- 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
Reasons proposed for use of sodium bicarbonate in DKA:
- treatment of severe acidaemia, which causes catecholamine resistance and myocardial depression
- treatment of severe hyperkalaemia
- 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-
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
- 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
- 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
- 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
- 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. PMC3224469.
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health, a Clinical Adjunct Associate Professor at Monash University, and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of LITFL.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of two amazing children.
On Twitter, he is @precordialthump.