Evaluation of severe growth retardation using cordocentesis--hematologic and metabolic alterations by etiology

Hematologic and respiratory blood gas parameters were studied in 21 fetuses with severe or early-onset (at or before 34 weeks) growth retardation and in 44 age-matched control fetuses. Diagnostic categories included uteroplacental insufficiency (N = 7) and uteroplacental insufficiency with associated fetal structural abnormality (N = 7), aneuploidy (N = 5), and congenital infection (N = 2). The mean (+/- 1 SEM) gestational age was 29.3 +/- 1 week. Compared with the control group matched for gestational age, the growth-retarded fetuses had higher hematocrits regardless of etiology. The platelet count was reduced in growth-retarded fetuses with aneuploidy (P less than .05). Leukopenia was observed in a fetus with congenital infection and in the group of fetuses with uteroplacental insufficiency unassociated with a structural abnormality (P less than .05). Leukocytosis was seen in growth-retarded aneuploid fetuses (P less than .01). The pH, pO2, and percent oxygen saturation were each lower in growth-retarded fetuses with either uteroplacental insufficiency or aneuploidy, and the pCO2 and bicarbonate were higher compared with controls (each P less than or equal to .05). Appropriately grown aneuploid fetuses had normal hematologic and respiratory blood gas measurements but were significantly more likely not to be trisomic (P = .04). Fetuses with uteroplacental insufficiency unassociated with a structural anomaly had significantly higher umbilical artery systolic/diastolic ratios than both the control group (P = .0002) and the group with uteroplacental insufficiency and a structural anomaly (P less than .008). This investigation confirms previous studies of fetuses suffering uteroplacental insufficiency and extends the observations to other etiologies.(ABSTRACT TRUNCATED AT 250 WORDS)