Hearing Loss In Preterm Infants Research Articles

Cumulative risk factors contributing to hearing loss in preterm infants

ObjectiveTo investigate individual and concomitant risk factors for hearing loss during neonatal care.DesignCase–control study.SettingCommunity.Population237 children born <32 weeks of gestation; 57 with hearing loss and 180 with normal hearing born...

The Hearing Status of Preterm Infant's ≤ 34 Weeks as Revealed by Otoacoustic Emissions (OAE) Screening and Diagnostic Brainstem Evoked Response Audiometry (BERA): A Tertiary Center Experience.

To know the prevalence of hearing loss in preterm infants & to evaluate the sensitivity & specificity of otoacoustic emission (OAE) in detecting hearing loss in preterm infants ≤ 34weeks. A total of 70 preterm babies from 28 to 34weeks of gestational age were enrolled in the study. Detailed prenatal, perinatal, postnatal & family history and physical examination of the babies were carried out. First OAE was done at discharge or two weeks after birth, whichever was earlier and the second OAE assessment was done at 36-40weeks of corrected age. Diagnostic brainstem evoked response audiometry (BERA) was done in all infants at 36-40weeks of corrected age, at the time of second OAE. Neonates with hearing impairment were advised for early hearing aid amplification and were referred to the rehabilitation center for further management. The sensorineural hearing loss (SNHL) in either one of the ears was identified in 13 (18.57%) preterm babies. Bilateral profound SNHL was found in 5 (7.14%) babies. Auditory neuropathy profile was found in 7 (53.8%) out of 13 babies who had hearing loss. The sensitivity, specificity, positive and negative predictive values of second TEOAE compared with diagnostic BERA was 46.15%, 85.96%, 42.85%, and 87.5% respectively. Neonatal jaundice (p = 0.009) and history of exchange transfusion (p = 0.019) were found to be significant risk factors of hearing loss in our study. Other risk factors like mode of delivery, birth asphyxia, low APGAR score, meningitis, ototoxic drugs, and seizures were not associated with hearing loss. The prevalence of hearing loss in preterm infants < 34weeks is very high. OAE alone is not an ideal screening test for high-risk neonates ≤ 34weeks because of its low sensitivity. OAE combined with diagnostic BERA should be done in all high-risk infants preterm neonates ≤ 34weeks to identify cases of auditory neuropathy spectrum disorders.

Congenital Hearing Loss among Pre-term infants in North India

Earlier investigations have reported congenital hearing loss in pre-term infants. Present study investigated hearing tests among pre-term infants to know the percentage of pre-term infants with hearing impairment. Two stage hearing assessment of pre-term infants showed congenital profound hearing loss in 16% of the infants. Present study showed the importance of TEOAE and ABR as efficient tool for hearing screening of high risk infants. Keywords: Preterm, Infants, India, Hearing Loss.

Hyperbilirubinemia and Follow-up Auditory Brainstem Responses in Preterm Infants.

Objectives. Neonatal hyperbilirubinemia is considered one of the most common causative factors of hearing loss. Preterm infants are more vulnerable to neuronal damage caused by hyperbilirubinemia. This study aimed to evaluate the effect of hyperbilirubinemia on hearing threshold and auditory pathway in preterm infants by serial auditory brainstem response (ABR). In addition, we evaluate the usefulness of the unconjugated bilirubin (UCB) level compared with total serum bilirubin (TSB) on bilirubin-induced hearing loss.Methods. This study was conducted on 70 preterm infants with hyperbilirubinemia who failed universal newborn hearing screening by automated ABR. The diagnostic ABR was performed within 3 months after birth. Follow-up ABR was conducted in patients with abnormal results (30 cases). TSB and UCB concentration were compared according to hearing threshold by ABR.Results. The initial and maximal measured UCB concentration for the preterm infants of diagnostic ABR ≥40 dB nHL group (n=30) were statistically higher compared with ABR ≤35 dB nHL group (n=40) (P=0.031 and P=0.003, respectively). In follow-up ABR examination, 13 of the ABR ≥40 dB nHL group showed complete recovery, but 17 had no change or worsened. There was no difference in bilirubin level between the recovery group and non-recovery group.Conclusion. UCB is a better predictor of bilirubin-induced hearing loss than TSB in preterm infants as evaluated by serial ABR. Serial ABR testing can be a useful, noninvasive methods to evaluate early reversible bilirubin-induced hearing loss in preterm infants.

