Acute Fatty Liver of Pregnancy (AFLP)

Coagulopathy decides the anesthetic - Unlike HELLP, AFLP is true hepatic synthetic failure: prolonged PT and INR with a low fibrinogen on top of a falling platelet count. Get a fresh coagulation panel, fibrinogen, and platelet count immediately before you place anything — the numbers move fast and a stale set is worthless.

Platelet product before operative delivery - Platelet transfusion is frequently needed before cesarean in AFLP. Confirm the current transfusion threshold against your institution's obstetric hemorrhage protocol rather than from memory; ⚠ transfusion targets are a moving guideline number and should not be quoted from a reference article.

General anesthetic when neuraxial is out - Coagulopathy usually takes the block off the table, so plan a rapid sequence induction and a secured airway for cesarean, with the blood bank notified and product in the room. Titrate induction agents down — this is an encephalopathic patient with a failing liver, not a healthy parturient.

Hypoglycemia - Hypoglycemia is characteristic of AFLP and is one of the findings that separates it from HELLP and preeclampsia. Check a point-of-care glucose on arrival and repeat it through the case and into the postpartum period; run dextrose rather than chasing the number.

Neuromuscular blockade - Liver failure disturbs volume of distribution, metabolism, biliary excretion, and esterase synthesis, so NMBA loading and maintenance doses are unpredictable. Monitor TOF and confirm reversal. If magnesium sulfate is running (given under 32 weeks for fetal neuroprotection), it antagonizes calcium at the neuromuscular junction and prolongs blockade further.

Emergence and encephalopathy - Hepatic encephalopathy with an elevated ammonia blunts airway reflexes and slows wake-up. Plan for a delayed emergence and an ICU bed rather than defaulting to extubation in the OR.

Renal and volume management - Creatinine and urine protein are part of the diagnostic workup, and renal failure is one of the things that kills these patients. Track urine output and creatinine, avoid nephrotoxins, and remember pulmonary edema from low oncotic pressure runs around 14% — crystalloid is not free here.

The postpartum period is not the end - Bleeding, hypoglycemia, and renal dysfunction all continue after delivery, so these patients go to the ICU. Liver function typically normalizes within about one to ten days; when it does not, liver transplantation is the next conversation.

Do not wait for diagnostic certainty - AFLP overlaps with and can coexist with HELLP and preeclampsia with severe features. The Swansea criteria support the diagnosis and liver biopsy is not required; management is largely the same across these entities, and delivery should not be delayed to make the distinction.

Acute fatty liver of pregnancy (AFLP) is microvesicular fatty infiltration of hepatocytes presenting in the third trimester, usually between 30 and 38 weeks, in roughly 1 in 7,000 to 20,000 pregnancies. Free fatty acids rise in late pregnancy to support fetoplacental growth; when their metabolism is defective — most importantly fetal long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency, present in about 20% of cases — fat accumulates in hepatocytes and injures them. What arrives in your room is acute liver failure in a parturient: jaundice, encephalopathy with elevated ammonia, hypoglycemia, coagulopathy with prolonged PT and INR and low fibrinogen, DIC, renal failure, and pulmonary edema from fallen oncotic pressure in about 14%. Delivery is the only definitive treatment and expectant management is not appropriate, so this is an obstetric emergency you will be called into.