A 33-year-old primigravida consulted the emergency department with a 40-week pregnancy and history of spontaneous rupture of membranes (SROM). The diagnosis of SROM was confirmed, and she was admitted to labor and delivery. Augmentation of labor was initiated, and approximately 2 hours after admission, fetal bradycardia was observed, and she was taken to an emergency cesarean delivery. During surgery, about 50% of placental abruption was diagnosed. No important bleeding was reported afterwards, and no surgical complications were reported. A healthy female newborn was obtained, who weighed 3.3 kgs, Apgar score was 8-9, and no neonatal complications were reported.
Fourteen hours after the surgery, the patient was noted jaundiced, oliguric, and hypoglycemic (glycemia: 40 mg/dL). She was conscious and alert, and no important obstetric bleeding was evidenced at the time. Her vital signs at that moment were the following: heart rate: 120 beats per minute (BPM), peripheral capillary oxygen saturation (SpO2): 95%, respiratory rate: 16 respirations per minute (RPM), temperature 36.3 degree Celsius, and blood pressure: 74/48 mmHg.
Laboratory tests evidenced important hepatic dysfunction (Total Bilirubin (TB) 7.9 mg/dL, Indirect Bilirubin (IB) 2.7 mg/dL, direct bilirubin (DB) 5.149 mg/dL, Aspartate Aminotransferase (ASAT) 170 U/L, and Alanine Aminotransferase (ALAT) 149 U/L), coagulopathy (prothrombin time (PT) 27 seconds, International Normalized Ratio (INR) 2.56, and fibrinogen 71 mg/dL), acute kidney injury (creatine 2.7 mg/dL) as well as hyperammonemia (126 mumol/L), low platelets (95 000), and leukocytosis (33 030/microliter). At this point, her hemoglobin level was 9.9 mg/dL, hematocrit 27.8%, and lactate dehydrogenase (LDH) 432 IU/L. Due to the laboratory anomalies, an abdominal ultrasound was ordered. The ultrasound revealed an echogenic liver with fatty infiltrates and mild hepatic steatosis.
It is important to note that on the days prior to her hospital admission, the patient had not presented with any symptoms suggesting hepatic failure, and she had no known exposure to virus or medications that could explain the clinical alterations. At this moment, the patient was considered to have 7 Swansea criteria and was admitted to the ICU with suspicion of AFLP.
In the ICU, resolution of the coagulopathy was initiated with blood products. The transfusion was guided by rotational tromboelastography (ROTEM). She required platelets (1 pool), fresh frozen plasma (1 unit), and cryoprecipitates (1 unit). The patient remained stable for the next 3 days.
On postoperative day 5, the patient deteriorated importantly. She turned disoriented and encephalopathic; she was coagulopathic (prolonged PT and INR > 5) once more and persistently hypoglycemic despite an adequate diet. Other causes of hepatic failure in pregnancy and postpartum were discarded, such as viral hepatitis. At this point, the decision to start plasma exchange therapy was made, she received a total of three sessions (one daily) of PE, and recovery of her neurological status and laboratory tests was reached on postoperative day 9.
Once the coagulation disorder was reversed, she was taken to a transjugular hepatic biopsy. The biopsy reported microvesicular steatosis, ballooning degeneration of hepatocytes, canalicular cholestasis, and cholangiolitis, findings suggesting AFLP considering the clinical context. On postoperative day 15, the patient was discharged home, with complete resolution of symptoms and normalization of hepatic and renal functions.