///2019 Abstract Details
2019 Abstract Details2019-07-13T07:45:15-05:00

Acute Liver Failure of Unclear Etiology in Pregnancy

Abstract Number: FCH-304
Abstract Type: Case Report Case Series

Vibha Mahendra MD1 ; Kelly West MD2; Jose Rivers MD3

Liver disease occurs in approximately 3% of pregnancies and while rare, acute liver failure during pregnancy is associated with a high mortality rate for both mother and fetus . This case report describes a twenty-seven year old parturient who developed acute and fulminant liver failure of unclear etiology at 27 weeks gestation.

Our patient was a 27 year old female, G4P0121 at gestational age 27 weeks, 2 days, with history of cervical insufficiency requiring cerclage placement at 20 weeks. She presented with five days of generalized malaise and chills, and was found to have a mild fever, tachycardia and transaminitis. Two days after beginning treatment for pyelonephritis, she developed high fevers and uterine fundal tenderness with cervical discharge. An uncomplicated urgent Cesarean delivery was performed under general anesthesia, for suspected chorioamnionitis. Despite delivery, her condition declined and she underwent a hysterectomy for source control, but pathology reports later indicated no evidence of infection in the uterus. Perioperatively, she developed hypotension requiring vasopressors and ICU admission, and evolved clinically from transaminitis and mild synthetic dysfunction to eventual DIC and encephalopathy. After a prolonged and complex ICU course, the patient was deemed to have irreversible and multifactorial acute liver failure, but due to immigration status was not a candidate for orthotopic liver transplantation. After 6 weeks, the patient expired due to multisystem organ failure.

The differential diagnosis for the patient’s liver failure included AFLP, HELLP, toxin/medication induced injury and Hemophagocytic Lymphohistiocytosis (HLH) . AFLP occurs primarily during the third trimester, causing elevations in transaminases <5 times the upper limit of normal, and is distinguished from HELLP by the presence of hypoglycemia . The treatment for AFLP is immediate delivery, and the characteristic liver biopsy finding is fatty infiltration of hepatocytes. Our patient’s liver biopsy showed large areas of necrosis with minimal inflammation (consistent with drug induced, ischemia, HELLP, and viral etiology). The patient’s prolonged exposure to hepatotoxic medications including meropenem and inhalational anesthetic agents likely intensified the underlying liver dysfunction and explain the biopsy findings.

While our patient had some characteristics of AFLP, HELLP and HLH, she did not perfectly meet any diagnosis or respond to treatment with IVIG or steroids. Exposure to hepatotoxins and periods of hypotension likely worsened her hepatic dysfunction and complicated the clinical and diagnostic picture. The complex nature of this case demonstrates the importance of early identification of liver dysfunction in pregnancy, avoidance of hepatotoxic medication exposure in at risk patients, and early initiation of supportive care.

SOAP 2019