Endotoxemia causing fetal bradycardia during urosepsis.

Abstract

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. 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. 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.