Non-reassuring fetal status

Need for developing case definitions and guidelines for data collection, analysis, and presentation for non-reassuring fetal status as an adverse event following immunization:

Non-reassuring fetal status is a term used to describe suspected fetal hypoxia and is meant to replace the more ubiquitous term “fetal distress.” Fetal distress, defined as progressive fetal hypoxia and/or acidemia secondary to inadequate fetal oxygenation, is a term that is used to indicate changes in fetal heart patterns, reduced fetal movement, fetal growth restriction, and presence of meconium stained fluid [1]. Although fetal distress may be associated with neonatal encephalopathy, the generic term has poor predictive value for neonatal outcomes; most neonates will be vigorous and healthy at birth despite a diagnosis of fetal distress. Fetal distress can only be observed indirectly, usually via electronic fetal heart rate monitoring which is subject to high intra- and inter-observer variability in data interpretation [2], [3], [4]. For this reason, many experts recommend abandoning the term fetal distress, and adopting the term non-reassuring fetal status to describe clinical interpretation of fetal well-being [1], [5], [6]. Consistent with current opinion in the field, we recommend use of the term non-reassuring fetal status for use in monitoring fetal response following immunization.

Non-reassuring fetal status is not an adverse event per se, but rather an indicator of an underlying condition resulting in temporary or permanent oxygen deprivation to the fetus which may lead to fetal hypoxia and metabolic acidosis. Since fetal oxygenation is dependent upon maternal oxygenation and placental perfusion, perturbations of maternal oxygenation, uterine blood supply, placental transfer or fetal gas transport may lead to fetal hypoxia and non-reassuring fetal status [7]. Conditions commonly associated with non-reassuring fetal status include maternal cardiovascular disease, anemia, diabetes, hypertension, infection, placental abruption, abnormal presentation of the fetus, intrauterine growth restriction and umbilical cord compression, among other obstetric, maternal or fetal conditions.

The fetus experiences three stages of deterioration when oxygen levels are depleted: transient hypoxia without metabolic acidosis, tissue hypoxia with a risk of metabolic acidosis, and hypoxia with metabolic acidosis [7], [8]. Fetal response to oxygen deprivation is regulated by the autonomous nervous system, mediated by parasympathetic and sympathetic mechanisms. The fetus is equipped with compensatory mechanisms for transient hypoxia during labor, but prolonged, uninterrupted fetal hypoxia may lead progressively to acidosis with cell death, tissue damage, organ failure and potentially death. In response to hypoxia, fetal compensatory mechanisms include 1) a decrease in heart rate; 2) a reduction in oxygen consumption secondary to cessation of nonessential functions such as gross body movements; 3) a redistribution of cardiac output to preferentially perfuse organs, such as the heart, brain, and adrenal glands; and 4) a switch to anaerobic cellular metabolism [9]. Prolonged fetal hypoxia is associated with significant perinatal morbidity and mortality with particular concern for short- and long-term complications including encephalopathy, seizures, cerebral palsy, and neurodevelopmental delay [10], [11]. The fetal heart rate changes markedly in response to prolonged oxygen deprivation, making fetal heart rate monitoring a potentially valuable and commonly used tool for assessing fetal oxygenation status in real time. Non-reassuring fetal heart rate patterns are observed in approximately 15% of labors [12].

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