Diabetic ketoacidosis in pregnancy — structured SAQ (15 marks)

(a) Working diagnosis and immediate investigations (4 marks)

One mark for the diagnosis with the euglycaemia caveat, one for the ketone test, one for the gas, one for the remaining bloods and the precipitant work-up. ^[1][3]

• Diabetic ketoacidosis, probably euglycaemic. Her glucose of 10.4 mmol/L is below 11.1 mmol/L, but she has known diabetes, so the 2024 consensus criteria still apply. Up to about 35 percent of pregnancy cases are euglycaemic.^[1][3]
• Capillary or venous beta-hydroxybutyrate — 3.0 mmol/L or more confirms significant ketonaemia. Do not rely on urine dipstick, which measures acetoacetate and underestimates ketosis early.^[1]
• Venous blood gas — pH below 7.30 or bicarbonate below 18 mmol/L confirms the acidosis. Remember maternal bicarbonate is physiologically low at about 18 to 22 mmol/L, so a "borderline" value is significant.^[1][6]
• Urea, electrolytes and creatinine with potassium, full blood count, lactate, calculated anion gap.^[1]
• Precipitant work-up: urine culture, blood cultures, assessment for chorioamnionitis, and a medication chart review.^[4]
• Continuous CTG and left lateral tilt; she is 31+4 weeks so the fetus is viable and monitored, but the trace is data, not an instruction.^[2]

The triad to write out for full marks: ^[1]

(b) Resuscitation in the first hour (5 marks)

One mark each for: fluid with a rate; insulin with a rate; the potassium rule; dextrose timing; and treating the precipitant plus escalation of care. ^[1]

• Fluid. Isotonic saline or a balanced crystalloid at 500 to 1000 mL/h for the first 2 to 4 hours, then correct the remaining deficit over 24 to 48 hours. Reassess after every litre — pregnancy is specifically named in the consensus as a state requiring caution about fluid overload.^[1]
• Insulin. A fixed-rate intravenous infusion of short-acting insulin at 0.1 units/kg/h, started as soon as the diagnosis is made. An initial 0.1 units/kg bolus only if intravenous access will be delayed. Continue her usual subcutaneous basal insulin alongside the infusion.^[1]
• Potassium — by the number.^[1]

• Dextrose. Add 5 to 10 percent dextrose once glucose falls below 13.9 mmol/L and reduce insulin to 0.05 units/kg/h. In this euglycaemic presentation, start dextrose at the same time as the insulin — she is already below that threshold.^[1][3]
• Precipitants and escalation. Stop the salbutamol. Continue proactive insulin escalation for the betamethasone effect. Treat any infection. Escalate to a high-dependency or delivery-suite bed with one-to-one nursing, and involve the physician or endocrinologist, anaesthetics and the neonatal team.^[4][5][1]
• Monitoring. Glucose hourly, beta-hydroxybutyrate every 1 to 2 hours, potassium at 2 hours then 4-hourly, continuous CTG.^[1]
• Do not give bicarbonate unless the pH is below 7.0.^[1]

(c) Response to the suggestion of immediate caesarean (3 marks)

One mark for the principle, one for the mechanism, one for naming the genuine exceptions. ^[2][6]

• The principle: correct the mother first. The fetal heart rate abnormality of maternal ketoacidosis usually recovers as maternal volume, glucose and acid–base status are corrected. Operating now converts one critically unwell patient into two.^[2]
• The mechanism: maternal ketones and hydrogen ions cross the placenta, maternal hypovolaemia and acidosis reduce uteroplacental perfusion, and maternal acidaemia impairs fetal oxygen delivery. Correct those and the trace improves.^[2][6]
• The anaesthetic argument: she is acidotic, volume-depleted and potentially hypokalaemic. General or regional anaesthesia in that state risks cardiovascular collapse and arrhythmia.^[6]
• The genuine exceptions, which you must name: a trace that does not recover after several hours of adequate maternal correction; a separate obstetric indication such as abruption, chorioamnionitis or severe preeclampsia; or maternal deterioration despite maximal therapy.^[2]
• Say the plan out loud: "Resuscitate hard, monitor continuously, review the trace against her biochemistry hourly, and involve the consultant now so the delivery decision is shared and documented."^[2]

(d) Precipitants and what you would have done differently (2 marks)

One mark for identifying the precipitants, one for the preventive change. ^[4][5]

• Precipitants here: vomiting, antenatal betamethasone, and intravenous salbutamol — plus the possibility of infection triggering the preterm labour. In the UK national cohort, vomiting and infection each accounted for 21 percent of episodes and steroid therapy for 13 percent.^[4]
• What I would have done differently: avoid a beta-agonist tocolytic in a woman with type 1 diabetes and use nifedipine instead; escalate insulin proactively before the betamethasone rather than reactively afterwards; and start hourly to two-hourly glucose with ketone testing from the first dose.^[5][2]
• Quote the size of the steroid effect: 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, so a fixed 25 percent increase is inadequate.^[5]

(e) Before discharge (1 mark)

One mark for a prevention plan with at least three concrete elements. ^[4][8]

• Written sick-day rules: never stop basal insulin, test ketones when unwell, increase insulin rather than reduce it, keep fluids and carbohydrate going, present early.^[8]
• A ketone meter and strips, and a phone number that reaches a clinician.^[4]
• A documented steroid plan for any future admission, review of the insulin regimen rather than restarting it unchanged, diabetes team follow-up, and social or mental-health support where relevant — 15 percent of women in the UK cohort had a second episode in the same pregnancy.^[4][5]