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.

Fetuses with relative uteroplacental insufficiency of labor (RUPI‐L) show normal features on the cardiotocography antenatally. With the onset of uterine contractions, they develop abnormal fetal heart rate patterns, potentially progressing to fetal deterioration if immediate action is not undertaken.

Abbreviations

CTG

cardiotocography

RUPI‐L

relative uteroplacental insufficiency of labor

Key message.

Fetuses with relative uteroplacental insufficiency of labor (RUPI‐L) show normal features on the cardiotocography antenatally. With the onset of uterine contractions, they develop abnormal fetal heart rate patterns, potentially progressing to fetal deterioration if immediate action is not undertaken.

1. INTRODUCTION

Placental insufficiency, or uteroplacental insufficiency, refers to the failure of the placenta to meet the fetus requirement for oxygen and nutrients during pregnancy. ¹ The resulting fetal hypoxia leads to impaired fetal growth, which in turn, represents a major risk factor for stillbirth and poor perinatal outcomes. ¹ , ² Traditionally, fetal “smallness” has been considered as a proxy for this condition and the leading cause of adverse perinatal outcomes due to antepartum or intrapartum hypoxia. ³ , ⁴ , ⁵ , ⁶ However, most of the adverse perinatal events secondary to hypoxic–ischemic events at or near term occur in normal‐sized fetuses, who are a priori considered to be at low risk of hypoxia. ⁷ , ⁸ Towards the end of the pregnancy, the fetal oxygen demands increase exponentially, while fetal nutritional demands begin to plateau. ⁹ Consequently, appropriately grown fetuses, may be exposed to a diminished placental function long before any noticeable impact on fetal growth occurs (i.e., subclinical placental insufficiency). ¹⁰ , ¹¹ , ¹² , ¹³ , ¹⁴ , ¹⁵ , ¹⁶

The onset of regular uterine activity may pose an additional challenge to the well‐being of these fetuses affected by subclinical placental insufficiency because uterine contractions cause intermittent reductions of the perfusion of the uteroplacental bed. ¹⁷ , ¹⁸ Such mechanical stress on both maternal and fetal side of the placenta is known to occur in all laboring women and causes raised intraplacental impedance to the blood flow as evidenced by abnormal Doppler findings. ¹⁹ Extrapolation of this research evidence would suggest that among fetuses that commence labor with subclinical placental insufficiency, regular uterine contractions may further diminish the oxygen supply to the fetus below the critical threshold leading to an increased risk of hypoxic perinatal events.

“Relative uteroplacental insufficiency of labor (RUPI‐L)” is a clinical condition where alterations in the fetal oxygen “demand–supply” equation becomes noticeable at the onset of regular uterine activity. Importantly, current external tocometry systems do not offer an accurate and reproducible method for measuring the intensity and duration of the uterine contractions, but only provide a somewhat reliable assessment of their frequency. Consequently, we are unable to establish a predetermined threshold of uterine activity that specifically triggers a RUPI‐L. The term RUPI‐L does not indicate an “absolute” uteroplacental insufficiency which presents before labor mostly with fetal growth restriction, but rather a condition of “relative” uteroplacental insufficiency which is relative, in response to a specific stressful circumstance, such as the onset of regular uterine activity. RUPI‐L may be more prevalent in fetuses where 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 conditions.

Prior to the onset of regular uterine activity (antepartum)—when uteroplacental oxygenation is not intermittently interrupted—fetuses affected by this condition exhibit a normal cardiotocography (CTG) tracing. 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. In other words, the intermittent reduction in oxygen supply to the fetus occurring during contractions can unveil a condition of relatively inadequate placental function that may have gone unnoticed until the onset of regular uterine activity. This condition, referred to as RUPI‐L, is characterized by distinctive CTG patterns which should be recognized by clinicians to ensure a timely intervention and reduce the risk of intrapartum fetal injury. We propose herein to revise the physiological CTG classification and introduce a new type of hypoxia observed in fetuses with RUPI‐L which cannot be classified as antepartum or intrapartum hypoxia but rather as hypoxia at the onset of regular uterine activity. ²⁰

2. UNDERLYING PATHOPHYSIOLOGICAL MECHANISMS THAT MAY CONTRIBUTE TO RELATIVE UTEROPLACENTAL INSUFFICIENCY OF LABOR (RUPI‐L).

