Implementation of a revised classification for intrapartum fetal heart rate monitoring and association to birth outcome: A national cohort study.

INTRODUCTION: A revised intrapartum cardiotocography (CTG) classification was introduced in Sweden in 2017. The aims of the revision were to adapt to the international guideline published in 2015 and to adjust the classification of CTG patterns to current evidence regarding intrapartum fetal physiology. This study aimed to investigate adverse neonatal outcomes before and after implementation of the revised CTG classification. MATERIAL AND METHODS: A before-and-after design was used. Cohort I (n = 160 210) included births from June 1, 2014 through May 31, 2016 using the former CTG classification, and cohort II (n = 166 558) included births from June 1, 2018 through May 31, 2020 with the revised classification. Data were collected from the Swedish Pregnancy and Neonatal Registers. The primary outcome was moderate to severe neonatal hypoxic ischemic encephalopathy (HIE 2-3). Secondary outcomes were birth acidemia (umbilical artery pH <7.05 and base excess < -12 mmol/L or pH <7.00), A-criteria for neonatal hypothermia treatment, 5-min Apgar scores <4 and <7, neonatal seizures, meconium aspiration, neonatal mortality and delivery mode. Logistic regression was used (period II vs period I), and results are presented as adjusted odds ratios (aORs) with 95% confidence intervals (95% CIs). RESULTS: There were no statistically significant differences in HIE 2-3 (aOR 1.27; 95% CI 0.97-1.66), proportion of neonates meeting A-criteria for hypothermia treatment (aOR 0.96; 95% CI 0.89-1.04) or neonatal mortality (aOR 0.68; 95% CI 0.39-1.18) between the cohorts. Birth acidemia (aOR 1.36; 95% CI 1.25-1.48), 5-min Apgar scores <7 (aOR 1.27; 95% CI 1.18-1.36) and <4 (aOR 1.40; 95% CI 1.17-1.66) occurred more often in cohort II. The absolute risk difference for HIE 2-3 was 0.02% (95% CI 0.00-0.04). Operative delivery (vacuum or cesarean) rates were lower in cohort II (aOR 0.82; 95% CI 0.80-0.85 and aOR 0.94; 95% CI 0.91-0.97, respectively). CONCLUSIONS: Although not statistically significant, a small increase in the incidence of HIE 2-3 after implementation of the revised CTG classification cannot be excluded. Operative deliveries were fewer but incidences of acidemia and low Apgar scores were higher in the latter cohort. This warrants further in-depth analyses before a full re-evaluation of the revised classification can be made.

Studies on the role of calcium phosphate in the process of calcium oxalate crystal formation.

Crystals of calcium phosphate (CaP) added to solutions with a composition corresponding to that at different levels of the collecting duct (CD) and with different pH were rapidly dissolved at pH 5.0, 5.25 and 5.5. Only minor or no dissolution was observed at higher pH levels. Despite this effect, CaP crystals induced nucleation or heterogeneous crystallization of CaOx up to a pH of 6.1, whereas CaP was the type of crystalline material that precipitated at higher pH. Accordingly, small crystal volumes were recorded at pH 5.5 and great volumes at pH 6.7 4 h after the addition of CaP crystals to the solutions. Dialyzed urine appeared to counteract the dissolution of CaP and to reduce the rate of secondary crystallization. The CaP induced crystallization of CaOx was confirmed by a reduction of (14)C-labeled oxalate in solution. The AP(CaOx) required for a nucleation or heterogeneous crystallization of CaOx in the presence of CaP was around 1.5 x 10(-8) (mol/l)(2). For CaP crystal formation on CaP, an AP(CaP) ((a)Ca(2+) x (a)PO(4)(3-)) of approximately 50 x 10(-14) (mol/l)(2) appeared to be necessary. The CaOx crystals formed were microscopically found in association with the CaP crystalline material and were most frequently of CaOx dihydrate type. Step-wise crystallization experiments comprising supersaturation with CaP (Step A), supersaturation with CaOx (Step B) and subsequently acidification (Step C) showed that CaOx crystal formation occurred when CaP crystals were dissolved and thereby served as a source of calcium. The ensuing formation of CaOx crystals is most likely the result from high local levels of supersaturation with CaOx caused by the increased concentration of calcium. These experimental studies give support to the hypothesis that crystallization of CaOx at lower nephron levels or in caliceal urine might be induced by dissolution of CaP formed at nephron levels above the CD, and that a low pH is prerequisite for the precipitation of CaOx. The observations accordingly provide additional evidence for the important role of calcium phosphate in the crystallization of calcium oxalate, that might occur both at the surface of Randall's plaques and intratubularly at the papillary tip.