mostly close to target and HbA1c was 6.6%. However, after that visit she failed to attend for her scheduled joint diabetes antenatal clinic review appointments and could not be contacted by the diabetes specialist midwife or her family doctor.
On initial assessment her pulse was 118 bpm, blood pressure 76/42 mmHg, respiratory rate 26 breaths/min, and Glasgow coma score (GCS) 8. There were no pointers to infection. Emergency bloods revealed blood glucose 33.2 mmol/L (603.6 mg/dL), urea 24.2 mmol/L (67.8 mg/ dL), creatinine 186 ฮผ mol/L (2.10 mg/dL), sodium 146 mmol/L (146 mEq/L), potassium 5.1 mmol/L (5.1 mEq/L), hemoglobin 13.4 g/L (1.34 g/dL), white cell count (WCC) โฒ 19.7 ร 10 6 /mL, pH 6.94, venous bicarbonate 4 mmol/L (4 mM), base excess -24, pO 2 25 kPa (on high -fl ow oxygen), and pCO 2 2.3 kPa. The friend who accompanied her to A & E reported that she had been depressed, had stopped testing her blood glucose, and had been taking her insulin only erratically.
A nasogastric tube was passed and 1.5 L of gastric content drained. One liter of plasma expander was infused over 30 minutes. Blood pressure rose to 90/48 mmHg and pulse reduced to 110 bpm. Urinary catheterization released 200 mL of concentrated urine containing ketones +++.
She was commenced on a standardized DKA protocol involving fl uid, insulin, and electrolyte replacement with frequent biochemical monitoring. Tinzaparin 4500 U was started subcutaneously (SC) once daily. By 12 hours from admission GCS was 15, nasogastric drainage had ceased, her pulse rate was 90 -100 bpm, and blood pressure 100 -110/60 -70 mmHg. Bedside capillary blood glucose was consistently in the range 5 -8 mmol/L (90 -145 mg/dL), venous pH was 7.32, and creatinine normal.
The fi rst dose of basal insulin was then administered while the nasogastric tube and urinary catheter were withdrawn. Intravenous (IV) fl uids and insulin were con-184 PRACTICE POINTS โข Diabetic ketoacidosis (DKA) is a very serious complication of pregnancy that threatens the mother ' s life and the health and viability of the fetus. โข DKA only occurs in situations of severe insulin defi ciency combined with increases in catabolic hormones. The metabolic physiology of pregnancy predisposes to DKA. โข Patients present with weakness, hypotension, vomiting, and abdominal pain. The diagnosis is confi rmed if there is hyperglycemia, ketonemia, and anion gap acidosis. โข To prevent hypovolemic shock, aspiration, cardiac dysrhythmias, thromboembolism or cerebral edema, prompt management, including fl uid and electrolyte replacement, insulin, airway protection, heparin and rigorous monitoring are essential. โข DKA in pregnancy is preventable if monitoring is intensive and corrective action prompt.