Hyperchloraemic metabolic acidosis slows recovery in children with diabetic ketoacidosis: A retrospective audit

Abstract

Hyperchloraemic metabolic acidosis (HMA) can occur in diabetic ketoacidosis (DKA), from urinary loss of bicarbonate precursors as ketones, or iatrogenically from chloride administration. To determine whether children with DKA given normal saline developed HMA, and whether HMA delayed their recovery. 13 Bed combined Paediatric Intensive Care/High Dependency Unit. Retrospective analysis of the venous biochemistry of 59 admissions with DKA, recording the times to recovery from acidosis and normalisation of anion gap, and total intravenous chloride load. Twenty-nine (49%) were newly diagnosed diabetics. The median age was 12 (interquartile range, IQR 8.2-15.4) years. The initial pH in 23 (39%) was <7.1. The median times to achieve pH>7.3, bicarbonate>15mmol/l and anion gap<16.1 were 14.2h (IQR 8.6-20.1), 12.9h (IQR 8.6-20.0) and 10.7h (IQR 8.2-15.0) respectively. For individual patients, the median difference between recovery times for bicarbonate and anion gap was 0.18h (IQR 0-5.3), p=0.0005. However, in 14 patients (24%), the difference was >6h. These patients did not differ significantly in age or initial pH but had a lower initial bicarbonate (median 5 versus 7.8mmol/l, p=0.002), narrower anion gap (median 29.5 versus 31.6mmol/l, p=0.038), and took longer to normalise the bicarbonate: median 26.1 versus 10.5h, p<0.0001. They tended to be newly diagnosed presentations. The anion gap (AG) normalises earlier than bicarbonate in children with DKA treated with normal saline, and children with persisting HMA recover from acidosis more slowly.