Over the years, animal experiments have studied the pathophysiology of abnormal Doppler flow patterns in chronic hypoxia. An experimental model using fetal sheep found that the progressive obliteration of placental vessels with plastic microspheres (embolization) from the fetal side induces alterations in the Doppler waveforms of the umbilical artery. Interestingly, according to these findings, it could be estimated that approximately more than 50% of the placental mass should be damaged before abnormal diastolic blood flow can be detected in the umbilical artery. ²¹ Gargon et al. induced a hypoxemic environment in sheep fetuses by performing daily fetal placental embolization. ²² This led to progressive fetal hypoxemia and a reduction in the umbilical vein flow with changes in umbilical artery Doppler flow velocity. Abnormal umbilical artery Doppler waveforms were followed by CTG changes, in this case, by an increase in the CTG baseline. Finally, Galan et al. induced placental insufficiency in an ovine model using a hyperthermic environment. The authors showed that placental insufficiency resulted in reduced fetal weight, increased blood pressure, and resistance of the umbilical arteries, and reduced umbilical vein flow. ²³ These experimental animal models indicate that a significant area of the placenta should be damaged prior to the onset of abnormal Doppler waveforms in the umbilical artery and that the latter precedes hypoxic changes in CTG tracing. ²² , ²⁴ , ²⁵

Research evidence from human studies suggests that extensive damage of the placental vascular bed may be caused by diverse placental lesions, including chorionic villous fibrosis, uteroplacental thrombosis, atherosis, placental infarcts, peri‐villous fibrin deposits, or a reduction in number and surface area of the villous capillary tree. ²⁶ , ²⁷ A vast anatomic disruption of the capillary tree is known to cause utero‐placental insufficiency which is responsible for fetal chronic hypoxia and fetal growth restriction ²⁶ , ²⁷ ; growth‐restricted fetuses often have multiple placental abnormalities, including also hemorrhagic vasculitis and infarction. ²⁸ Additionally, some environmental or metabolic factors are known to exert a detrimental effect on placental function even in the absence of overt disruption of the chorionic plate, such as low‐grade inflammation from inappropriately sugar and fat‐rich diet, obesity or pollution, apoptosis, and villi crowding. ²⁹ , ³⁰ , ³¹ , ³² , ³³

Several studies have highlighted the features of chronic hypoxia on the CTG if placental insufficiency continues to progress leading to the onset of metabolic acidosis and depression of the fetal brain. ³⁴ , ³⁵ , ³⁶ , ³⁷ Features of chronic hypoxia on the CTG, as described below, are mostly encountered in growth‐restricted fetuses and represent the “end stage” of a progressive uteroplacental insufficiency. ²⁸ , ³⁸ , ³⁹ , ⁴⁰ , ⁴¹ However, in some circumstances fetuses experience during pregnancy a placental damage which is not as extensive (>50%); to cause a high grade or long duration of chronic hypoxia before birth. These fetuses do not demonstrate overt clinical manifestations of placental insufficiency—such as fetal smallness, abnormal Doppler or antepartum CTG abnormalities—until the occurrence of a super‐imposed stress (eg uterine activity) that induces an intermittent reduction in the blood supply to the placenta. ⁷ This subclinical condition is better defined as a “relative utero‐placental insufficiency of labor” (RUPI‐L) rather than a proper “absolute” placental insufficiency.

Fetus with a relatively mild alteration in their oxygen “demand–supply” equation, may not show any abnormal changes in the CTG at rest. However, with the onset of regular uterine activity, which transiently reduce uteroplacental oxygenation due to the compression of spiral uterine arteries and/ or compression of the umbilical cord, ¹⁸ the available oxygen may not be sufficient to meet the fetal metabolic and respiratory requirements. The deprivation of oxygen will become critical, as uterine contractions intensify in strength and frequency, and inevitably result in cardiovascular changes to ensure aerobic metabolism within the fetal “high‐priority” central organs. ² , ³⁹ This is similar to an adult with mild coronary artery stenosis not showing any clinical signs—that is, breathlessness or tachycardia—at rest, but rapidly becoming symptomatic when undertaking a physical exercise. ⁴² Subsequently, fetuses affected by RUPI‐L start to manifest abnormal CTG patterns of hypoxia as soon as uterine contractions become sufficiently strong to cause intermittent obstructions of uteroplacental circulation.

