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

Abstract

Introduction: Hyperchloraemic metabolic acidosis (HMA) can occur in diabetic ketoacidosis (DKA), from urinary loss of bicarbonate precursors as ketones, or iatrogenically from chloride administration.

Objective: To determine whether children with DKA given normal saline developed HMA, and whether HMA delayed their recovery.

Setting: 13 Bed combined Paediatric Intensive Care/High Dependency Unit.

Methods: 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.

Results: 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.

Conclusion: 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.