Hearing loss in neonatal encephalopathy

Around 34 million children are estimated to have hearing loss.Estimated prevalence in low-and middle-income countries (LMICs) (2.4%) is five times higher than high income countries (0.5%) with well-established universal neonatal hearing screening programs. 1 major contributor to childhood hearing loss is Neonatal Encephalopathy (NE).Sensorineural hearing loss in NE may occur due to a variety of reasonsdamage to the outer hair cells, cochlear nucleus or pathways between the auditory cortex to cochlear nucleus or due to other co-morbidities or ototoxic drugs.Most studies indicate that the occurrence of hearing loss is proportional to the severity of original brain injury.In a large retrospective study involving 776 babies who received whole body hypothermia for NE in Japan, Kennosuke Tsuda and colleagues recorded parent-reported hearing loss requiring amplification in 17 (20.5%)babies with severe NE and in 10 (3.6%) babies with moderate NE, while babies with mild NE did not have hearing loss requiring amplification. 2 This might suggest that hearing deficit are probably due to involvement of central auditory areas as a part of global cerebral hypoxia.Babies with severe NE are also likely to receive more ototoxic drugs and have less ability to clear these due to renal impairment.In contrast, another retrospective cohort study from Turkey involving 197 babies (124 cooled) showed no relation between hearing screening failure assessed using otoacoustic emissions and severity of encephalopathy.Hearing screen failure was reported in 10 of the 51 (19%) babies with mild encephalopathy, 20 of the 105 (19%) with moderate encephalopathy and 5 of the 21 (23%) babies with severe encephalopathy in this study. 3There is also evidence to suggest that even short periods of oxygen deprivation may damage outer hair cells leading to hearing loss, which may or may not be detected during neonatal screening using otoacoustic emissions. 4oes cooling reduce the occurrence of hearing loss in NE?The pooled data from cooling trials involving a total of 1505 babies from high income countries does not suggest so, although such analysis would be underpowered due to the low (3%) occurrence of hearing loss requiring amplification in these trials. 5Most of these cooling trials used parent-reported hearing loss at 18 months or more.Nevertheless, cooling does alter aminoglycoside metabolism and hearing loss may easily occur if there is genetic predisposition. 6In the United Kingdom, screening for mitochondrial genetic variant m.1555A > G is clinically used before aminoglycoside therapy. 7hat about the situation in LMIC where the occurrence of childhood hearing loss is five times higher than in high-income countries, 1 and cooling therapy is ineffective? 8The higher occurrence may be related to ototoxic drugs, co-morbidities, growth restriction and less established screening programs.The health and economic impact of hearing loss in LMIC may be higher than in high-income countries as effective remedial programs may not be available.In this systematic review, Pawale and colleagues pooled data on 5821 babies with NE from observational studies as well as randomized controlled trials to examine the incidence of hearing loss.They report 2 to 4% of babies with NE in high income countries and 7 to 8% in LMIC had hearing loss.The review is extensive and includes large number of babies.Hence these estimates provide important information for clinical practice and future research.These data are particularly useful for LMICs where cooling therapy is not effective, 8 and newer therapies that do not involve induced hypothermia are being developed.