Gentamicin Exposure and Sensorineural Hearing Loss in Preterm Infants.

ObjectiveTo evaluate the impact of gentamicin exposure on sensorineural hearing loss (SNHL) in very low birth weight (VLBW) infants.MethodsExposure to gentamicin was determined in infants born between 1993 and 2010 at a gestational age < 32 weeks and/or with a birthweight < 1500 g, who presented with SNHL during the first 5 years of life. For each case, we selected two controls matched for gender, gestational age, birthweight, and year of birth.ResultsWe identified 25 infants affected by SNHL, leading to an incidence of SNHL of 1.58% in our population of VLBW infants. The proportion of infants treated with gentamicin was 76% in the study group and 70% in controls (p = 0.78). The total cumulated dose of gentamicin administered did not differ between the study group (median 10.2 mg/kg, Q1-Q3 1.6–13.2) and the control group (median 7.9 mg/kg, Q1-Q3 0–12.8, p = 0.47). The median duration of gentamicin treatment was 3 days both in the study group and the control group (p = 0.58). Maximum predicted trough serum levels of gentamicin, cumulative area under the curve and gentamicin clearance were not different between cases and controls.ConclusionThe impact of gentamicin on SNHL can be minimized with treatments of short duration, monitoring of blood levels and dose adjustment.

Preconditioning crush increases the survival rate of motor neurons after spinal root avulsion.

OBJECTIVE:A meta-analysis of published randomized controlled trials investigating the long-term effect of dexamethasone on the nervous system of preterm infants.DATA SOURCES:Online literature retrieval was conducted using The Cochrane Library (from January 1993 to June 2013), EMBASE (from January 1980 to June 2013), MEDLINE (from January 1963 to June 2013), OVID (from January 1993 to June 2013), Springer (from January 1994 to June 2013) and Chinese Academic Journal Full-text Database (from January 1994 to June 2013). Key words were preterm infants and dexamethasone in English and Chinese.STUDY SELECTION:Selected studies were randomized controlled trials assessing the effect of intravenous dexamethasone in preterm infants. The quality of the included papers was evaluated and those without the development of the nervous system and animal experiments were excluded. Quality assessment was performed through bias risk evaluation in accordance with Cochrane Handbook 5.1.0 software in the Cochrane Collaboration. The homogeneous studies were analyzed and compared using Revman 5.2.6 software, and then effect model was selected and analyzed. Those papers failed to be included in the meta-analysis were subjected to descriptive analysis.MAIN OUTCOME MEASURES:Nervous system injury in preterm infants.RESULTS:Ten randomized controlled trials were screened, involving 1,038 subjects. Among them 512 cases received dexamethasone treatment while 526 cases served as placebo control group and blank control group. Meta-analysis results showed that the incidence of cerebral palsy, visual impairment and hearing loss in preterm infants after dexamethasone treatment within 7 days after birth was similar to that in the control group (RR = 1.47, 95%CI: 0.97–2.21; RR = 1.46, 95%CI: 0.97–2.20; RR = 0.80, 95%CI: 0.54–1.18; P > 0.05), but intelligence quotient was significantly decreased compared with the control group (MD = −3.55, 95%CI: −6.59 to −0.51; P = 0.02). Preterm infants treated with dexamethasone 7 days after birth demonstrated an incidence of cerebral palsy and visual impairment, and changes in intelligence quotient similar to those in the control group (RR = 1.26, 95%CI: 0.89–1.79; RR = 1.37, 95%CI: 0.73–2.59; RR = 0.53, 95%CI: 0.32–0.89; RR = 1.66, 95%CI: −4.7 to 8.01; P > 0.05). However, the incidence of hearing loss was significantly increased compared with that in the control group (RR = 0.53, 95%CI: 0.32–0.89; P = 0.02).CONCLUSION:Dexamethasone may affect the intelligence of preterm infants in the early stages after birth, but may lead to hearing impairment at later stages after birth. More reliable conclusions should be made through large-size, multi-center, well-designed randomized controlled trials.

