Abstract
Although uncommon during pregnancy, cirrhosis results in multiple medical complications impacting both mother and fetus. Previous reports suggest liver dysfunction in pregnancy causes accumulation of neurotoxins within the maternal compartment that increases neonatal morbidity through placental transfer. We present a case of a 36-year-old G2P1 female with history of biliary cirrhosis presenting at 32-weeks' gestation with hepatic congestion progressing to hepatic encephalopathy prompting delivery. Umbilical cord sampling and postnatal infant testing demonstrated elevated ammonia levels which resolved by 12 hours of life without intervention. At discharge, the infant did not demonstrate evidence of neurologic deficit. We conclude that acute maternal hepatic encephalopathy and hyperammonemia due to chronic liver disease do not portend adverse neonatal outcomes, notably encephalopathy.
Highlights
Due to deleterious effects of maternal hepatic derangements on fertility, pregnancy is uncommon in women with advanced liver dysfunction [1]
Infant complications related to metabolic derangements, such as inherited uric acid cycle dysfunction, have been described to cause hyperammonemia leading to encephalopathy [4]
We present a case of pregnancy complicated by iatrogenic biliary cirrhosis with worsening hepatic congestion that resulted in delivery of a viable infant without neurological consequences from in utero exposure of chronic maternal hyperbilirubinemia and acute hyperammonemia
Summary
Due to deleterious effects of maternal hepatic derangements on fertility, pregnancy is uncommon in women with advanced liver dysfunction [1]. We present a case of pregnancy complicated by iatrogenic biliary cirrhosis with worsening hepatic congestion that resulted in delivery of a viable infant without neurological consequences from in utero exposure of chronic maternal hyperbilirubinemia and acute hyperammonemia. Persistent hepatobiliary dysfunction necessitated transjugular intrahepatic portosystemic shunt (TIPS) for esophageal varices and percutaneous biliary drainage with radiographically guided exchange of biliary drainage tubes every three months. She denied prior episodes of hepatic encephalopathy or neurologic deficiencies and was using a titrated lactulose therapy. EKG, chest, and abdominal plain films were unremarkable Her symptomatology was attributed to hypervolemia and hepatic congestion without overt decompensation.
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