Endocrine Abstracts

Introduction: Diabetic ketoacidosis (DKA) remains a common presentation of type 1 diabetes (T1D) in children. During the COVID-19 pandemic, rates of presentation in DKA increased. Electrolyte abnormalities can occur during DKA treatment, but they are uncommon at presentation. We report a teenage girl with new-onset T1D presenting in severe DKA, complicated by profound hypokalaemia and hypernatremia.

Case Report: A previously healthy 13-year-old girl was admitted during the COVID-19 pandemic with 9-week history of polyuria, polydipsia, and weight loss. Initial laboratory findings showed: blood glucose 32 mmol/l, ketone 7 mmol/l, pH 7.06, bicarbonates 8.3 mmol/l; potassium 1.9 mmol/l, sodium 134 mmol/l. She showed severe dehydration, Kussmaul breathing and tachycardia (126 bpm); Glasgow coma scale (GCS) was initially 15. She also tested positive for Sars-Cov2, despite being asymptomatic. Following initial fluid management based on BSPED guidelines, potassium infusion was started via central line and rates increased to the maximum due to profound hypokalaemia (lowest value: 1.7 mmol/l), associated with runs of bradycardia (40-50 beats/min) and premature ventricular beats on ECG. Due to persistent hypokalaemia, intravenous insulin was delayed for 15 h, and started at a modified rate of 0.03 units/kg/h, once serum potassium was >2.5 mmol/l, and rates gradually increased in intensive care. Over the first 24 h, she remained acidotic, hypertensive and GCS dropped to 8. She was treated with hypertonic saline and mannitol due to suspicion of cerebral oedema. Over the next 24-32h, GCS gradually improved, and potassium levels normalised. However, corrected sodium increased up to 172 mmol/l. Thus fluids were changed to 0.45% saline and free water through NG commenced. Acidosis, ketosis and blood glucose gradually normalised. The girl made full recovery without any neurological deficit and discharged after 5 days on a basal-bolus insulin regimen.

Conclusions: This case highlights the challenges associated with profound hypokalaemia at DKA presentation, requiring delaying and reducing insulin infusion rates. It also underscores the importance of judicious use of hypertonic saline fluid in management of suspected cerebral oedema, especially if sodium levels are on the rise. The severity of the DKA episode in this patient may have been precipitated by the concomitant COVID-19 infection.