Umbilical cord pH (UC-pH) level is an important objective indicator of intrapartum fetal hypoxia and is used to predict neonatal morbidity and mortality. A UC-pH value of less than 7.00 is often defined as a threshold for severe acidosis, but existing evidence is divergent and largely based on UC-pH measurements from selected populations; consequently, the results are challenging to interpret.

Umbilical cord blood acid–base sampling is routinely performed at many hospitals. Recent studies have questioned this practice and the association of acidosis with cerebral palsy.

脐动脉血气是评估胎儿氧合和酸碱代谢异常的重要指标，是诊断新生儿窒息的重要补充。建议高危孕产妇分娩后及产时可疑胎儿窘迫者常规行脐动脉血气分析，根据血气结果进行高危儿随访和治疗，可最大限度降低近期缺血缺氧性脑病和远期脑瘫等神经系统功能异常的发生率。

\n Objective The aim of this study is to determine the association between mild acidemia (umbilical artery [UA] pH: 7.11–7.19) and neonatal morbidity in neonates at term.

Neonatal hypoxic ischaemic encephalopathy (HIE) is the most common cause of encephalopathy in the neonatal period and carries a high risk of mortality and long‐term morbidity.

Although abruptio placentae causes hypoxia in the infant and thus leading to cerebral palsy (CP), its incidence and clinical features at a nationwide level have not been demonstrated.To determine the proportion of abruptio placentae among antenatal and intrapartum causative factors leading to cerebral palsy (CP) and clinical features of such abruptio placentae.A review was conducted in 107 infants with CP in whom CP was determined to be due to antenatal and or intrapartum hypoxic conditions by the Japan Council for Quality Health Care until April 2012.Abruptio placenta was responsible for 28 (26%) of the 107 CP infants, and was the single leading causative factor of CP. Of these 28 women, 22 (79%) exhibited non-reassuring fetal status on admission to obstetric facilities at 36.2 ± 2.6 weeks of gestation and had neonates with umbilical cord arterial blood pH (base excess) of 6.728 ± 0.164 (-25 ± 5.4 mmol/L). In these 22 women, strong abdominal pain and/or profuse vaginal bleeding occurred 159 ± 99 min prior to admission to an obstetric facility, and the interval until delivery after admission was 47 ± 31 min. Hypertension or isolated proteinuria preceded clinical events in one (4.5%) and five (23%) of these 22 women, respectively.Abruptio placentae was responsible for CP in one quarter of all cases determined to be due to antenatal and/or intrapartum hypoxic conditions in Japan. New strategies to shorten the interval until admission to an obstetric facility after onset of symptoms are urgently needed.Copyright © 2012 Elsevier Ltd. All rights reserved.

This study aimed to identify risk factors for the onset of cerebral palsy (CP) in neonates due to placental abruption and investigate their characteristics.

Placental abruption is a complete or partial separation of the placenta from the uterine decidua. Clinical manifestations include vaginal bleeding, abdominal pain, uterine contractions, and abnormalities in the fetal heart rate tracing. Placental abruption occurs in 0.4% to 1.0% of all pregnancies. However, the pathophysiology remains incompletely understood. We present a review of the pathophysiology, diagnosis, and management of placental abruption, exploring overlapping processes which contribute to premature placental separation. Classic findings and limitations of ultrasound in evaluating placental abruption are explained. Finally, we discuss the management of placental abruption based on gestational age, fetal status, and maternal hemodynamic stability.Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.

Our objective was to identify factors associated with hypoxic-ischemic encephalopathy (HIE) among newborns with an umbilical pH < 7.00.Case-control study during a four-year study period in a single academic tertiary-center, including all neonates ≥35 weeks with an umbilical pH < 7.00. Cases were neonates with HIE, regardless of Sarnat classification, and controls were neonates without signs of HIE. We used univariate and multivariate analysis to compare the maternal, obstetric, and neonatal characteristics of cases and controls.Among 21,211 births, 179 neonates≥35 weeks (0.84%) had an umbilical pH < 7.00. One hundred and forty-seven(82.1%) newborns had severe asphyxia without HIE, 32(17.9%) had HIE and 21(11.7%) needed therapeutic hypothermia. Neonates with HIE were significantly more likely to have 5-minute Apgar score<7(75% versus 15.7% P < 0.01), together with a lower mean umbilical arterial pH (6.84 versus 6.95, P < 0.01) and lower mean base deficits (-17.0 versus -12.7, P < 0.01). Factors significantly associated with HIE were the mother being overweight(28.1% for cases versus 14.3% for controls, adjusted OR=4.6[1.4-15.2]) or obese(25.0% versus 13.6%, aOR=15.5[1.1-12.5]), smoking(18.7% versus 5.4%, aOR=5.8[1.6-21.2]), a sentinel event as cord prolaps or placenta abruption (34.4% versus 13.6%, aOR=2.7[1.1-7.2]), and decreased fetal heart rate variability(68.7% versus 44.2%, aOR=2.8[1.1-6.9]).Among neonates with an umbilical cord pH < 7.00, those with HIE had a more severe metabolic acidosis. Maternal factors associated with HIE among newborns with an umbilical pH < 7.00, were being overweight or obese, and smoking, and the associated obstetric factors were a sentinel event and decreased fetal heart rate variability.Copyright © 2019 Elsevier B.V. All rights reserved.

Relative uteroplacental insufficiency of labor (RUPI‐L) is a clinical condition that refers to alterations in the fetal oxygen “demand–supply” equation caused by the onset of regular uterine activity. The term RUPI‐L indicates a condition of “relative” uteroplacental insufficiency which is relative to a specific stressful circumstance, such as the onset of regular uterine activity. RUPI‐L may be more prevalent in fetuses in which the ratio between the fetal oxygen supply and demand is already slightly reduced, such as in cases of subclinical placental insufficiency, post‐term pregnancies, gestational diabetes, and other similar conditions. Prior to the onset of regular uterine activity, fetuses with a RUPI‐L may present with normal features on the cardiotocography. However, with the onset of uterine contractions, these fetuses start to manifest abnormal fetal heart rate patterns which reflect the attempt to maintain adequate perfusion to essential central organs during episodes of transient reduction in oxygenation. If labor is allowed to continue without an appropriate intervention, progressively more frequent, and stronger uterine contractions may result in a rapid deterioration of the fetal oxygenation leading to hypoxia and acidosis. In this Commentary, we introduce the term relative uteroplacental insufficiency of labor and highlight the pathophysiology, as well as the common features observed in the fetal heart rate tracing and clinical implications.