K Sterrenburg1, W Visser2, L S Smit3, J Cornette1. 1. Department of Obstetrics and Gynaecology, University Medical Centre Erasmus, Rotterdam, the Netherlands. 2. Department of Obstetrics and Gynaecology, Internal Medicine, University Medical Centre Erasmus, Rotterdam, the Netherlands. 3. Department of Pediatrics, Division of Neonatology, University Medical Centre Erasmus, Rotterdam, the Netherlands; Department of Neurology, Division of Pediatric Neurology, University Medical Centre Erasmus, Rotterdam, the Netherlands.
Abstract
BACKGROUND: Intrahepatic cholestasis of pregnancy is a cholestatic disorder with an increased risk for adverse perinatal outcome. The mechanism underlying intrauterine demise is poorly understood. CASE: A nulliparous woman with gestational age of 36 plus 6 weeks presented with suspected intrahepatic cholestasis. Continuous CTG monitoring evolved from a normal pattern towards a non-reassuring pattern. A male neonate was delivered by caesarean section. Apgar scores 0, 1 and 4 at 1, 5 and 10 min. Fetal cord gas analysis showed pH 6.98, base deficit -15 mmol/L. Blood results showed maternal serum bile acid concentration of 220 µmol/L. CONCLUSION: Our case suggests gradual evolution towards hypoxia and acidosis. It is unknown whether certain components in the bile acid concentrations might contribute to a fetal metabolic component of the acidosis.
BACKGROUND:Intrahepatic cholestasis of pregnancy is a cholestatic disorder with an increased risk for adverse perinatal outcome. The mechanism underlying intrauterine demise is poorly understood. CASE: A nulliparous woman with gestational age of 36 plus 6 weeks presented with suspected intrahepatic cholestasis. Continuous CTG monitoring evolved from a normal pattern towards a non-reassuring pattern. A male neonate was delivered by caesarean section. Apgar scores 0, 1 and 4 at 1, 5 and 10 min. Fetal cord gas analysis showed pH 6.98, base deficit -15 mmol/L. Blood results showed maternal serum bile acid concentration of 220 µmol/L. CONCLUSION: Our case suggests gradual evolution towards hypoxia and acidosis. It is unknown whether certain components in the bile acid concentrations might contribute to a fetal metabolic component of the acidosis.
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