/1 in more than 50% of the cases.3 After i.v. gentamicin (2-5 mg/kg) its C.S.F. concentration is very low (by bioassay4) or undetectable (by radioimmunoassay5). The minimum inhibitory concentration against infecting gram-negative rods usually exceeds 5 mg/1 for ampicillin and 1 mg/1 for gentamicin, the figures in four cases of Escherichia coli infection being (mg/1) >20, 16, 4, and 10 for ampicillin and 1, 2, 2, and 2.55 for gentamicin. Before 1972, of the last eight patients we treated with i.v. antibiotics alone one fully recovered, three were mentally retarded, and four died. From 1972 we added daily intraventricular instillation with 2 mg gentamicin to the i.v. therapy. This has been reported to result in adequate, non-toxic levels both in the ventricular fluid (2.4-10 mg/1) and in the spinal fluid (3.1-5 mg/1) up to 21-30 h after the injection.4 The intrathecal therapy was started as soon as the diagnosis of ventriculitis was made (more than 200 polymorphonuclears/µl with c.s.F. glucose below 30 mg/dl, or a positive culture). Combined i.v. and intrathecal therapy was applied to all infants with meningitis due to gram-negative organisms and to group-B streptococci. Indeed, group-B streptococci are much less sensitive to ampicillin than are group-A streptococci. In addition, the minimal bactericidal concentration frequently surpasses the minimal inhibitory concentration, even by a factor of 100, and usually exceeds 8 mg/1 for ampicillin. Bacterial killing is much accelerated when ampicillin and gentamicin are used in combination.6 The daily instillations were repeated (during an average of 7 days) until the white-cell count in the C.S.F. was less than 100/ul. Systemic antibiotic therapy consisted of ampicillin (100 mg/kg every 6 h) and gentamicin (2-5 mg/kg every 8 h). 29 meningitis patients (mainly with gram-negative bacteria) have been treated in this way and all have survived, seventeen with complete recovery and only eight (27%) with residual problems after a follow-up of 1-5 years. The chance of a full recovery depends on the time of diagnosis and treatment--of nine patients diagnosed within 24 h of symptoms only one had sequels, while only one of six patients diagnosed later made a full recovery.
clearly
L. CORBEEL K. DE BOECK N. LOGGHE
E. EGGERMONT P. CASAER
Departments of Pædiatrics Bacteriology, University of Leuven, 3000 Leuven, Belgium
and
R. EECKELS J. VANDEPITTE L. VERBIST
1. Lancet, 1976, ii, 778. 2 Yeung, C. Y. Archs Dis.
Childh., 1976, 51, 686. 3. Bessard, G., Rambaud, P., Gavend, M., Beaudoing,
A.
Pediatrie, 1976, 31,
649.
4. Moellering, R. C., Fischer, E. G. J. Pediat. 1972, 81, 534. 5. Pickering, L. K., Ericsson, C. D., Ruiz-Palacios, G., Blevins, J., Miner, M E. Am. J. Dis. Child. 1978, 132, 480. 6. Schauf, V., Deveikis, A., Riff, L., Serota, A. J. Pediat. 1976, 89, 194.
may be the
et
al.’
cause
available incubators in current use. Nevertheless, we agree that careful attention must be paid to ambient noise levels in newborn nurseries, particularly since in addition to
cially
motor-driven incubators, monitoring devices with noise are being increasingly used. Departments of Obstetrics and Pædiatrics, and Royal Ear Hospital, University College Hospital and Medical School, London WC1
signals
ANN STEWART
SOLOMON ABRAMOVICH
AVAILABLE OXYGEN IN PRETERM BABIES
SIR,-We support the note of caution in your editorial (Feb. 24, p. 419) about transfusion of fresh blood to infants and believe that 5-7-day-old blood, screened for hepatitis and and very unlikely to transmit cytomegalovirus, is safer. Despite the increase in Hb-02 affinity on storage of
syphilis
1. Douek, E., Bannister, L. H., Dodson, H. C., Ashcroft, P. Lancet, 1976, ii, 1110. 2. Harris, F., Pickup, D. S., Eastwood, M., Collins, D. H., Williams, S. Jl. R. Soc. Med. 1978, 71, 852. 3. Schulte, F. J., Stennert, E. Archs Dis. Child. 1978, 53, 269. 4. Spector, G. J., Pettit, W. J., Davis, G., Strauss, M., Rauchbach, E. Laryngoscope, 1978, 88, 764. 5. Abramovich, S., Gregory, S., Slemick, M., Stewart, A. Archs Dis. Child. (in the press).
