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OG12.1-11,OG16.4 | Medical Disorders in Pregnancy — PBL Case
CLINICAL SETTING
Mrs Kavitha, a 27-year-old primigravida at 34 weeks of gestation, is brought to the emergency department at 2 a.m. by her husband. Over the past 36 hours she has developed generalised pruritus, yellow discolouration of the eyes and skin, dark-coloured urine, and has vomited three times. She also reports right upper quadrant discomfort that started this evening. Her previous antenatal visits were reportedly normal. She has no past history of liver disease, alcohol use, or blood transfusion. She was screened HIV-negative at booking. Her blood group is O-negative; her husband is B-positive. On examination: she is icteric, mildly distressed, BP 128/82 mmHg, pulse 98 bpm, temperature 37.8°C. Her uterus is appropriately sized for 34 weeks. The fetal heart rate is 148 bpm on CTG monitoring. Fundal height is 32 cm (2 cm lag for dates).
Trigger 1: First investigations return
Urgent bloods show: Hb 11.2 g/dL, WBC 14,800/µL, platelets 210,000/µL, serum bilirubin (total) 4.8 mg/dL (conjugated 3.2 mg/dL), AST 68 IU/L, ALT 74 IU/L, alkaline phosphatase 320 IU/L, serum bile acids 52 µmol/L, blood glucose 4.8 mmol/L, prothrombin time 12.5 sec (control 12 sec), serum albumin 3.2 g/dL. Ultrasound abdomen shows a slightly echogenic liver with no biliary dilatation; no gallstones; normal common bile duct. The fetus has an estimated weight on the 12th centile. Umbilical artery Doppler shows mildly elevated pulsatility index.
DISCUSSION POINTS
- What is the most likely diagnosis at this point, and what clinical and biochemical features support it? Which pregnancy-specific liver diseases are on your differential and how do you discriminate between them based on the available data?
- What is the significance of the serum bile acids level of 52 µmol/L specifically for fetal well-being, and what does the Doppler finding add to your concern about fetal outcome?
Click to reveal Trigger 2: The Rh blood group triggers a new concern (discuss previous trigger first!)
Trigger 2: The Rh blood group triggers a new concern
The midwife notes that Mrs Kavitha is O-negative and her husband is B-positive. Her booking indirect Coombs test (ICT) from 12 weeks is retrieved from the records — it was reported as negative. However, she discloses that she had a spontaneous miscarriage at 9 weeks in a previous pregnancy and is uncertain whether she received any injection at the time. A repeat ICT today returns positive: anti-D titre 1:4. Middle cerebral artery (MCA) peak systolic velocity Doppler is performed: result is 1.2 MoM.
DISCUSSION POINTS
- What is the mechanism of Rh iso-immunization in this woman? What sensitising events may have occurred, and at what point in her obstetric history could sensitisation have been prevented?
- How do you interpret an MCA PSV of 1.2 MoM in the context of a positive ICT? What would change your decision to intervene?
Click to reveal Trigger 3: Thyroid function results arrive (discuss previous trigger first!)
Trigger 3: Thyroid function results arrive
A thyroid function panel (requested because the patient mentioned fatigue, cold intolerance, and constipation 'since early pregnancy') returns: TSH 5.6 mIU/L (trimester-specific reference range at 34 weeks T3: 0.3–3.0 mIU/L), free T4 10.2 pmol/L (low-normal). Anti-thyroid peroxidase antibodies (anti-TPO) are strongly positive. The treating team debates whether this finding is incidental or clinically significant at this gestational stage.
DISCUSSION POINTS
- Is this thyroid function result normal or abnormal for 34 weeks of pregnancy? Explain why the non-pregnant reference range must not be used, and what the clinical implications of subclinical-to-overt hypothyroidism at this stage are for the fetus.
- What treatment decision do you make now, and how does the fundal height lag (possible IUGR) change the urgency of your decision?
