Fetal acidosis in prolonged pregnancy cannot be attributed to cord compression alone.

ABSTRACT

Fetal heart rate abnormalities associated with prolonged pregnancy have been attributed to umbilical cord vulnerability rather than placental insufficiency. Although intrapartum fetal heart rate patterns indicative of umbilical cord compression are common beyond 41 weeks' gestation, fetal intolerance to labor develops only in a subset of such patients. To test the hypothesis that suboptimal placental function contributes to reduced amniotic fluid volume and, ultimately, to fetal intolerance to labor, we prospectively collected biochemical and clinical data on 112 prolonged pregnancies. Data analysis was blinded to outcome and included cord blood acid-base measurements and intrapartum fetal heart rate interpretation. We observed a high incidence of umbilical cord compression (46.4%), but this finding was not predictive of emergent delivery in 32 of 52 cases (61.5%). Fetal acidosis (arterial pH less than 7.20) occurred more often in patients with cord compression, but the anticipated increase in carbon dioxide tension was not observed. Instead, a primary metabolic or combined acidosis was encountered in those fetuses delivered emergently. The additional findings of lower amniotic fluid volume and diminished birth weight in those patients delivered for fetal intolerance to labor suggest a direct role for suboptimal placental function in selected patients with prolonged pregnancy.