Letters
to
the Editor
suggested that ambient noise in incubaof the sensory neural hearing-loss which has been reported to be prevalent among premature infants. Harris et al. expressed a similar concern after recording sound-pressure levels in incubators and head boxes. Exposure to increased levels of noise is as undesirable for the newborn immature infant as it is for any other individual, but, like Schulte and Stennert,3 we cannot accept that ambient noise in incubators is alone the cause of sensory neural hearing-loss among low-birth-weight survivors. These infants are at risk of hypoxia and hyperbilirubinaemia, both of which may cause sensory neural hearing-loss. They are also liable to bleed into the subependymal matrix of the brain and into the ventricles. Extension of these haemorrhages into the inner ear has been reported in infants who died after receiving ventilatory support for respiratory distress.4 All these factors, therefore, must be considered when attempting to evaluate the influence of ambient noise on the hearing of low-birth-weight infants nursed in incubators. We have examined the hearing of a group of 111 infants who weighed 1500 g at birth.5 These infants represented 86% of the surviving infants of this birth-weight who were cared for in the neonatal unit of University College Hospital in the years 1966-72. All these infants were nursed in commercially available incubators for periods ranging from 2 to 80 days (mean 37 days). None received continuous positive airway pressure from a head box. Sound-pressure levels at all octave frequencies in our incubators were similar to those reported by Harris et al .2 10 (9%) of these infants had sensory neural hearing-loss (mean 51 dB) when tested at a mean age of 6-5years. None of the audiograms of these 10 children showed notches at 4000 Hz, which are considered to be characteristic of damage to the cochlea due to long-term noise exposure. They all had either a gradual fall of threshold towards the high frequencies, or an abrupt loss at 8000 Hz only. The mean duration of incubator stay did not differ between the infants with sensory neural hearing-loss and those without. In contrast, perinatal illnesses, particularly those known or likely to have caused hypoxia in the newborn period, including apnoca, were significantly associated with sensory neural hearing-loss. Jaundice seemed to have an additive effect. We conclude that sensory neural hearing-loss in very-lowbirth weight infants is probably caused by hypoxia in the newborn period and is not due to the ambient noise in commerSIR,-Douek
tors
TREATMENT OF PURULENT MENINGITIS IN INFANTS
SIR,-When treated with intravenous antibiotics purulent meningitis in infants less than 2 months of age has a high fatality-rate (40-70%’,2). This is explained by the low concentration of the antibiotics in cerebrospinal fluid (c.s.F.). For example, ampicillin, given at a dosage as high as 400 mg/kg/day results in c.s.F. levels lower than 4 mg/1 in more than 50% of the cases.3 After i.v. gentamicin (2-5 mg/kg) its C.S.F. concentration is very low (by bioassay4) or undetectable (by radioimmunoassay5). The minimum inhibitory concentration against infecting gram-negative rods usually exceeds 5 mg/1 for ampicillin and 1 mg/1 for gentamicin, the figures in four cases of Escherichia coli infection being (mg/1) >20, 16, 4, and 10 for ampicillin and 1, 2, 2, and 2.55 for gentamicin. Before 1972, of the last eight patients we treated with i.v. antibiotics alone one fully recovered, three