Click to reveal Trigger 4: Clinical deterioration overnight (discuss previous trigger first!)
Trigger 4: Clinical deterioration overnight
At 6 a.m. the on-call registrar is called: Mrs Kavitha has developed palpitations and is breathless at rest. Her BP is now 135/88 mmHg, pulse is 118 bpm irregularly irregular. Oxygen saturation is 94% on room air. A 12-lead ECG confirms new-onset atrial fibrillation with rapid ventricular response. Bedside echo shows moderate mitral stenosis (mitral valve area 1.4 cm²) with a heavily scarred valve, consistent with rheumatic heart disease — not previously diagnosed. She has no prior cardiac history documented.
DISCUSSION POINTS
- Why do you think the cardiac diagnosis was missed in this pregnancy until now, and what physiological changes of pregnancy precipitated this decompensation?
- What is the immediate management of new-onset AF with rapid ventricular rate in a pregnant woman with rheumatic mitral stenosis? Identify the drug that must NEVER be used in the third stage of labour for this patient and explain why.
Click to reveal Trigger 5: Delivery decision (discuss previous trigger first!)
Trigger 5: Delivery decision
The team now faces a complex multi-system decision. Mrs Kavitha has: (1) intrahepatic cholestasis of pregnancy (ICP) with bile acids 52 µmol/L; (2) Rh iso-immunization (positive ICT, MCA PSV 1.2 MoM, no active fetal anaemia yet); (3) newly detected hypothyroidism (TSH 5.6 mIU/L on Hashimoto's background); (4) rheumatic mitral stenosis with acute AF, now rate-controlled on IV beta-blocker; (5) likely IUGR (EFW 12th centile, raised umbilical artery PI). She is at 34+3 weeks.
DISCUSSION POINTS
- Construct a delivery decision framework for this patient: which condition is driving the timing of delivery most urgently? What is the threshold bile acid level at which ICP guidelines recommend delivery, and does she meet it?
- Write a brief multidisciplinary team (MDT) management summary for handover — identify which specialist should lead each problem (cardiologist, hepatologist, obstetrician, haematologist, neonatologist) and the single most important action each team must complete before delivery.
Group Task Assignments
- Construct a problem list for Mrs Kavitha in order of clinical urgency and justify the prioritisation.
- Draw a timeline of when each complication could have been detected and prevented — identify the missed opportunities at each antenatal visit.
- Compare the investigation findings of ICP, AFLP, and HELLP syndrome in a structured table to explain why AFLP and HELLP were excluded in this case.
- Write a management plan for the cardiac complication (AF with mitral stenosis) that specifies which drugs are safe in pregnancy and identifies the absolute contraindication at delivery.
- Role-play the MDT handover for Trigger 5: each student takes a specialist role (obstetrician, cardiologist, haematologist, neonatologist) and states the single most important action their specialty must contribute before delivery.
Learning Issues
Research these questions and bring your findings to the discussion.
- [OG12.6] How does intrahepatic cholestasis of pregnancy differ from HELLP and AFLP in terms of presentation, biochemistry, and fetal risk — and what bile acid threshold guides delivery timing?
- [OG12.4] Why does rheumatic mitral stenosis decompensate in the third trimester, why is ergometrine absolutely contraindicated, and what is the appropriate rate-control agent in pregnancy?
- [OG12.8] What sensitising events place an Rh-negative woman at risk of iso-immunization, and how does MCA PSV Doppler guide the decision between watchful waiting and intrauterine transfusion?
- [OG12.9] Why must trimester-specific TSH reference ranges be used in pregnancy, and what are the fetal consequences of undiagnosed hypothyroidism in the third trimester?
- [OG12.11] How does umbilical artery Doppler staging (normal → raised PI → absent EDF → reversed EDF) guide the timing and mode of delivery in suspected IUGR?
- [OG12.5] When is UTI in pregnancy treated irrespective of symptoms, and what is the complication rate of untreated asymptomatic bacteriuria that drives this policy?