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:Â 21906367; PubMed Central PMCID:Â PMC3224469.
In particular about the pediatric DKA. The recommendation is strongly against NaCHO3
http://www.adanatriham.blogspot.com/2014/01/dka-and-cerebral-edema-are-fluids-to.html
Dear Chris. I am a paediatric intensivist and I use 60 mls of 8.4% NaHCO3 in 940 mls of 0.45% saline with 5% dextrose and 40 mmol of KPO4 to try to create a balanced solution for pts with DKA. Does this present a risk for cerebral oedema? I have never seen this described before.
To add, the dextrose is added once serum glucose is less than 15mmol/l. Initially the fluid is as described without the dextrose.