BSPED2024 Poster Presentations Miscellaneous/Other 1 (9 abstracts)
Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom
An 8-year-old girl presented with a new diagnosis of diabetes mellitus in severe diabetic ketoacidosis (DKA) (pH 6.8, BE -31.5 mmol/l, glucose 25 mmol/l, ketones 4 mmol/l). She had abdominal pain, vomiting, and Kussmaul breathing on a background of osmotic symptoms for a few months. She was treated with fluid resuscitation, replacement fluids and intravenous insulin in the high dependency setting. Initial laboratory sodium levels were low, 122 mmol/l (corrected for glucose 17.1 mmol/l) and plasma reported to have a milky appearance due to severe hypertriglyceridaemia (HTG) 187.5 mmol/l (0.55-1.9 mmol/l). Haemoglobin A1c was 131 mmol/ mmol. Correction of the perceived hyponatraemia with hypertonic saline was avoided as parallel blood gas sampling sodium was 152 mmol/l. Adjusting the laboratory sodium of 122 mmol/l for the triglyceride level of 187.5 mmol/l, would have given a value of 155 mmol/L, a 33 mmol/L difference. Acute pancreatitis was suspected as she developed worsening abdominal pain requiring morphine. Serial amylase rose from 234 IU/l to 375 IU/l (25-125 IU/l) and lipase was elevated 545 IU/l (8-78 IU/l). The visualised portions of the pancreas were not inflamed on ultrasound. Severe HTG is a rare but serious complication of DKA, where insulin deficiency results in lipolysis and release of free fatty acids. Very low-density lipoprotein production is increased in response to free fatty acid uptake by the liver, resulting in HTG. HTG-induced acute pancreatitis is well reported in adults, but less established in the paediatric population. Pancreatitis can lead to septic shock and multiorgan failure. In this case, a higher rate of intravenous insulin infusion (0.1units/kg/hour) was sufficient to treat HTG, however refractory cases may require plasmapheresis. Probable pancreatitis was successfully treated with conservative management (piperacillin/tazobactam, proton pump inhibitor and low-molecular-weight heparin) and correction of HTG. This case highlights the potential for lipaemia to interfere with indirect laboratory electrolyte assays, a phenomenon known as the electrolyte exclusion effect, describing falsely low electrolyte concentrations in the presence of severe lipaemia. It is important that lipaemia is recognised quickly, due to the risk of HTG-induced acute pancreatitis, and the interpretation of laboratory assays which should be adjusted for lipaemia. If in doubt, direct blood gas assays should be used.