OG12.6 | Liver Disease in Pregnancy — Summary & Reflection

KEY TAKEAWAYS

Liver disease in pregnancy spans a spectrum from the common pruritus of ICP to the obstetric emergencies of AFLP and HELLP syndrome. The trimester of onset and the biochemical profile discriminate between conditions. ICP (obstetric cholestasis) causes pruritus due to bile acid accumulation; bile acids ≥40 µmol/L define severe disease with a doubled stillbirth risk; treatment is UDCA 10–15 mg/kg/day with delivery at 37–38 weeks (mild) or 35–36 weeks (severe). AFLP is caused by mitochondrial fatty-acid oxidation failure (often LCHAD-fetal link); the Swansea criteria (≥6 of 14 features) confirm diagnosis; hypoglycaemia, coagulopathy, and encephalopathy are the hallmarks; delivery is always the treatment. HELLP is a pre-eclampsia-spectrum microangiopathy with MAHA + thrombocytopaenia + hepatic necrosis; ergometrine is absolutely contraindicated; delivery is definitive management. Hepatitis E has 20–25% maternal mortality in pregnant Indian women (genotype 1, third trimester) and requires ICU support + expedited delivery in late pregnancy. Viral hepatitis B requires tenofovir from 28 weeks (high DNA load) and neonatal HBV vaccine + HBIG within 12 hours.

REFLECT

Consider a woman from a rural area presenting at 35 weeks with jaundice and confusion. She has been referred from a primary health centre with a diagnosis of 'viral hepatitis'. Her blood glucose is 1.9 mmol/L and her PT is 22 seconds. Reflecting on Kolb's learning cycle: What concrete experience do you now carry into this scenario from this module? What conceptualisation helps you discriminate AFLP from HEV hepatitis at the bedside? What active experiment would you plan in the next 30 minutes — and which condition changes your management most urgently? Now apply this: would you delay delivery while awaiting more investigations, or act immediately? Reflect on the role of rapid bedside glucose testing as the single most discriminating emergency investigation in this scenario.