were mentally retarded, and four died. From 1972 we added daily intraventricular instillation with 2 mg gentamicin to the i.v. therapy. This has been reported to result in adequate, non-toxic levels both in the ventricular fluid (2.4-10 mg/1) and in the spinal fluid (3.1-5 mg/1) up to 21-30 h after the injection.4 The intrathecal therapy was started as soon as the diagnosis of ventriculitis was made (more than 200 polymorphonuclears/µl with c.s.F. glucose below 30 mg/dl, or a positive culture). Combined i.v. and intrathecal therapy was applied to all infants with meningitis due to gram-negative organisms and to group-B streptococci. Indeed, group-B streptococci are much less sensitive to ampicillin than are group-A streptococci. In addition, the minimal bactericidal concentration frequently surpasses the minimal inhibitory concentration, even by a factor of 100, and usually exceeds 8 mg/1 for ampicillin. Bacterial killing is much accelerated when ampicillin and gentamicin are used in combination.6 The daily instillations were repeated (during an average of 7 days) until the white-cell count in the C.S.F. was less than 100/ul. Systemic antibiotic therapy consisted of ampicillin (100 mg/kg every 6 h) and gentamicin (2-5 mg/kg every 8 h). 29 meningitis patients (mainly with gram-negative bacteria) have been treated in this way and all have survived, seventeen with complete recovery and only eight (27%) with residual problems after a follow-up of 1-5 years. The chance of a full recovery depends on the time of diagnosis and treatment--of nine patients diagnosed within 24 h of symptoms only one had sequels, while only one of six patients diagnosed later made a full recovery.
clearly
L. CORBEEL K. DE BOECK N. LOGGHE
E. EGGERMONT P. CASAER
Departments of Pædiatrics Bacteriology, University of Leuven, 3000 Leuven, Belgium
and
R. EECKELS J. VANDEPITTE L. VERBIST
1. Lancet, 1976, ii, 778. 2 Yeung, C. Y. Archs Dis.
Childh., 1976, 51, 686. 3. Bessard, G., Rambaud, P., Gavend, M., Beaudoing,
A.
Pediatrie, 1976, 31,
649.
4. Moellering, R. C., Fischer, E. G. J. Pediat. 1972, 81, 534. 5. Pickering, L. K., Ericsson, C. D., Ruiz-Palacios, G., Blevins, J., Miner, M E. Am. J. Dis. Child. 1978, 132, 480. 6. Schauf, V., Deveikis, A., Riff, L., Serota, A. J. Pediat. 1976, 89, 194.
may be the
et
al.’
cause
available incubators in current use. Nevertheless, we agree that careful attention must be paid to ambient noise levels in newborn nurseries, particularly since in addition to
cially
motor-driven incubators, monitoring devices with noise are being increasingly used. Departments of Obstetrics and Pædiatrics, and Royal Ear Hospital, University College Hospital and Medical School, London WC1
signals
ANN STEWART
SOLOMON ABRAMOVICH
AVAILABLE OXYGEN IN PRETERM BABIES
SIR,-We support the note of caution in your editorial (Feb. 24, p. 419) about transfusion of fresh blood to infants and believe that 5-7-day-old blood, screened for hepatitis and and very unlikely to transmit cytomegalovirus, is safer. Despite the increase in Hb-02 affinity on storage of
syphilis
1. Douek, E., Bannister, L. H., Dodson, H. C., Ashcroft, P. Lancet, 1976, ii, 1110. 2. Harris, F., Pickup, D. S., Eastwood, M., Collins, D. H., Williams, S. Jl. R. Soc. Med. 1978, 71, 852. 3. Schulte, F. J., Stennert, E. Archs Dis. Child. 1978, 53, 269. 4. Spector, G. J., Pettit, W. J., Davis, G., Strauss, M., Rauchbach, E. Laryngoscope, 1978, 88, 764. 5. Abramovich, S., Gregory, S., Slemick, M., Stewart, A. Archs Dis. Child. (in the press).
