Association of Nonreassuring Fetal Heart Rate Patterns and Subsequent Cerebral Palsy in Pregnancies with Intrauterine Bacterial Infection

Abstract

We evaluated an association of nonreassuring fetal heart rate (FHR) patterns and subsequent cerebral palsy (CP) in pregnancies with intrauterine bacterial infection. Among 10,030 infants born during 1995 to 2000, 139 were complicated with acute intrauterine bacterial infection in labor. The FHR patterns 2 hours immediately before delivery were interpreted according to the guidelines of the National Institute of Child Health and Human Development. The correlations between the FHR patterns and umbilical blood gases, as well as FHR patterns and CP were studied. Statistics included unpaired t test, contingency table with chi (2) and Fisher test, and one-way analysis of variance with Bonferroni/Dunn test. Fifteen infants (11%) developed CP at 2 years or older. Nonreassuring FHR patterns including recurrent late deceleration, severe variable deceleration, and prolonged deceleration occurred in 24% of pregnancies with intrauterine infection. Incidence of CP was not different according to the FHR deceleration patterns or umbilical pH values. Multiple logistic regression analysis revealed that fetal tachycardia (OR, 11; 95% CI, 1.8 to 67) and lower gestational age (< 34 weeks; OR, 9.4; 95% CI, 0.96 to 93) was associated with CP in intrauterine infection. Nonreassuring FHR patterns were increased in intrauterine infection. CP occurred more frequently and was associated with tachycardia and lower gestational age, but not with FHR deceleration patterns or acidemia, suggesting different pathophysiology from acute hypoxia-ischemia.

Are we (mis)guided by current guidelines on intrapartum fetal heart rate monitoring? Case for a more physiological approach to interpretation

“…Current electronic FHR monitoring technology is not designed to detect FSIRS. In one study, tachycardic fetuses with infection had an increased risk of encephalopathy and cerebral palsy, but had no acidaemia or bradycardia, 54 suggesting that infection may exert neurological injury directly or via a non-hypoxia pathway. Further still, fetal inflammation and hypoxia appear to act synergistically to increase the risk of encephalopathy and cerebral palsy exponentially.…”

Histological Chorioamnionitis as a Risk Factor for Preterm Birth without Disturbing Fetal Heart Rate: A Case-Control Study

“…Third, all evaluation items of the FHR pattern were categorical variables. The absence or decrease of variability is thought to represent a state of fetal acidosis (Siira et al 2013), and we focused on decreased variability as reported in other studies (Salafia et al 1998;Sameshima et al 2005 induced by lipopolysaccharides (LPS) was associated with a transient increase in FHR variability and loss of FHR variability by repeated exposure to LPS (Lear et al 2014), so rigorous FHR evaluation including increased variability might be required in future studies focused on the evaluation of intrauterine infection. Furthermore, in certain cases, variability is not determined quantitatively but judged subjectively based on the recorded data, and, thus, quantitative analysis in observational study might be also required.…”

“…However, the present study did not show any association between histological CAM and abnormal FHR patterns indicative of a hypoxic state or acidemia. A previous study reported that FHR deceleration was not associated with intra-amniotic infection in patients who subsequently developed cerebral palsy (Sameshima et al 2005). An observational study also reported that intrauterine histological CAM is not associated with fetal acidosis (Holcroft et al 2004).…”

“…In this analysis, we referred to the previous study that examined the correlation between FHR patterns 2 hours before delivery and the presence of cerebral palsy during pregnancy with intrauterine bacterial infection (Sameshima et al 2005). The FHR patterns taken 1 to 2 hours before delivery were retrospectively evaluated by a single obstetric specialist certified by the Japan Society of Perinatal and Neonatal Medicine.…”

Asphyxie périnatale et infirmité motrice d’origine cérébrale (I- Le diagnostic)

“…Asphyxie foetale progressive au cours du travail selon le modèle dit de Hon avec des ralentissements tardifs, montrant l'association des ralentissements de type hypoxique (tardifs) à une tachycardie progressive et à une perte d'oscillations en cas d'acidose manifeste (tracé B au cours d'une grossesse prolongée avec un pH AO à 7,04), alors que le tracé A manifeste une hypoxie débutante (pH AO à 7,21). développer une atteinte de la substance blanche, même si la perte de variabilité et les décélérations restent des témoins de l'acidose métabolique, ce qui suggère un mécanisme physiopathologique différent d'une hypoxie-ischémie, d'autant plus que l'IMOC apparaît fréquemment associée au faible âge gestationnel et à la tachycardie témoignant d'infection intra-utérine [89][90][91].…”