Abstract Rationale Infants are susceptible to sleep apnea due to physiological immaturity of sleep drive and anatomical predisposition of their upper airway. Despite this susceptibility, there is paucity of data regarding prognosis of infant sleep apnea, particularly in infants who do not have any risk for Obstructive Sleep Apnea (OSA). We hypothesized that infants without any risk factors for OSA will demonstrate improvement in sleep apnea without any need for intervention. Methods In an ongoing observational study, we collected data on infants who had their first sleep study within their first year of life and a follow-up sleep study within first four years of life, excluding infants who had craniofacial anomalies, genetic conditions associated with OSA, or prematurity. Infants were grouped into non-intervention (non-I), or intervention (I) group, where they had surgical intervention (i.e. supraglottoplasty/adenoidectomy/tonsillectomy) or non-surgical intervention (i.e. low flow oxygen supplementation/PAP therapy). Time between visits was categorized as short (7.5 months) or long (7.5 months). For each subgroup, differences in apnea-hypopnea index ( AHI) between the visits were compared using a t-test. Associations of follow-up group, age, gender, and laryngomalacia with change in AHI were examined with a linear mixed model. Results Our study included 60 infants (42 non-I group). For the non-I and I group, there were 16 and 8 females, and median age at first sleep study was 2.6 vs. 2.9 (IQR = (0.6,14.3) vs. (0.5,18.9) months, respectively. Median age at the follow up sleep study was 8.8(1.3,38.3) months. LZ1 Prevalence of laryngomalacia in non-I group was 17(40.5%) and in I group was 7(38.9%). There was a significant improvement in AHI between visits in the non-I group (average decrease=12.4, 95%CI = (5.6, 19.2), p = 0.006) and I group (average decrease=18.5, 95%CI = (1.4, 35.7), p = 0.035). Age at first sleep study (β=-1.5,SE=0.61,p = 0.019) and short follow-up time group (β=-13.8,SE=4.18,p = 0.001) was significantly associated with change in AHI in the non-I group, adjusting for other covariates. In the I group, short follow-up group (β=-19.9,SE=9.85,p = 0.045) was significantly associated with change in AHI, after adjusting for other covariates. Conclusion In infants without risk factors predisposing them to OSA, AHI improved with and without intervention. Age of presentation and severity of sleep apnea was associated with improvement in AHI in infants without intervention. Future studies correlating neurocognitive outcome with severity of sleep apnea may be useful in determining need for intervention in this population. This abstract is funded by: None
Bandyopadhyay et al. (Fri,) studied this question.