AFLP at 34 weeks — structured oral station (12 minutes)

Opening prompt — "Talk me through your reading of these results and your immediate plan."

Model response — say it in this order:[1][2]

• "This is acute fatty liver of pregnancy — third-trimester microvesicular liver failure. She meets at least eight Swansea criteria: vomiting, abdominal pain, encephalopathy, elevated bilirubin, hypoglycaemia, elevated urate, leucocytosis, ascites/bright liver on USS, elevated transaminases, elevated ammonia, renal impairment and coagulopathy. The normal blood pressure, normal platelets and negative urinalysis make HELLP less likely."
• "AFLP is a multi-disciplinary emergency. I will call my consultant, the anaesthetist, haematology, hepatology or a specialist liver unit, the major-haemorrhage coordinator and the neonatal team. I will declare the diagnosis."
• "While the team mobilises I will correct the four biochemical pillars: hypoglycaemia with IV dextrose — 50 mL of 50% as a bolus, then a 10% infusion; coagulopathy with fresh frozen plasma 12-15 mL/kg, cryoprecipitate to keep fibrinogen above 1.5-2 g/L, and vitamin K 10 mg IV; encephalopathy with lactulose and head-up positioning."
• "Delivery is the treatment. Once she is stabilised I will expedite delivery, by induction if achievable within hours and the maternal/fetal condition allows, by caesarean otherwise, with the coagulopathy corrected before any operative delivery."[2][4]

Examiner is listening for: Swansea recognition, the AFLP-vs-HELLP discriminator, the supportive bundle with doses, and the unambiguous delivery-is-the-cure statement.[1]

Probe 1 — "Why not HELLP? She has elevated transaminases and right-upper-quadrant pain."

• "HELLP shares third-trimester timing, transaminitis, right-upper-quadrant pain and elevated urate — none of these discriminate. The discriminators are the four biochemical pillars of AFLP: hypoglycaemia, hyperammonaemia, coagulopathy and lactic acidosis, plus encephalopathy. HELLP, by contrast, is defined by hypertension, proteinuria, haemolysis and thrombocytopenia. This patient has normal blood pressure, normal platelets and a negative urinalysis — that is strongly against HELLP."[4]

Probe 2 — "She improves after two units of FFP. Could you delay delivery for 48 hours to give steroids for fetal lung maturity?"

• "No. Delivery is the treatment of AFLP — there is no role for expectant management regardless of gestational age. The fetal-placental unit is the source of the toxic fatty-acid metabolites causing maternal hepatocyte injury; delivery removes the source and recovery follows. Steroids for fetal lung maturity are appropriate where they can be given without delaying delivery, but they are not a reason to defer."
• "If she is at 34 weeks, the balance of risks already favours delivery, given the severity of the maternal metabolic derangement."[2][4]

Probe 3 — "On day 5 postpartum her liver function is not improving and she is somnolent. What now?"

• "I will refer urgently to a specialist liver unit for liver transplant assessment, while continuing all supportive measures. The Westbrook 2010 King's College Hospital series showed that an admission lactate over 2.8 mg/dL plus encephalopathy had 90% sensitivity and 86% specificity for death or transplant — she meets both. The classical King's College Criteria perform poorly in pregnancy-related liver failure, so I will not rely on them."
• "I will continue IV dextrose, FFP and cryoprecipitate to correct coagulopathy, lactulose for encephalopathy, head-up positioning, and frequent neuro-observations. The transplant centre will decide between continued medical support and listing for transplant."[3]

Probe 4 — "Her partner asks why this happened, and whether it will happen again."

This is a scored communication domain. Demonstrate it out loud:[6]

• Sit at his eye level, use his name, acknowledge the fear: "This must be terrifying — let me explain what we know."
• "Acute fatty liver of pregnancy is rare — about five in every hundred thousand pregnancies. We understand it now as a problem with how the fetus metabolises fats. The baby inherits a gene change from both parents that prevents the breakdown of long-chain fatty acids. The toxic products cross the placenta and injure the mother's liver. The good news is delivery removes the source, and your partner's liver will recover."
• "For a future pregnancy with the same partner, the chance of the fetus inheriting the same gene change from both of you is one in four. We will arrange testing of you, your partner and the baby to confirm. We will plan a future pregnancy with that information."[6]

Probe 5 — "What will you do for the baby?"

• "We will screen the baby for fatty-acid oxidation disorders — long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency and trifunctional protein (TFP) deficiency. Babies with these disorders can present in the first days or weeks of life with hypoketotic hypoglycaemia, cardiomyopathy, or sudden death. The neonatal team will be aware, and we will start feeds early and avoid fasting. Genetic counselling for the family follows."[6]