FRCA Notes

Liver Disease in Obstetrics

This page forms part of a series of pages on liver disease across a spectrum of patient cohorts.

Liver disease in pregnancy hasn't yet been a CRQ, though questions on hepatic pathology have featured in 3 of the past 5 CRQ papers.

Resources

  • Liver disease in pregnancy mostly arises due to disorders specific to the parturient, namely:
    • Pre-eclampsia with hepatic impairment (49%)
    • HELLP syndrome (22%)
    • Intrahepatic cholestasis of pregnancy (17%)
    • Acute fatty liver of pregnancy (4%)
  • The above-linked BJA Education article covers disorder
  • Patients with hepatic impairment from PET/HELLP should be managed in an HDU setting, as the syndrome is unpredictable and can progress rapidly
  • Clinical features include:
    • Hepatic angina i.e. RUQ or epigastric abdomnial pain
    • Haemolysis, although rarely significant enough to cause anaemia
    • Thrombocytopaenia which requires close monitoring (2hrly FBC)
    • Hepatic haematoma or hepatic rupture (rare but high mortality)

    • Chest pain and tachycardia due to PE
    • AKI
    • Standard symptoms of pre-eclampsia
  • ALT is raised (at least 2x and up to 30x) but bilirubins and bile acids are typically normal

  • Management
    • As for pre-eclampsia, with foetal delivery at a time which balances maternal and neonatal risk
    • Treatment of cardiovascular shock, which occurs in 50% of those with HELLP

  • Presents in the late third trimester, more commonly in those with multiple pregnancy or low BMI
  • It is associated with a high maternal (<2%) and perinatal (up to 50%) mortality
  • Diagnosed by presence of six features of the Swansea criteria without other explanation, supported by cross-sectional imaging
  • There is normally a markedly evelated ALT and bilirubin (both 2 - 15x normal) but normal bile acids

  • Clinical features
    • A prodrome of non-specific nausea, vomiting and malaise which may last weeks
    • Hypertension & proteinuria (akin to PET) and pruritus (akin to cholestasis of pregnancy)
    • Acute kidney injury (90%)
    • Those of fulminant hepatic failure i.e. hypoglycaemia, coagulopathy and encephalopathy
  • Complications include ARDS and pancreatitis

  • Management is with expedited delivery following suitable resuscitation (i.e. correction of hypoglycaemia & coagulopathy)
  • Symptoms can deteriorate post-partum and HDU monitoring for at least 48hrs is required

  • Impaired excretion of bile acids leads to a generalised pruritus
  • Bile acids (up to 15x) and ALT (up to 8x) are raised, although bilirubin is normal
  • Although it rarely requires HDU management, the condition can lead to vitamin K malabsorption and therefore clotting should be checked
  • It can be a marker of other liver disease

  • MDT management including haematology (if coagulopathy) and early liaison with the regional liver unit
  • Careful monitoring in an HDU or ITU setting
    • Lactate >2.8 + the presence of encephalopathy is the best predictor of clinical deterioration requiring transplant
  • No evidence that use of NAC is harmful

Anaesthetic considerations

  • Regional techniques are not contraindicated but should be cautious with regards to coagulopathy
  • Amide local anaesthetics undergo hepatic metabolism so need to monitor for toxicity

  • If GA is required:
    • Propofol and thiopentone are suitable induction agents
    • Suxamethonium or cis(atracurium) is the NMBA or choice, or rocuronium + sugammadex
    • Volatile anaesthetics are suitable for maintenance

  • Reduced-dose paracetamol may be acceptable
  • Avoid NSAIDs
  • Caution with opioids; fentanyl or oxycodone may be preferable to morphine

  • The commonly used uterotonics are hepatically metabolised but should be used in full doses for those with PPH
  • Avoid the IM route in those with coagulopathy