Pediatric pulmonology · 2022
A simple noninvasive biomarker can reflect both the acute and chronic pulmonary impact of patent ductus arteriosus shunting.
СтатьяНазвание и аннотация: Перевод в очереди
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Bin-Nun Alona, Shchors Irina, Abu-Omar Rawan, Kasirer Yair, Mimouni Francis, Hammerman Cathy
Аннотация
AIM: The SFR (SpO2 /FiO2 ratio) offers a continuous, noninvasive reflection of pulmonary function regardless of whether the baby is ventilated or breathing spontaneously. We hypothesized that significant patent ductus arteriosus (PDA) shunting would impair pulmonary oxygen diffusion, reflected by decreased SFR; and that early PDA related decreases in SFR predict subsequent chronic lung disease (CLD).
METHODS: We retrospectively examined records from preterm neonates ≤30 weeks gestational age. Ductal shunting was graded for severity by first week echocardiogram. SFR was calculated as SpO2 /FiO2 and recorded on Day 7 of life and 36 weeks postmenstrual age (PMA).
RESULTS: We studied 104 infants: 65 with closed duct, 17 with hemodynamically insignificant PDA, and 22 with hemodynamically significant (hsPDAs). CLD developed in 9 (14%) of those with closed ducts; 6 (35%) of those with hisPDA; and in 12 (55%) of those with hsPDA (p = 0.005). SFR values at 1 week postnatally were decreased in those with hsPDA and with hisPDA as compared with those with closed ducts (closed ducts 452 [448-457] vs. hisPDA 396 [294-442] vs. hsPDA 327 [235-369]; p = 0.00001). However, at 36 weeks only SFRs of babies with hsPDA remained significantly lower (467 [461-467] vs. 467 [413-471] vs. 369 [262-436] for closed vs. hisPDA vs. hsPDA respectively; p = 0.000148). Using ROC curve analysis, Week 1 SFR was strongly associated with hsPDA (area under curve [AUC] = 0.770; p < 0.0001) and highly predictive (AUC = 0.801; p < 0.0001) of CLD at 36 weeks PMA.
CONCLUSION: Early decreases in SFR reflect both the acute and chronic pulmonary impact of PDA shunting, possibly providing the missing link supporting an association between hemodynamically significant PDA and subsequent CLD.
METHODS: We retrospectively examined records from preterm neonates ≤30 weeks gestational age. Ductal shunting was graded for severity by first week echocardiogram. SFR was calculated as SpO2 /FiO2 and recorded on Day 7 of life and 36 weeks postmenstrual age (PMA).
RESULTS: We studied 104 infants: 65 with closed duct, 17 with hemodynamically insignificant PDA, and 22 with hemodynamically significant (hsPDAs). CLD developed in 9 (14%) of those with closed ducts; 6 (35%) of those with hisPDA; and in 12 (55%) of those with hsPDA (p = 0.005). SFR values at 1 week postnatally were decreased in those with hsPDA and with hisPDA as compared with those with closed ducts (closed ducts 452 [448-457] vs. hisPDA 396 [294-442] vs. hsPDA 327 [235-369]; p = 0.00001). However, at 36 weeks only SFRs of babies with hsPDA remained significantly lower (467 [461-467] vs. 467 [413-471] vs. 369 [262-436] for closed vs. hisPDA vs. hsPDA respectively; p = 0.000148). Using ROC curve analysis, Week 1 SFR was strongly associated with hsPDA (area under curve [AUC] = 0.770; p < 0.0001) and highly predictive (AUC = 0.801; p < 0.0001) of CLD at 36 weeks PMA.
CONCLUSION: Early decreases in SFR reflect both the acute and chronic pulmonary impact of PDA shunting, possibly providing the missing link supporting an association between hemodynamically significant PDA and subsequent CLD.