Acute fatty liver of pregnancy (AFLP) is a rare but life-threatening obstetric emergency that occurs exclusively in the third trimester of pregnancy (typically between 30-38 weeks gestation), characterized by microvesicular fatty infiltration of hepatocytes leading to acute liver failure. The estimated incidence is 1 in 7,000 to 1 in 16,000 pregnancies, but the mortality rate has historically been 75-85% and, even with modern intensive care and prompt delivery, remains 7-18% for the mother and 9-23% for the fetus. The registered nurse must recognize the often subtle and nonspecific early symptoms of AFLP to facilitate rapid diagnosis and emergency delivery, which is the only definitive treatment. The underlying pathogenesis of AFLP is linked to a defect in mitochondrial fatty acid oxidation, specifically a deficiency of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) in the fetus. LCHAD is a key enzyme in the mitochondrial beta-oxidation pathway that breaks down long-chain fatty acids into acetyl-CoA for energy production. When the fetus is homozygous for an LCHAD mutation (the most common being the G1528C mutation in the HADHA gene), it cannot properly oxidize long-chain fatty acids. These...