Background: Intrahepatic cholestasis of pregnancy is a reversible cholestasis typically beginning in the second or third trimester and associated with increased rates of stillbirth, preterm birth, fetal asphyxia, and neonatal care unit admission. The etiology of adverse outcomes in gestational cholestasis seems related to maternal bile acids levels, but recommendations for management, particularly regarding fetal surveillance and timing of delivery, have been limited due to the paucity of data and the low-quality of the evidence. Case: A patient with severe gestational cholestasis (bile acids level >100 µmol/L) was hospitalized at 32.3 weeks of gestation for close fetal surveillance inclusive of non-stress test three times daily, and maternal treatment. At 34.1 weeks, fetal bradycardia lasting 7 minutes was noted at fetal heart rate monitoring. At emergency cesarean delivery a liveborn appropriately grown infant was found, with Apgar scores of 5, 7 and 8 at 1, 5 and 10 minutes, respectively, and umbilical artery acidemia (pH of 7.19, base excess of -5.4 mMol/L). The child did eventually well. Conclusion: Severe maternal cholestasis can cause acute fetal acidemia; close inpatient surveillance or delivery could be necessary in such cases to prevent stillbirth.
Amatucci, N., Pintucci, A., Consonni, S., Locatelli, A., Ghidini, A. (2024). Sudden Fetal Deterioration in Severe Intrahepatic Cholestasis of Pregnancy. JOURNAL OF CLINICAL AND MEDICAL IMAGES AND SHORT REPORTS, 7, 1-4.
Sudden Fetal Deterioration in Severe Intrahepatic Cholestasis of Pregnancy
Amatucci, N;Locatelli, A;
2024
Abstract
Background: Intrahepatic cholestasis of pregnancy is a reversible cholestasis typically beginning in the second or third trimester and associated with increased rates of stillbirth, preterm birth, fetal asphyxia, and neonatal care unit admission. The etiology of adverse outcomes in gestational cholestasis seems related to maternal bile acids levels, but recommendations for management, particularly regarding fetal surveillance and timing of delivery, have been limited due to the paucity of data and the low-quality of the evidence. Case: A patient with severe gestational cholestasis (bile acids level >100 µmol/L) was hospitalized at 32.3 weeks of gestation for close fetal surveillance inclusive of non-stress test three times daily, and maternal treatment. At 34.1 weeks, fetal bradycardia lasting 7 minutes was noted at fetal heart rate monitoring. At emergency cesarean delivery a liveborn appropriately grown infant was found, with Apgar scores of 5, 7 and 8 at 1, 5 and 10 minutes, respectively, and umbilical artery acidemia (pH of 7.19, base excess of -5.4 mMol/L). The child did eventually well. Conclusion: Severe maternal cholestasis can cause acute fetal acidemia; close inpatient surveillance or delivery could be necessary in such cases to prevent stillbirth.| File | Dimensione | Formato | |
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