Clinical overview
Abnormal liver tests, abdominal pain, vomiting, jaundice or encephalopathy in pregnancy require a differential that crosses obstetrics, medicine and surgery. Pregnancy-specific disease—HELLP syndrome, acute fatty liver of pregnancy (AFLP), intrahepatic cholestasis and hyperemesis-related injury—can resemble viral, drug-induced, autoimmune, vascular or gallstone disease. Delay is dangerous because delivery is disease-modifying in HELLP and AFLP, while acute liver failure, cholangitis, perforation and infected urinary obstruction require specialist support or source control.
Pregnancy changes the reference frame. Alkaline phosphatase rises from placental production and albumin falls through haemodilution; aminotransferases and bilirubin are not expected to rise substantially merely because of pregnancy. A new transaminitis, synthetic dysfunction, hypoglycaemia or jaundice demands explanation.
Core knowledge
Pattern the liver injury
Start by identifying hepatocellular, cholestatic or mixed injury, then assess severity. Aminotransferase magnitude describes injury, not liver function. Function is reflected by glucose handling, coagulation, bilirubin trajectory, mental state and lactate/acid–base context. INR can be altered by anticoagulants or DIC; interpret with fibrinogen, platelets and bleeding.
Key pregnancy comparisons:
| Syndrome | Timing and clues | Critical action |
|---|---|---|
| HELLP | Usually later pregnancy/postpartum; hypertension may be present, haemolysis, raised AST/ALT/LDH, low platelets | Stabilise, magnesium/BP treatment as indicated, plan delivery; evaluate DIC/TMA |
| AFLP | Usually third trimester; vomiting, abdominal symptoms, jaundice, hypoglycaemia, coagulopathy, AKI, encephalopathy | Correct glucose/coagulopathy, critical care and prompt delivery |
| Intrahepatic cholestasis | Pruritus, raised bile acids, usually preserved synthetic function | Fetal/obstetric risk management; seek another cause if organ failure |
| Hyperemesis-related injury | Early pregnancy, vomiting/starvation, modest liver abnormalities | Fluids/electrolytes, thiamine, nutrition and exclusion of alternate disease |
| Viral/drug/autoimmune/vascular | Exposure, medicine, serology, imaging and systemic context | Cause-specific treatment; transplant-centre discussion if acute failure |
HELLP, TTP/aHUS and AFLP overlap. A profoundly abnormal smear/haemolysis pattern, neurological injury, severe persistent renal failure or lack of improvement after delivery should trigger urgent haematology/nephrology reassessment rather than assuming all abnormalities will resolve as HELLP.
Figure M14.1 — Pregnancy-associated liver injury is patterned before severity is judged: aminotransferases describe injury, while glucose, coagulation, bilirubin trajectory, mental state and lactate expose failure and distinguish pregnancy-specific syndromes from competing disease.
Acute liver failure
Acute liver failure is acute hepatic injury with coagulopathy and encephalopathy in a patient without established cirrhosis. Causes include paracetamol toxicity, viral/autoimmune hepatitis, drug injury, ischaemia and pregnancy-specific disease. Manage in critical care with early transplant-centre consultation; do not wait for advanced encephalopathy.
Priorities include airway protection when consciousness falls, frequent glucose correction, haemodynamic and renal support, infection surveillance, electrolyte management and cerebral-oedema precautions. Give N-acetylcysteine promptly for paracetamol toxicity; specialist teams may use it in selected non-paracetamol acute liver failure. Avoid routine plasma merely to normalise INR because it obscures trajectory and adds volume; use haemostatic products for bleeding or an indicated procedure.
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