Predictors of umbilical artery acidosis in preterm delivery.
OBJECTIVE
The purpose of this study was to investigate the significance of preterm acidosis and its risk factors.


METHODS
From a cohort of 786 consecutive singleton neonates who were born after spontaneous or iatrogenic preterm delivery at 24.0-33.6 weeks of gestation from January 1993 to December 2005 with an evaluation of umbilical artery pH at delivery, we extracted demographic, obstetric, neonatal, and placental histologic variables and related them to umbilical artery evidence of fetal acidemia, which was defined as pH <7.10. Excluded were stillbirths and neonates with major congenital anomalies. Fetal distress was defined as nonreassuring fetal hearth rate tracing or biophysical profile or appearance of thick meconium at delivery. Statistical analysis included 1-way analysis of variance and logistic regression with a probability value of <.05 considered significant.


RESULTS
Neonates with umbilical cord evidence of acidosis (n = 34) were born more frequently after abruption (P < .001), fetal distress (P < .001), and by cesarean delivery (P < .04) and were born less frequently after a complete course of corticosteroids (P = .03) and labor (P = .05) than nonacidotic babies (n = 752). Acute inflammatory lesions at placental histologic evaluation were less frequent (P = .049), and placental vascular lesions were more common in acidotic than in nonacidotic preterm neonates (P = .039). Logistic regression analysis demonstrated that cord acidosis was associated independently with the occurrence of abruptio placentae (odds ratio, 7.3; 95% CI, 2.9, 18.8), fetal distress (odds ratio, 12.0; 95% CI, 4.9, 18.3), and vascular placental lesions (odds ratio, 2.8; 95% CI, 1.2, 6.8)


CONCLUSIONS
In preterm infants, umbilical artery acidosis is significantly more common in the presence of placental abruption, fetal distress, and histologic evidence of placental vascular disease.
Andreani
Marianna
M
Department of Obstetrics and Gynecology, San Gerardo Hospital, University of Milano-Bicocca, Monza, Italy. marianna.andreani@gmail.com
Locatelli
Anna
A
Assi
Francesca
F
Consonni
Sara
S
Malguzzi
Silvia
S
Paterlini
Giuseppe
G
Ghidini
Alessandro
A
D000037:Abruptio Placentae / Q000378:metabolism; D000138:Acidosis / Q000175:diagnosis*; D000328:Adult; D001784:Blood Gas Analysis; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D005316:Fetal Distress / Q000150:complications / Q000378:metabolism; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000097:blood / Q000378:metabolism*; D010920:Placenta / Q000098:blood supply; D010922:Placenta Diseases / Q000378:metabolism*; D011247:Pregnancy; D047928:Premature Birth / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D012307:Risk Factors; D014469:Umbilical Arteries