Effect of dexamethasone on intelligence and hearing in preterm infants: a meta-analysis

In a previous study, heat shock protein 27 was persistently upregulated in ventral motor neurons following nerve root avulsion or crush. Here, we examined whether the upregulation of heat shock protein 27 would increase the survival rate of motor neurons. Rats were divided into two groups: an avulsion-only group (avulsion of the L4 lumbar nerve root only) and a crush-avulsion group (the L4 lumbar nerve root was crushed 1 week prior to the avulsion). Immunofluorescent staining revealed that the survival rate of motor neurons was significantly greater in the crush-avulsion group than in the avulsion-only group, and this difference remained for at least 5 weeks after avulsion. The higher neuronal survival rate may be explained by the upregulation of heat shock protein 27 expression in motor neurons in the crush-avulsion group. Furthermore, preconditioning crush greatly attenuated the expression of nitric oxide synthase in the motor neurons. Our findings indicate that the neuroprotective action of preconditioning crush is mediated through the upregulation of heat shock protein 27 expression and the attenuation of neuronal nitric oxide synthase upregulation following avulsion.

Postnatal risk factors associated with hearing loss among high-risk preterm infants: tertiary center results from Turkey

The aim of this study was to determine the postnatal risk factors associated with hearing loss as well as the prevalence of hearing loss among high-risk preterm infants in newborn hearing screening (NHS). We performed a retrospective study of high-risk preterm infants born with a gestational age ≤32 weeks and/or a birth weight ≤1,500 g. A NHS procedure was performed by automated auditory brainstem response (AABR) and automated evoked otoacoustic emission (TEOAE). Infants who failed TEOAE or AABR or both tests were referred to a tertiary audiology center for diagnosis confirmation and management. Postnatal risk factors associated with hearing loss were evaluated and compared for preterm infants with and without hearing loss. 1,360 high-risk preterm infants were assessed. Permanent hearing loss was found in 19 (1.4%) infants. Multivariate analysis revealed that proven sepsis (p = 0.019), mechanical ventilation ≥5 days (p = 0.024), loop diuretics (p = 0.001), patent ductus arteriosus ligation (p = 0.018) and operation for retinopathy of prematurity (ROP) (p = 0.034) were significant related factors for the hearing loss. This study showed a low prevalence of hearing loss and an association between operation for ROP and hearing loss in preterm infants, which has not been defined previously. Our results suggest that every neonatal intensive care unit should determine their own risk factors and take precautions to prevent hearing loss for these high-risk preterm infants.

Conductive hearing loss in preterm infants with bronchopulmonary dysplasia.

To determine the risk of conductive hearing loss in preterm infants with bronchopulmonary dysplasia (BPD) and preterm controls. The study population consisted of 78 infants with BPD of 26-33 weeks gestation and 78 controls of similar gestational age matched for broad-based birthweight categories. An auditory brainstem response (ABR) audiology was performed shortly before hospital discharge. Visual reinforcement orientation audiometry (VROA) and impedance audiometry were performed at 8-12 months corrected for prematurity. Infants with persistent audiological abnormalities were referred for evaluation to paediatric ENT surgeons. Infants with BPD had a significantly higher rate of ABR abnormalities (BPD: 22%, controls: 9%; P = 0.028). On VROA and impedance audiometry, the infants with BPD also had a higher rate of persistent abnormalities. Following ENT assessment, 22.1% of infants with BPD and 7.7% of controls had persistent conductive dysfunction requiring myringotomy and grommet tube insertion (P = 0.03). Most of these infants had normal ABR audiometry at hospital discharge. Preterm infants with BPD are at high risk of persistent conductive hearing loss late in the first year of life compared to controls. An ABR audiology conducted at the time of hospital discharge does not predict accurately later conductive hearing problems. Infants with BPD should have routine audiological evaluation toward the end of the first year of life.

