Sodium Bicarbonate and Diabetic Ketoacidosis

Reviewed and revised 28 January 2014

OVERVIEW

• The correction of the acidaemia in DKA is achieved by correcting the underlying pathophysiology with fluid replacement and insulin
• The role of sodium bicarbonate (NaHCO3) as a therapy for diabetic ketoacidosis (DKA) is controversial
• Different sources have different values for the cut off pH which requires treatment, and other sources advise against NaHCO3 use in DKA completely — there is no consensus

RATIONALE

Reasons proposed for use of sodium bicarbonate in DKA:

• treatment of severe acidaemia, which causes catecholamine resistance and myocardial depression
• treatment of severe hyperkalemia
• replacement of bicarbonate loss from Renal or GI tract — theoretical potential for giving HCO3- with renal wasting of HCO3- or GI loss if delta ratio is <1 (as is usual for DKA)
• ketoacids lost in urine (hence delta ratio <1) cannot be converted into HCO3-

DISADVANTAGES

Side effects of sodium bicarbonate

• Worsening of intracellular acidaemia
• hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-)
• hyperosmolality (cause arterial vasodilation and hypotension)
• volume overload
• rebound or ‘overshoot’ alkalosis
• hypokalaemia
• ionised hypocalcaemia
• impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve
• removal of acidotic inhibition of glycolysis by increased activity of PFK
• CSF acidosis
• hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis)
• severe tissue necrosis if extravasation takes place
• bicarbonate increases lactate production by:
  — increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis
  — shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues

EVIDENCE

• A 2011 systematic review by Chua et al found no evidence supporting the use of NaHCO3 in DKA
• High level evidence is lacking
• No evidence for the use of HCO3- to treat acidaemia or improve cardiac contractility
• Some evidence for the use of HCO3- in hyperkalaemia as a temporising measure, assuming underlying renal function is maintained
• Evidence suggests that HCO3- is associated with worse outcome  in paediatrics, in patients who presented sicker (lower PaCO2 and higher urea on presentation)
  — this may not be causative and paediatric patients can compensate for longer

CONCLUSION

• Do not use NaHCO3 routinely in the management of DKA
• Despite the lack of evidence many intensivists have a personal cut-off pH at which they consider giving HCO3- in severe acidemia due to DKA (typically < pH 6.9 to 7.1) as a ‘last ditch’ measure

References and Links

Journal articles

• Chua HR, Schneider A, Bellomo R. Bicarbonate in diabetic ketoacidosis – a systematic review. Ann Intensive Care. 2011 Jul 6;1(1):23. doi: 10.1186/2110-5820-1-23. PubMed PMID: 21906367; PubMed Central PMCID: PMC3224469.