Pregestational diabetes in pregnancy — structured SAQ (15 marks)

(a) Immediate medication changes (4 marks)

One mark per correct change with a justification. Maximum four. ^[1][6]

• Stop ramipril today. Angiotensin-converting enzyme inhibitors cause fetopathy; substitute labetalol, nifedipine or methyldopa if antihypertensive cover is needed for her blood pressure and nephropathy.^[1][6]
• Stop atorvastatin today. Statins are not recommended in pregnancy and there is no urgency to lipid control over nine months.^[6]
• Start folic acid 5 mg orally daily and continue to the end of the first trimester. She is already at 9+3 weeks, so this will not undo the neural-tube risk window, but it remains indicated for the rest of organogenesis.^[1][6]
• Start aspirin 100–150 mg orally at night before 16 weeks and continue to 36 weeks, for preeclampsia prophylaxis in a woman with pregestational diabetes, hypertension and nephropathy.^[4]
• Intensify insulin now with a target HbA1c as close to below 6.5 percent (48 mmol/mol) as tolerable, and offer continuous glucose monitoring.^[6][9]
• Also acceptable: iodine 150 micrograms daily, and a review of any over-the-counter medication.^[1]

(b) Investigations and surveillance (3 marks)

One mark each for the retinal plan, the renal plan and the fetal plan. ^[1][5]

• Retina: dilated retinal examination or retinal photography now, and repeat at 28 weeks. She has documented background retinopathy, so screen more frequently — pre-existing retinopathy carries a relative risk of progression of about 4.5, and rapid glycaemic normalisation from an HbA1c of 9.4 percent is itself a progression risk.^[5]
• Kidneys: serum creatinine with eGFR and repeat urine albumin-to-creatinine ratio. Her value of 14 mg/mmol indicates significant albuminuria, predicting preeclampsia, growth restriction and preterm birth; establish a baseline now so a later rise can be interpreted.^[1]
• Fetus: dating scan, first-trimester screening, a detailed anatomy scan at 18–20 weeks with dedicated fetal echocardiography, then serial growth scans with liquor from 28 weeks.^[3][8]
• Also credit: thyroid function, full blood count and ferritin, blood pressure monitoring plan, and a downloaded review of her glucose data rather than a verbal report.^[9]

(c) Counselling about risk to the baby (3 marks)

One mark for using her actual HbA1c as the modifier, one for the anomaly pattern, one for the population outcome figures. ^[2][3]

• Anchor the risk to her number. In a prospective series of 933 type 1 diabetic pregnancies, the risk of serious adverse pregnancy outcome — major malformation or perinatal death — rose significantly once periconceptional A1C exceeded 6.9 percent, and reached about 16 percent in women with A1C above 10.4 percent. At 9.4 percent she sits in the high-risk band.^[2]
• Name the anomaly pattern: neural tube defects, congenital heart disease (particularly conotruncal and septal lesions, the commonest group), renal tract anomalies, and caudal regression.^[3]
• Give the population figures: in the CEMACH-era population study, perinatal mortality was roughly four times and major congenital anomaly roughly double the background rate in women with type 1 or type 2 diabetes.^[3]
• Add the stillbirth figure: Victorian population data show a stillbirth relative risk of 2.68 in pre-existing diabetes, rising to about four in fetuses above the 97th centile.^[8]
• Be honest but not fatalistic: organogenesis risk is fixed, but improving control from now reduces macrosomia, stillbirth, preterm birth and neonatal morbidity — and that is why the next 30 weeks still matter.^[2][6]

(d) Insulin across the pregnancy and in labour (3 marks)

One mark for the trimester pattern, one for the intrapartum plan, one for the immediate postpartum reduction. ^[6][1]

• First trimester: requirements often fall between about 8 and 16 weeks; warn her about severe hypoglycaemia and hypoglycaemia unawareness, and teach her partner glucagon use.^[6]
• From 18 to 20 weeks: a steep rise driven by placental hormones; expect the total daily dose to double or more by the third trimester, titrating every 2 to 3 days against downloaded continuous glucose monitoring data.^[6][9]
• Late pregnancy: a plateau or modest fall is normal; a large unexplained fall warrants fetal assessment for placental insufficiency.^[6]
• In labour: variable-rate intravenous insulin infusion with concurrent dextrose, hourly capillary glucose, target 4 to 7 mmol/L.^[1]
• At delivery of the placenta: reduce immediately to approximately her pre-pregnancy dose, or roughly half the late-pregnancy dose. Warn about further hypoglycaemia with breastfeeding and advise carbohydrate before night feeds.^[1][6]

(e) Glycaemic management with betamethasone (2 marks)

One mark for anticipating the magnitude and duration, one for the monitoring and escalation plan. ^[7]

• Expect about 72 hours of hyperglycaemia and escalate insulin proactively, before the glucose rises, rather than chasing it.^[7]
• Expect a large increase. An Australian prospective cohort using an intensified protocol still measured median insulin requirement increases of 50 percent on day 1, 106 percent on day 2 and 133 percent on day 3, with only 35.3 percent of readings in target and no maternal hypoglycaemia — so older protocols using a fixed 25 percent bump are inadequate.^[7]
• Monitoring: hourly to two-hourly capillary glucose (or continuous glucose monitoring with alarms), with a low threshold to convert to a variable-rate intravenous insulin infusion if she is persistently above target or ketotic.^[7][1]
• Never withhold basal insulin, and check ketones — corticosteroids are a recognised precipitant of ketoacidosis in pregnancy.^[1]
• Alert the neonatal team, since maternal hyperglycaemia before birth predicts neonatal hypoglycaemia.^[6]