3. DIFFERENT TYPES OF FETAL HEART RATE CHANGES IN RESPONSE TO DIFFERENT TYPES OF HYPOXIC STRESS

In the recently introduced physiological CTG classification of intrapartum monitoring, the authors recommended to differentiate the features of antepartum or chronic hypoxia from the features of primarily intrapartum hypoxia. ⁴³ , ⁴⁴ In the former group, abnormal CTG findings, such as reduced/absent variability and cycling with or without increased CTG baseline and shallow decelerations, are expected to appear on the CTG before onset of regular uterine activity; and are related to a hypoxic antepartum injury or an autonomic dysfunction of the fetal brain. ³⁴ In the latter group, abnormal CTG findings are related to an ongoing hypoxic stress which occurs primarily during active labor (i.e., repetitive compression of the umbilical cord and/or intermittent disruption in uteroplacental oxygenation) ⁴⁵ in fetuses who commence labor with adequate placental reserves. Based on the duration, frequency, and intensity of the hypoxic stress, intrapartum hypoxia may be further classified as acute, subacute, or slowly evolving; all of which elicit a different fetal response and present with specific CTG patterns (Table 1). ⁴⁶ , ⁴⁷ Both types of fetal hypoxia (antepartum and intrapartum) do not apply to fetuses with RUPI‐L, whose abnormal CTG findings appear neither before labor nor during advanced labor, but rather at the onset of regular uterine activity.

TABLE 1.

Physiological cardiotocography classification based on International Expert Consensus Guidelines on Physiological Interpretation of Cardiotocography (CTG).

Hypoxia	Features	Management
No Hypoxia	Baseline appropriate for gestational age Normal variability and cycling No repetitive decelerations	Consider whether the CTG needs to continue. If continuing the CTG, perform routine hourly review. (see CTG Assessment Tool below)
Evidence of Hypoxia
Chronic Hypoxia	Higher baseline than expected for gestational age Reduced variability and/ or absence of cycling Absence of accelerations Shallow decelerations Consider the clinical indicators: reduced fetal movements, thick meconium, bleeding, evidence of chorioamnionitis, postmaturity fetal growth restriction	Avoid further stress Expedite delivery, if delivery is not imminent
Gradually Evolving Hypoxia	Compensated	Likely to respond to conservative interventions (see below) Regular review every 30–60 min to assess for signs of further hypoxic change, and that the intervention resulted in improvement. Other causes such as reduced placental reserve MUST be considered and addressed accordingly.
	Rise in the baseline (with normal variability and stable baseline) preceded by decelerations and loss of accelerations
	Decompensated	Needs urgent intervention to reverse the hypoxic insult (remove prostaglandin pessary, stop oxytocin infusion, tocolysis) Delivery should be expedited, if no signs of improvement are seen
	Reduced or increased variability Unstable/ progressive decline in the baseline (step ladder pattern to death)
Subacute Hypoxia	More time spent during decelerations than at the baseline May be associated with saltatory pattern (increased variability)	First Stage
		Remove prostaglandins/stop oxytocin infusion If no improvement, needs urgent tocolysis If still no evidence of improvement within 10–15 min, review situation and expedite Delivery
		Second Stage
		Stop maternal active pushing during contractions until improvement is noted. If no improvement in noted, consider tocolysis if delivery is not imminent or expedite delivery by operative vaginal delivery
Acute Hypoxia	Prolonged deceleration (>3 min)	Preceded by reduced variability and lack of cycling or reduced variability within the first 3 min
		Immediate delivery by the safest and quickest route
		Preceded by normal variability and cycling and normal variability during the first 3 min of the deceleration (see 3‐min rule above)
		Exclude the 3 accidents (i.e. cord prolapse, placental abruption, uterine rupture ‐ if an accident is suspected prepare for immediate delivery) Correct reversible causes If no improvement by 9 min or any of the accidents diagnosed, immediate delivery by the safest and quickest route
Unable to ascertain fetal wellbeing (Poor signal quality, uncertain baseline, possible recording of the maternal heart rate)		Escalate to senior team Consider Adjunctive Techniques, if appropriate Consider the application of fetal scalp electrode to improve signal quality

Using an example from a non‐medical context, the journey of human labor can be compared to an adult running a 100 m race (Figure 1). In this comparison, a fetus with RUPI‐L would be the runner who is unable to cope with the physical exercise, needing to stop shortly after starting; the fetus with antepartum hypoxia (pre‐existing injury) would be the runner that is not fit enough to start running; and the fetus with intrapartum hypoxia would be the runner that undergoes progressive or sudden decompensation later into the race due to his inability to sustain a prolonged effort.

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.

