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Life in the Fast Lane • LITFL • Medical Blog

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Critical Care Compendium | Sodium Bicarbonate and Diabetic Ketoacidosis

Sodium Bicarbonate and Diabetic Ketoacidosis

by Chris Nickson, Last updated January 28, 2014

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.

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About Chris Nickson

FCICM FACEM BSc(Hons) BHB MBChB MClinEpid(ClinTox) DipPaeds DTM&H GCertClinSim

Chris is an Intensivist at the Alfred ICU in Melbourne and is an Adjunct Clinical Associate Professor at Monash University. He is also the Innovation Lead for the Australian Centre for Health Innovation and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He has 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 since completed further training in emergency medicine, clinical toxicology, clinical epidemiology and health professional education. 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 Lifeinthefastlane.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.

Reader Interactions

Comments

  1. itango2 says

    February 5, 2014 at 2:19 am

    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

    Reply
  2. Kuban Naidoo says

    June 12, 2015 at 7:16 am

    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.

    Reply
  3. Kuban Naidoo says

    June 12, 2015 at 7:22 am

    To add, the dextrose is added once serum glucose is less than 15mmol/l. Initially the fluid is as described without the dextrose.

    Reply

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