Objective: Our purpose was to test the hypothesis that placental histologic lesions reflect abnormal placental respiratory function in preterm gestations.
Study design: A retrospective study of preterm deliveries from 22 to 32 weeks revealed 431 patients with umbilical venous or arterial blood gas values. Excluded were stillbirth, multiple gestations, placenta previa, maternal medical diseases, and fetal anomalies. Charts were reviewed for principal indication of delivery, diagnosis of labor, and mode of delivery. Blood gases were studied within 10 minutes of delivery on a model 178 automatic pH analyzer (Corning Med, Boston). Placental data included uteroplacental vascular lesions and related villous lesions, lesions of acute inflammation, chronic inflammation, and coagulation. Contingency tables and analysis of variance considered p < 0.05 as significant.
Results: Mean +/- SD umbilical vein pH was 7.36 +/- 0.07 (range 6.94 to 7.56) and umbilical artery pH was 7.30 +/- 0.08 (range 6.83 to 7.55). Increasing severity of uteroplacental thrombosis, villous lesions reflective of uteroplacental vascular pathologic mechanisms, avascular villi, histologic evidence of abruptio placentae, chronic villitis, and increased circulating erythrocytes were associated with decrease in umbilical vein and artery pH, increase in umbilical vein and artery PCO2, and decrease in umbilical vein and artery PO2. Histologic evidence of acute infection and villous edema were associated with a higher pH and PO2 and a lower PCO2 in both umbilical vein and artery. Umbilical vein or artery base excess was not related to placental lesions. Labor was not related to blood gas values in this data set, although a subset of cases of extremely preterm premature rupture of membranes and preterm labor who labored and were delivered by cesarean section had significantly poorer umbilical venous and fetal arterial blood gas values (all p < 0.005). Lesions related to poorer blood gas values were significantly more frequent in preterm preeclampsia and nonhypertensive abruptio placentae than in premature rupture of membranes or preterm labor.
Conclusions: Changes in umbilical vein and artery pH, PO2, and PCO2 are significantly related to lesions of uteroplacental vascular pathologic mechanisms and intraplacental thrombosis. Placental lesions may be associated with chronic fetal distress by altering fetal oxygen availability and acid-base status. Placental immaturity resulting from prematurity may be associated with inefficient placental respiratory function and an increased likelihood of cesarean delivery in cases of premature rupture of membranes or preterm labor. Altered fetal acid-base balance plus excess numbers of circulating nucleated erythrocytes suggests that placental respiratory function is functionally abnormal when these lesions are present and leads to fetal tissue hypoxia.