Relative uteroplacental insufficiency of labor

Abstract

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.

Keywords: active labor; baseline fetal heart rate; cardiotocography; catecholamine response; decelerations; fetal growth restriction; fetal heart rate variability; fetal heart trace tracing; fetal hypoxia; hypoxic stress.; labor; neonatal acidosis; placental insufficiency; uterine contractions.

FIGURE 1

The journey of human labor compared to a 100 m race. This schematic representation describes the different types of fetal hypoxia that may occur before or during labor. RUPI‐L, relative uteroplacental insufficiency of labor.

FIGURE 2

Cardiotocographic trace of a fetus at term that underwent induction of labor with prostaglandins due to prolonged pre‐labor rupture of the membranes. The cardiotocography was initiated when the patient reported regular uterine activity. Vaginal examination reported a cervical dilation less than 2 cm. Note the presence of wide and deep decelerations that immediately stop after the administration of terbutaline (black arrow). The fetal heart rate baseline does not progress further than the upper limit of the normal range (160–170 bpm) due to the chronic release of adrenal‐derived catecholamines in fetuses exposed to subclinical hypoxia. Paper speed at 1 cm/min.

FIGURE 3

Cardiotocography of a term fetus following induction of labor at 41 weeks of gestation. Note the appearance of repetitive decelerations following augmentation of the uterine contractile activity with oxytocin. Vaginal examination revealed a closed cervix. Upon discontinuation of oxytocin (black arrow), a reduction in contractile activity and disappearance of decelerations can be observed. The baseline fetal heart rate between decelerations is increased due to the chronic release of adrenal‐derived catecholamines in fetuses exposed to subclinical hypoxia. Paper speed at 1 cm/min.

FIGURE 4

Cardiotocography of a fetus following induction of labor due to fetal macrosomia at 39 weeks of gestation. Note the abrupt increase in the fetal heart rate baseline, variability—that is, “Zig‐Zag pattern” (black circle)—and decelerations lasting more than 60 s and deeper than 60 bpm which disappeared as soon as uterine contractions were abolished by tocolysis (black arrow). Vaginal examination revealed an unfavorable Bishop score. Paper speed at 1 cm/min.

FIGURE 5

Cardiotocography of a fetus at 41 weeks of gestation with features of relative uteroplacental insufficiency of labor. The patient underwent induction of labor due to post‐term pregnancies with prostaglandins. Shortly after the onset of regular uterine activity, the cardiotocography showed a progressive increase in the fetal heart rate baseline (around 150–160 bpm) without any significant preceding repetitive decelerations. Paper speed at 1 cm/min.