Endocrine Abstracts

Background: Children presenting with diabetic keto-acidosis (DKA) as an initial presentation of diabetes mellitus are often unwell, with associated increases in mortality and morbidity. While electrolyte imbalances such as hypokalaemia and hypophosphataemia are well recognised, the incidence of hypercalcaemia is less well documented.

Case: A previously healthy 12-year-old boy presented to hospital with a history suggestive of new onset diabetes. Initial bloods indicated DKA: pH 6.84, BE −28.9 and plasma glucose 30.4 mmol/l. Clinically he was severely dehydrated (estimated 8%). Despite standard management according to national guidelines he developed a reduced GCS, presumed secondary to cerebral oedema, requiring intubation and ventilation.

He remained severely acidotic, which was initially secondary to keto- and lactic-acidosis but was then propagated by hyperchloraemia. Over the next few hours he gradually developed acute severe hypercalcaemia, with maximum corrected calcium of 3.75 mmol/l. Possible causes for hypercalcaemia including hyperparathyroidism, malignancy, and thyrotoxicosis were ruled out. He developed mild-moderate renal failure (maximum creatinine 269 mmol/l). He was treated cautiously with rehydration as part of a neuro-protective strategy and latterly treated with frusemide infusion and hydrocortisone. Calcium levels and renal function normalised within a week.

Discussion: Potassium and phosphate disturbances are common in DKA, however significant abnormalities in calcium haemostasis are less common. Severe hypercalcaemia in DKA is likely due to diminished bone formation mediated in part by metabolic acidosis, paired with increased bone resorption due to severe insulin deficiency and metabolic acidosis. We suggest that calcium concentrations are checked routinely in all DKA patients.