• Patho/Etiology
    • A rare but life-threatening complication of the third trimester or early postpartum period.
    • Caused by a defect in mitochondrial beta-oxidation of fatty acids.
    • Strongly associated with fetal long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency, an autosomal recessive disorder.
    • Unmetabolized fetal fatty acids enter the maternal circulation, overwhelming the mother’s (often a heterozygous carrier) enzymatic capacity and leading to microvesicular fatty infiltration of hepatocytes.
  • Clinical Presentation
    • Insidious onset of nausea/vomiting, RUQ/epigastric pain, malaise, anorexia, and headache.
    • Can rapidly progress to fulminant liver failure, presenting with jaundice, hepatic encephalopathy (e.g., confusion), and profound hypoglycemia.
    • Patients may also present with polydipsia (excessive thirst) and polyuria.
  • Diagnosis
    • A clinical diagnosis based on presentation and lab findings; liver biopsy is the gold standard but rarely performed due to bleeding risk.
    • Labs:
      • Profound hypoglycemia is a hallmark feature.
      • ↑↑ Bilirubin and ↑↑ Ammonia.
      • Moderately elevated aminotransferases (AST/ALT usually < 500 IU/L).
      • Coagulopathy: ↑ PT/PTT, ↓ fibrinogen, thrombocytopenia.
      • Leukocytosis and elevated uric acid are common.
  • Differential Diagnostics
    • HELLP Syndrome: A major differential. Key features distinguishing AFLP from HELLP include:
      • AFLP: More severe liver dysfunction (significant jaundice, hypoglycemia, coagulopathy, ↑ ammonia).
      • HELLP: Dominated by Hemolysis (schistocytes), Elevated Liver enzymes, and severe Low Platelets. Hypertension is more common and severe in HELLP.
    • Pre-eclampsia with severe features: Presents with HTN and proteinuria, but LFT elevation is typically milder.
    • Viral Hepatitis: Presents with much more dramatic elevation of aminotransferases (AST/ALT often >1,000 IU/L).
  • Management
    • IMMEDIATE DELIVERY of the fetus is the only definitive treatment, regardless of gestational age.
    • Aggressive supportive care in an ICU setting is critical.
      • IV dextrose to correct hypoglycemia.
      • Correction of coagulopathy with blood products like fresh frozen plasma (FFP) and cryoprecipitate.
      • Monitoring and support for multi-organ failure (e.g., renal failure, pancreatitis).
    • Liver transplantation is rarely needed but may be considered if liver function does not improve after delivery.
  • Key Associations/Prognosis
    • Risk factors include nulliparity, multiple gestations, and carrying a male fetus.
    • Maternal and fetal mortality was once very high but has significantly improved with early diagnosis and prompt delivery.
    • The infant should be screened for LCHAD deficiency post-delivery.
    • The condition can recur in future pregnancies, with a genetic chance of 25%.