Is it time to end the use of base deficit for fetal well-being assessment?

Authors have expressed reservations regarding the use of base deficit on umbilical artery blood samples to assess fetal well-being during the course of labor and predict neonatal neurological morbidity. Despite its integration into clinical practice for over fifty years, obstetricians and maternal fetal medicine specialists may not realize that this marker has significant limitations in accurately assess identifying neonatal metabolic acidosis as a proxy of fetal well-being. In brief, there are two large family of base deficit: whole blood and extracellular fluid. Both rely on equations using normal adult acid-base characteristics (pH 7.40 and pCO2 40 mmHg) which overlook the specificity of the normal in-utero acid-base status with pH 7.27 and pCO2 54 mmHg. Additionally, it ignores the unique characteristic of in utero fetal response to acute hypoxia. Dependence on placental circulation for carbon dioxide (CO2) elimination may lead to extremely high values (up to 130 to 150 mmHg) during hypoxic events, a phenomenon absent in adults with acute metabolic acidosis who can hyperventilate. The dispute over whether to include the correction for high pCO2 on bicarbonate estimation, as presented in the "Great Trans-Atlantic Debates" (1), remains unresolved. The key constants computed for adult acid-base physiology in current base deficit algorithms, without accounting for the impact of high pCO2 or other fetal characteristics of buffering capacity (e.g., differences in body water content composition, plasma protein, and hemoglobin attributes), may lead to an overestimation of metabolic acidosis, especially in newborns experiencing hypercarbia during the early stages of hypoxic response. These unrecognized limitations impact the base deficit results and may mislead clinicians on fetal well-being assessment when discussing management of the fetal heart rate monitoring and neonatal outcomes. Based on our arguments, we believe it is prudent to consider an alternative to base deficit for drawing conclusions regarding fetal well-being during the course of birth management. We propose a marker specifically related to newborn acid-base physiology - the neonatal eucapnic pH correction. This marker can be added to arterial cord blood gas analysis, and we have described how to interpret it as a marker of neonatal metabolic acidosis.