Caldeyro‐Barcia et al. reported the effects of both normal and abnormal uterine contractions that occur during labor in human fetuses. ¹⁸ , ⁴⁸ , ⁴⁹ Most fetuses without pre‐existing uteroplacental insufficiency are likely to tolerate the transient interruption in oxygenation caused by each uterine contraction without displaying alterations in the CTG. In contrast, fetuses with RUPI‐L may struggle to maintain the required cardiac output and central organ perfusion once regular uterine activity commences and are more likely to exhibit alterations in the CTG during episodes of transient reduction in oxygenation.

4. CTG FEATURES OF RELATIVE PLACENTAL INSUFFICIENCY OF LABOR (RUPI‐L)

In fetuses affected by RUPI‐L, alterations in the CTG manifest simultaneously at the onset of regular uterine activity, regardless of whether labor commenced spontaneously or was induced. However, due to the increased intensity and duration of uterine contractions following induction of labor with prostaglandins or oxytocin, CTG alterations indicative of RUPI‐L may be observed earlier and may be more remarkable with induced rather than spontaneous contractions. These alterations reflect a decrease in fetal oxygenation as uterine contractions reach a certain level of intensity leading to a reduction in utero‐placental oxygenation.

The fetal heart rate patterns frequently observed on the CTG in fetuses with RUPI‐L are described below and summarized in Table 2:

• Wide and deep decelerations as soon as regular uterine activity—either spontaneous or secondary to the use of oxytocin or administration of prostaglandins—begins. (Figures 2, 3, 4).

• Decelerations lasting longer than 60 s, or with a drop of the fetal heart rate of more than 60 bpm, or with a nadir lower than 60 bpm (Figures 2, 3, 4).

• The decelerations disappear or reduce their width and depth as uterine contractions decrease in intensity and frequency (Figures 2, 3, 4).

• Fetal heart rate baseline between fetal decelerations commonly on the upper limit of the normal range. This occurs as a result of the catecholamines release and aims to increase the perfusion to the peripheral tissue when oxygen supply is restored in the pause between uterine contractions (Figures 2, 3, 4).

• An increase in the fetal heart rate baseline in the absence of repetitive decelerations, (Figure 5) as a result of the chronic release of adrenal‐derived catecholamines in fetuses with a long‐standing exposure to subclinical hypoxia. ⁵⁰ , ⁵¹

TABLE 2.

Common cardiotocographic features associated with relative uteroplacental insufficiency of labor.

Feature	Likely underlying mechanism
Onset of wide and deep decelerations as soon as regular uterine activity begins	Relative reduction in the utero‐placental reserve, which compels the fetus to reduce myocardial workload in response to a sudden and transient cessation of oxygenation
Decelerations lasting longer than 60 s, or with a drop of the fetal heart rate of more than 60 bpm, or with a nadir lower than 60 bpm
The decelerations disappear or reduce their width and depth as uterine contractions decrease in intensity and frequency
Fetal heart rate baseline between fetal decelerations commonly on the upper limit of the normal range	This occurs as a result of the catecholamines release and aims to increase the perfusion to the peripheral tissue when oxygen supply is restored in the pause between uterine contractions
An increase in the fetal heart rate baseline in the absence of repetitive decelerations	Chronic release of adrenal‐derived catecholamines in fetuses with a long‐standing exposure to subclinical hypoxia

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.

5. RECOGNITION OF RELATIVE PLACENTAL INSUFFICIENCY OF LABOR (RUPI‐L): CLINICAL APPLICATION

The latest Cochrane Systematic Review on electronic fetal heart rate monitoring concluded that the use of continuous CTG for fetal assessment using “normal, suspicious, pathological” or “category I. II & III” classification systems have not resulted in a reduction in the incidence of cerebral palsy or perinatal deaths, but has led to an increase in the rate of cesarean sections and operative vaginal births. ⁵² This is accompanied by a recent meta‐analysis evaluating the three‐tiered system of the American College of Obstetrics and Gynecology for fetal heart rate monitoring to predict adverse neonatal acidosis. The authors found that there was no difference in the incidence of hypoxic–ischemic encephalopathy between categories I and II; but most importantly, that almost 98% of fetuses with category II tracings did not present acidosis at birth. ⁵³ Consequently, the role of the traditional practice of CTG has been questioned. ⁵⁴

Recent studies using the international consensus guideline on physiological CTG interpretation—which was produced by 44 experts from 14 countries ⁴⁴ —have not only shown a correlation between the types of fetal hypoxia with umbilical cord gases at birth, ⁵⁵ , ⁵⁶ but also with the pattern of brain injury on the neonatal magnetic resonance imaging scans. ⁵⁷ , ⁵⁸ Additionally, this newly introduced CTG interpretation system seems to have a better predictive capacity to predict neonatal acidemia compared to other classification systems. ⁵⁹ Emerging scientific evidence indicates a reduction of more than 50% in the incidence of hypoxic–ischemic encephalopathy ⁴⁶ , ⁶⁰ , ⁶¹ and other adverse pregnancy outcomes ⁶² after implementation of the physiological CTG interpretation.

