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Fetal lactic acidosis with epidural anesthesia

  • Clarel Antoine
    Affiliations
    From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, New York University School of Medicine and Bellevue Hospital, New York, New York
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  • Bruce K. Young
    Correspondence
    Department of Obstetrics and Gynecology, 530 First Ave., Suite 5G, New York, New York 10016
    Affiliations
    From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, New York University School of Medicine and Bellevue Hospital, New York, New York
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      Three hundred thirty-six consecutive cesarean deliveries performed under epidural anesthesia were reviewed. Twenty per cent of mothers suffered at least a 20% fall in blood pressure following administration of epidural anesthesia. An additional 24% required ephedrine, a vasopressor with predominantly beta activity, when other corrective measures failed. Thus, 44% of these patients suffered significant hypotension. Forty-one percent of all elective repeat cesarean sections were treated with ephedrine because of maternal hypotension. Fifty-one patients delivered by scheduled repeat cesarean section were divided into ephedrine-treated and untreated groups. There were no differences in Apgar scores among infants of both groups. Fetal acidosis was proportional to the severity of hypotension and the ephedrine dose. The metabolic abnormalities were most pronounced when severe hypotension, requiring over 15 mg of ephedrine, was present. Following restoration of blood pressure with conventional measures and ephedrine therapy, lactic acidosis persisted until delivery, whereas Po2 and Pco2 reverted toward normal values. The hypoperfusion of the intervillous space was the most likely cause of the observed significant umbilical venous and arterial lactic acidosis. Maternal hypotension remains a significant problem complicating conduction anesthesia.
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