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Hypoglycemia, DIC and Delayed Emergence in a Cesarean Section
Abstract Number: S2C-6
Abstract Type: Case Report/Case Series
In the US, AFLP affects 1 in 7000-16,000 deliveries, is more common in primiparous women and most commonly presents during the 35th week of pregnancy. Maternal mortality is 12.5-18%, with a neonatal mortality rate of 7-66%.
27 years G1P0 with history of placenta previa presents at 37 weeks with vaginal bleeding. A STAT Cesarean section was planned. All prenatal labs were within normal limits, including coagulation profile and platelet count of 257. General endotracheal anesthesia was induced and fetus was delivered uneventfully. At completion of the surgery, patient was breathing spontaneously at RR 15 and tidal volumes of 300, but minimally responsive to painful stimuli. Naloxone was titrated with no improvement. Labs sent prior to C-Section showed glucose 70, INR 2.1, fibrinogen 130 and platelets146. A bolus of D5NS was given. At this time, profuse vaginal bleeding was noticed and patient was reopened. Methylergonovine and carboprost were given; massive transfusion protocol initiated. Radial arterial line inserted. Repeat labs showed glucose 182, INR 2.5, fibrinogen 92, platelets 91000, creatinine 2.8, elevated LFTs and LDH. Patient was transferred intubated to IR for uterine artery embolization. She received 7 PRBC, 7 FFP, 3 platelet and 4 cryoprecipitate. Placed on a D10W infusion in SICU for glucose in the 60s which resolved on postop day 2. She was discharged home on postop day 10.
Acute fatty liver of pregnancy (AFLP) is a complication characterized by microvesicular steatosis in the liver, due to a mitochondrial dysfunction in the oxidation of fatty acids and accumulation in hepatocytes, causing acute liver insufficiency, N/V, RUQ pain, upper GI hemorrhage, acute renal failure, pancreatitis, hypoglycemia, or fulminant liver failure with hepatic encephalopathy. ARF and hypoglycemia differentiate from HELLP. These patients are more likely to have a heterozygous long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency, which is involved in the beta oxidation of long-chain fatty acids. If fetus is homozygous for this mutation, it is unable to oxidize fatty acids, which are passed to the mother and leads to AFLP.
Treatment is delivery of the fetus and supportive care: 5% dextrose, replacement of coagulation factors, postpartum plasma exchange or hemodiafiltration. Anesthetic considerations include regional anesthesia if no coagulopathy is present or general anesthesia with avoidance of hepatotoxic agents.