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ENDOTOXEMIA CAUSING FETAL BRADYCARDIA DURING UROSEPSIS

Buhimschi, Catalin MD; Weiner, Carl P. MD

CASE REPORTS
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Background Fetal bradycardia is a recognized response to maternal hypothermia associated with hypoglycemia, tocolysis with magnesium sulfate, or urosepsis, and it is thought to be a direct response to the decrease in the maternal core temperature.

Case A 25-year-old white woman, gravida 1, para 0, at 31 1/7 weeks' gestation was admitted with a diagnosis of pyelonephritis. The baseline fetal heart rate was 120 beats per minute with accelerations. Within 3 hours of admission, the patient became hypothermic (35.1C) and, concomitantly, the fetal heart rate baseline declined to 90 beats per minute with marked variability. Despite sustained maternal hypothermia, the fetal heart rate baseline rose to 120 beats per minute. It was another 6 hours before the patient's temperature rose above 38.5C. Her urine and blood cultures were positive for Serratia rubidacea infection. The patient delivered a healthy infant at 39 weeks' 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.

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.

Department of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland.

Address reprint requests to: Catalin Buhimschi, MD, Department of Obstetrics, Gynecology & Reproductive Sciences, University of Maryland School of Medicine, 655 W. Baltimore Street, Baltimore, MD 21201. E-mail: cbuhi001@umaryland.edu

Received September 25, 2000. Received in revised form October 26, 2000. Accepted December 12, 2000.

© 2001 The American College of Obstetricians and Gynecologists