Abstract

Identifying biomarkers for hearing impairments (HIs) in patients with neonatal hypoxic–ischemic encephalopathy (HIE), to initialize early hearing habilitation, is crucial. Seventy-eight neonates with HIE were divided into the following two groups: those with HIs and those without HIs. We compared those patients with 11,837 newborns without HIE, and analyzed the risk factors of HIs among neonatal HIE. Of the 78 patients, 11 were confirmed to have an HI, which is a substantially higher percentage than in the 11,837 newborns without HIE (14.1% vs. 0.87%; p < 0.001). More patients with moderate-to-severe HIE had confirmed HIs (p = 0.020; odds ratio, 8.61) than those with mild HIE. Clinical staging, and blood lactate and glucose levels could be predictive factors for HIs among patients with HIE. The patients who exhibited HIs had significantly higher lactate (104.8 ± 51.0 vs. 71.4 ± 48.4; U = 181, p = 0.032) and serum glucose (159.5 ± 86.1 vs. 112.1 ± 62.3; U = 166, p = 0.036) levels than those without HIs. A higher prevalence of HIs was noted in the patients with stage III HIE than those with stage II HIE (43.8% vs. 10%; p = 0.008). The degree of HI correlated with brain anomalies and neurodevelopmental outcomes at 1 year of age. Clinical staging, and blood lactate and glucose levels could be predictive factors for HIs among patients with HIE.

Highlights

  • Hearing impairments (HIs) in newborns can cause a serious obstacle to their development in language, cognition, and education [1,2,3], and can have considerable effects on their future development if the HI is not managed [1]

  • As identifying the risk factors for HIs is valuable for managing neonatal Hypoxic–ischemic encephalopathy (HIE), to avoid further damage, we investigated the risk factors of hearing damage in patients with neonatal HIE

  • We retrospectively reviewed the records of patients with neonatal HIE at Chung Shan Medical University Hospital, located in central Taiwan, by identifying those with a clinical history of fetal distress, metabolic acidosis, or needing positive-pressure ventilation immediately after birth

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Summary

Introduction

Hearing impairments (HIs) in newborns can cause a serious obstacle to their development in language, cognition, and education [1,2,3], and can have considerable effects on their future development if the HI is not managed [1]. The development of an HI after birth can be caused by numerous etiologies, including congenital infection, a stay in the neonatal intensive care unit for more than 5 days, assisted ventilation, exposure to ototoxic medications or loop diuretics, hyperbilirubinemia that requires an exchange transfusion, craniofacial anomalies, neurodegenerative disorders, or meningitis [4]. Hypoxic–ischemic encephalopathy (HIE) is a common cause of neonatal death, neurodevelopmental delays, and HI. Moderate-to-severe cases can cause irreversible cerebral cell damage and death, leading to a syndrome of HIE. HIE may lead to an altered conscious state, autonomic instability, absence of primitive reflexes, neonatal seizures, and death. Long-term consequences include epilepsy, intelligence disability, cerebral palsy, and hearing and visual impairment. A proportion of neonates with HIE will develop various degrees of HIs, despite the use of rescue hypothermia, which is standard care for those with moderate-to-severe neonatal HIE

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