Hyponatremia and Sensorineural Hearing Loss in Preterm Infants

In a case-control study the role of hyponatremia in the hearing loss of preterm infants was investigated. One hundred and sixty-four premature infants treated at the neonatal intensive care unit were screened with transient evoked otoacoustic emission (TEAOE). In 32 infants TEAOE results indicated the need for further investigations. Auditory brainstem response was performed and 22 of 32 cases had bilateral hearing impairment (HI). The birth weight and gestational age in the HI group were 1,425 ± 528 g and 30.4 ± 3.7 weeks. The matched control group consisted of 25 infants with a mean birth weight and gestational age of 1,410 ± 280 g and 31.1 ± 2.1 weeks. Significant differences were found between the HI and control groups: Apgar score (p < 0.05), pH value (p < 0.01) and pO₂ level (p < 0.05) were lower; the total dose of aminoglycosides (p < 0.01), furosemide usage (p < 0.01), the maximum pCO₂ level (p < 0.01), incubator stay (p < 0.05) and hyponatremia (p < 0.01) were higher, and the duration of hyponatremia (p < 0.05) was longer in the HI group. Multivariate logistic regression revealed that aminoglycoside treatment and hyponatremia were the two most significant factors in the development of hearing impairment. These results suggest that hyponatraemia is an additional risk factor for hearing loss in preterm infants.

Risk factors of sensorineural hearing loss in preterm infants.

Among 547 preterm infants of < or = 34 weeks gestation born between 1987 and 1991, 8 children (1.46%) developed severe progressive and bilateral sensorineural hearing loss. Perinatal risk factors of infants with hearing loss were compared with those of two control groups matched for gestation and birth weight and for perinatal complications. Our observations demonstrated an association of hearing loss with a higher incidence of perinatal complications. Ototoxicity appeared closely related to a prolonged administration and higher total dose of ototoxic drugs, particularly aminoglycosides and furosemide. Finally, we strongly recommend to prospectively and regularly perform audiologic assessment in sick preterm children as hearing loss is of delayed onset and in most cases bilateral and severe.

The effect of preterm birth on brainstem, middle latency and cortical auditory evoked responses (BMC AERS)

Recent studies on the maturation of auditory brainstem evoked responses (ABRs) present conflicting results, whereas only sparse reports exist with respect to the maturation of middle latency auditory evoked responses (MLRs) and auditory cortical evoked responses (ACRs). The present study reports the effect of preterm birth on the maturation of auditory evoked responses in low risk preterm infants (27–34 weeks conceptional age). The ABRs indicate a consistent trend towards longer latencies for all individual ABR components and towards longer interpeak latencies in preterm infants. The MLR shows longer latencies for early component PO in preterm infants. The ACRs show a remarkable difference between preterm and term infants. At 40 weeks CA the latencies of ACR components Na and P2 are significantly longer in term infants, whereas at 52 weeks CA the latencies of the same ACR components are shorter in term infants. The results support the hypothesis that retarded myelination of the central auditory pathway is partially responsible for differences found between preterm infants and term infants with respect to late ABR components and early MLR component PO. Furthermore, mild conductive hearing loss in preterm infants may also play its role. A more complex mechanism is implicated to account for the findings noted with respect to MLR component Na and ACR components Na and P2.