Chua HR, Schneider A, Bellomo R. Bicarbonate in diabetic ketoacidosis – a systematic review. Ann Intensive Care. 2011;1(1):23.

What We Already Know About the Topic

DKA is either a absolute or relative deficiency of insulin. Ketones are generated with the liver’s metabolism of free fatty acids. Accumulation of anions occurs through various mechanisms with severe dehydration as clinical manifestation. Sulphate, urate and phosphate are accumulated.

Metabolic acidemia has prompted some physicians to administer bicarbonate given the thought process that a base is required to reverse an acidosis.

The concern is that side effects of bicarbonate (namely intracellular worsening of acidosis) outweigh the potential benefits in acidemia.

Why is This Study Important?

Looked not only at important outcomes like mortality and hospitalization, but also looked at physiolgical data like acidosis or ketosis resolution.

Purpose (PICO format)

Adult and pediatric patients with DKA treated with bicarb or no bicarb for emergent treatment; outcomes were mortality and hospitalization duration.


Multiple centers


Systematic search by two investigators identified 508 potentially relevant citations. Any disagreements were adjudicated by a third independent investigator.

Outcome Measures

Primary outcomes of length of hospitalization and mortality. Secondary outcomes of resolution of acidosis, ketosis, potassium balance, tissue oxygenation, CSF acidosis, neurologic deterioration, and hemodynamic parameters.

Inclusion Criteria

Adult and pediatric patients with DKA and treated with bicarbonate were reviewed for inclusion

Exclusion Criteria

No review articles

No commentaries/letters/editorials

Articles not related to cerebral edema, bicarb, or acid/base in DKA


Of the 508 potentially relevant articles, 44 were selected and reviewed. There was only one double-blinded RCT and two nonblinded RCTs; the majority of studies were case-controlled studies.

No apparent impact on LOS; also, no published study in bicarb in DKA was able to comment on mortality–though, most studies excluded the severely ill DKA (i.e. severe metabolic acidemia).

The studies that seemed to see physiological benefit in RCTs found improved pH and bicarb levels at 2h; however, 24h later, there was no difference.

Paradoxical worsening of ketonemia; specifically, slower decline in the ketonemia in the first hour of bicarbonate infusion.

Variable results on the potassium or rate of decline in blood lactate. Furthermore, there was a variable, non-statistically significant difference in CSF pH and bicarb levels within 24 hours in bicarb and control groups.

A small number of the analyzed studies included outcomes like neurologic performance or hemodynamics but found no significant differences.


Most of the studies included in this systematic review excluded critically ill/severe metabolic acidemia DKA cases. The pH threshold for bicarbonate administration varied between < 7.00 to < 7.20. Dosages varied with more recent dosing strategies 120-150 mmol for adults. More recent studies were preferentially using slow infusions of half-isotonic or isotonic preparations (approx 1%) or small intermittent boluses.

Conclusions of the Authors of the Study

Data heterogenous and without clear signal for benefit in bicarbonate administration for DKA; potential for worsening ketonemia and requirements for potassium. However, there could be a transient improvement in acidosis without clinical outcome changes.

Take Home Points for Us

The potential for worsening ketonemia and potassium requirements seems minor; furthermore, bicarb’s transient improvement in acidosis bears no clinically relevant outcome. The minor, transient improvement in pH could be useful in severe acidemia as a brief temporizing measure in rare situations but remains unproven.

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