Endotoxemia causing fetal bradycardia during urosepsis

Background: Fetal bradycardia is a recognized response to maternal hypother mia associated with hypoglycemia, tocolysis with magnesium sulfate, or uros epsis, and it is thought to be a direct response to the decrease in the mat ernal core temperature. Case: A 25-year-old white woman, gravida 1, para 0, at 31 1/7 weeks' gestat ion was admitted with a diagnosis of pyelonephritis. The baseline fetal hea rt rate was 120 beats per minute with accelerations. Within 3 hours of admi ssion, the patient became hypothermic (35.1C) and, concomitantly, the fetal heart rate baseline declined to 90 beats per minute with marked variabilit y. Despite sustained maternal hypothermia, the fetal heart rate baseline ro se to 120 beats per minute. It was another 6 hours before the patient's tem perature rose above 38.5C. Her urine and blood cultures were positive for S erratia rubidacea infection. The patient delivered a healthy infant at 39 w eeks' gestation. Conclusion: Fetal bradycardia in the presence of urosepsis might be due to the release of endotoxin from gram-negative bacteria, triggering production of cardiotoxic cytokines, rather than to maternal hypothermia alone. (C) 2 001 by The American College of Obstetricians and Gynecologists.