Which feature is most consistent with acute fatty liver of pregnancy, and what is definitive treatment?

Which feature is most consistent with acute fatty liver of pregnancy, and what is definitive treatment?

• A. N/V, RUQ pain, jaundice, hypoglycemia; delivery is definitive treatment
• B. Hypertension, proteinuria; give magnesium
• C. Hyperglycemia, polydipsia; initiate insulin therapy
• D. Severe edema and anemia; plasmapheresis

Answer: (A)

In acute fatty liver of pregnancy, the hallmark features come from liver dysfunction in late gestation: nausea and vomiting, right upper quadrant pain, jaundice, and often hypoglycemia. This combination reflects the developing hepatic failure that characterizes AFLP. The definitive treatment is urgent delivery, which removes the source driving the maternal hepatic crisis and typically leads to rapid improvement in liver function after the fetus is born. To place this in context, AFLP occurs in the third trimester due to problems with fatty acid metabolism in the liver, causing microvesicular steatosis and potential coagulopathy and hypoglycemia. Delivery is the key intervention because it halts the progression of the disease for the mother. The other described scenarios reflect different pregnancy-related conditions. Hypertension with proteinuria points to preeclampsia, for which magnesium is used for seizure prevention but isn’t the treatment for AFLP itself. Hyperglycemia with polydipsia suggests diabetes mellitus, where insulin therapy addresses glucose control. Severe edema and anemia aren’t characteristic of AFLP, and plasmapheresis isn’t a standard definitive therapy for AFLP.

In acute fatty liver of pregnancy, the hallmark features come from liver dysfunction in late gestation: nausea and vomiting, right upper quadrant pain, jaundice, and often hypoglycemia. This combination reflects the developing hepatic failure that characterizes AFLP. The definitive treatment is urgent delivery, which removes the source driving the maternal hepatic crisis and typically leads to rapid improvement in liver function after the fetus is born.

To place this in context, AFLP occurs in the third trimester due to problems with fatty acid metabolism in the liver, causing microvesicular steatosis and potential coagulopathy and hypoglycemia. Delivery is the key intervention because it halts the progression of the disease for the mother.

The other described scenarios reflect different pregnancy-related conditions. Hypertension with proteinuria points to preeclampsia, for which magnesium is used for seizure prevention but isn’t the treatment for AFLP itself. Hyperglycemia with polydipsia suggests diabetes mellitus, where insulin therapy addresses glucose control. Severe edema and anemia aren’t characteristic of AFLP, and plasmapheresis isn’t a standard definitive therapy for AFLP.