Abstract :
Keywords Extreme prematurity; Mortality; Bronchopulmonary dysplasia; Chronic lung disease; Intraventricular hemorrhage; Retinopathy of prematurity Highlights * Mortality among extremely premature infants was highest during the first 3 months. * Mortality decreased with higher gestational age and in more recent years. * Bronchopulmonary dysplasia increased the risk of mortality versus no complications. * Mortality risk also increased in infants with severe intraventricular hemorrhage. Abstract Background Preterm birth is a leading cause of infant mortality, particularly for those born extremely prematurely (EP; Aims To examine the epidemiology, complications, and mortality/survival among EP infants. Study design Retrospective analysis of electronic medical records from the Kaiser Permanente Northern California database. Subjects EP infants live-born between 22 and Outcome measures Cumulative all-cause mortality/survival were analyzed and stratified by GA (22 to Results 2154 EP infants were identified; of these, 916 deaths were recorded. Mortality was highest during the first 3 months (41.7 % cumulative mortality), and few were reported after 2 years (42.5 % cumulative mortality). Mortality decreased with higher GA and over more recent birth periods. BPD/CLD and IVH grade 3/4 were associated with increased mortality risk versus no complications (adjusted hazard ratios 1.41 and 1.78, respectively). Conclusions The risk of mortality is high during the first few months of life for EP infants, and is even higher for those with BPD and IVH. Despite an overall trend toward increased survival for EP infants, strategies targeting survival of EP infants with these complications are needed. Abbreviations BPD, bronchopulmonary dysplasia; CLD, chronic lung disease; EMR, electronic medical record; EP, extremely premature; GA, gestational age; HR, hazard ratio; ICD, International Classification of Diseases; IVH, intraventricular hemorrhage; PMA, post-menstrual age; ROP, retinopathy of prematurity Author Affiliation: (a) Global Evidence and Outcomes, Takeda Development Center Americas, Lexington, MA, USA (b) College of Allied Health Sciences, Augusta University, Augusta, GA, USA (c) Division of Research, Kaiser Permanente Northern California, Oakland, CA, USA * Corresponding author at: Global Evidence and Outcomes, Takeda Pharmaceutical Company Limited, 300 Shire Way, Lexington, MA 02421, USA. Article History: Received 27 January 2022; Accepted 15 June 2022 (footnote)1 Affiliation at the time of the study. Byline: Csaba Siffel [csaba.siffel@takeda.com] (a,b,*), Andrew K. Hirst (c), Sujata P. Sarda (a,1), Michael W. Kuzniewicz (c), De-Kun Li (c)