Recognizing CTG features of RUPI‐L when active labor starts or uterine activity increases in terms of strength or frequency is important for optimizing perinatal outcomes. Allowing labor to continue without intervention may result in a rapid progress from compensation to decompensation, leading to fetal hypoxia and acidosis.

The optimal management of RUPI‐L has not yet been clearly defined, as this condition is being introduced for the first time in this Commentary. Although our management recommendations have not undergone testing in a controlled interventional study, they are supported by the current knowledge on fetal physiology during labor and the collective clinical experience of the authors. In cases of RUPI‐L, the fetus demonstrates unexpectedly an inability to cope with labor when regular uterine activity starts. Based on our preliminary experience and the discussed pathophysiology of this condition, continuous exposure to regular uterine contractions may swiftly lead to fetal deterioration, resulting in fetal acidosis.

The use of intrauterine resuscitation (eg tocolysis) and discontinuation of oxytocin/prostaglandins may temporarily abolish the hypoxic stress caused by uterine contractions, allowing the fetus to rectify the imbalanced “demand–supply” equation and ensure sufficient utero‐placental oxygenation during labor. However, these measures may be insufficient to guarantee a safe vaginal delivery, given that these fetuses are in the early or even latent stages of labor. Considering that the frequency, duration, and strength of uterine contractions progressively increase as the labor advances, these fetuses with evidence of RUPI‐L may not be able mount and maintain their effective compensatory responses as labor progresses. Therefore, in the presence of RUPI‐L, it is key to avoid any superimposed hypoxic stress (i.e., augmentation of uterine activity) and to evaluate the speed of spontaneous labor progression. Moreover, we advocate for expediting delivery and considering cesarean section as a reasonable option to prevent rapid deterioration of fetal oxygenation which may result in an irreversible fetal brain damage. The only exception, in the opinion of the authors, may be cases with an apparent fast and spontaneous labor progression (i.e., parous women) without any signs of fetal deterioration on the CTG trace. In these rare circumstances, continuation of labor may be safely allowed under strict surveillance, and the option of vaginal delivery may be pursued without increasing the risk of intrapartum hypoxic injury.

6. CONCLUSION

In this Commentary, we have described a new clinical entity defined as RUPI‐L, which includes fetuses with normal CTG findings antepartum, who rapidly develop CTG alterations as soon as regular uterine activity commence. However, this newly described clinical entity cannot be classified among the spectrum of antepartum nor intrapartum hypoxia in the current physiological CTG classification. Therefore, it would be appropriate to include a new subgroup—that is, relative uteroplacental insufficiency of labor (RUPI‐L)—in the physiological CTG interpretation system ²⁰ for those fetuses who demonstrate features of RUPI‐L at the onset of regular uterine activity. Recognition of the features of RUPI‐L on the CTG may help make frontline clinicians to take appropriate management decisions based on the overall clinical context, and ensure timely interventions to avoid hypoxic–ischemic injuries as a result of the rapid deterioration of fetal oxygenation as labor continues.

Future studies should address whether the description of this new subset of fetal hypoxia and a wider awareness of its features among clinicians might translate into improved perinatal outcomes.

AUTHOR CONTRIBUTIONS

Stefania Fieni, Ruben Ramirez Zegarra, Susana Pereira and Andrea Dall'Asta were responsible for drafting the paper and conducting literature research. Tullio Ghi and Edwin Chandraharan contributed to the conceptualization, drafting the paper, and final review.

CONFLICT OF INTEREST STATEMENT

The authors report no conflict of interest.

Ghi T, Fieni S, Ramirez Zegarra R, Pereira S, Dall’Asta A, Chandraharan E. Relative uteroplacental insufficiency of labor. Acta Obstet Gynecol Scand. 2024;103:1910‐1918. doi: 10.1111/aogs.14937