Critically evaluate the  use of sodium bicarbonate therapy in Diabetic Ketoacidosis

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College Answer

Critically   evaluate   the   use   of   sodium   bicarbonate   therapy   in   Diabetic

•    Definition of DKA and it pathophysiological consequences
•    The possible rationale for the use of sodium bicarbonate
o   Severe acidaemia (generally pH < 7.10 although no hard data)
o   Severe hyperkalemia
o   Bicarbonate loss from Renal or GI tract
•    The possible problems of giving sodium bicarbonate
o   Worsening of intracellular acidaemia
o   Hypokalaemia & Hypernatraemia
o   Large bolus of hypertonic solution
•    No  evidence   for  the  use  of  HCO3-    to  treat  acidaemia,   or  improve   cardiac contractility. In fact many different texts have different values for the cut off pH which
requires treatment, suggesting no real consensus.
•    The   correction   of   the   acidaemia   is   achieved   by   correcting   the   underlying pathophysiology with fluids and insulin
•    Some evidence for the use of HCO3-  in hyperkalaemia,  as a temporising measure, assuming underlying renal function is maintained
•    Theoretical potential for giving HCO3-  with renal wasting of HCO3-  or GI loss if delta ratio is <1 (usual for DKA)
•    Evidence suggesting that HCO3- is associated with worse outcome, however this in paediatrics, in patients who presented sicker (lower PaCO2 and higher urea on presentation).  However this does not assume causality and paediatric patients can compensate for longer.
•    Despite the lack of evidence it would appear that most intensivists have a personal cut-off pH at which they consider giving HCO3-


The "critically evaluate" questions should be approached in a structured manner.


  • DKA is a systemic illness associated with impaired glucose metabolism due to a lack of insulin (in IDDM) or due to insulin resistance (NIDDM). The decreased oxidative phosphorylation of glucose leads to a switch in metabolism, favouring lipolysis and the use of fatty acids for the purpose of ketone body synthesis. The ketone bodies dissociate into a conjugate base and hydrogen ion, acting as acids and thereby inducing acidosis.

Rationale for this practice

  • Sodium bicarbonate is an alkaline compound used to correct metabolic acidosis; it acts as an exogenous source of bicarbonate buffer, and titrates the pH of the body fluids.
  • The administration of bicarbonate in metabolic acidosis is expected to reverse the physiological disadvantages of acidosis, including cardiovascular instability
  • Ketones in DKA are lost in the urine and therefore cannot be metabolised (which would absorb the H+ ion ) - the urinary loss of ketones therefore represents the urinary loss of bicarbonate, and exogenous bicarbonate needs to be given to replace this.


  • Return of pH to normality = restoration of normal cellular enzyme function
  • Normalisation of pH also restores normal catecholamine receptor-ligand affinity relationships, resulting in the improvement of haemodynamic performance.
  • Administration of Na+ cations results in an increase of the strong ion difference, which maintains the improvement in pH.
  • In the event of severe hyperkalemia, sodium bicarbonate administration causes a intracellular shift of potassium, which may be useful in the context of DKA.


  • Return of pH to normality may be unnecessary, as many intracellular mechanisms of compensation for acidosis function optimally in the presence of acidosis. For instance, ketone body and lactate metabolism are delayed by bicarbonate administration.
  • The administration of hyperosmolar solution may result in fluid shifts of significant magnitude, particularly dangerous in those patients who have significant cardiac comorbidities.
  • The administration of a large volume of sodium bicarbonate to an already hypokalemic patient may result in worsening hypokalemia and cardiac arrest
  • Sodium bicarbonate may be converted to CO2 and internalised into cells, where it may counterproductively cause an intracellular acidosis.
  • Sodium bicarbonate may be rapidly turned into CO2 by the act of buffering, and thus may increase PaCO2 contributing to respiratory acidosis.
  • Oveshoot may occur, resulting in metabolic alkalosis
  • The alkalinisation of body fluid will result in a decrease in the ionised fraction of Ca++ leading to tetany and muscle spasm
  • Rapid correction of acidosis with bicarbonate may impair oxygen delivery to tissues resulting in tissue hypoxia (by counteracting the rightward shift of the oxyhemoglobin dissociation curve, which is the result of acidosis).

Evidence against the use of bicarbonate in DKA

Own practice

  • The only situations in which I personally would give bicarbonate for DKA:
    • Haemodynamic instability with escalating vasopressor requirements, coupled with a blood gas pH of less than 7.00
    • A serum bicarbonate level which is approaching 0, suggesting that the endogenous buffer systems are all but depleted.


This LITFL article offers a balanced and concise overview of this topic.

Chua, Horng Ruey, Antoine Schneider, and Rinaldo Bellomo. "Bicarbonate in diabetic ketoacidosis-a systematic review.Annals of intensive care 1.1 (2011): 1-12.

Hale, P. J., J. Crase, and M. Nattrass. "Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis." British medical journal (Clinical research ed.) 289.6451 (1984): 1035.

Soler, N. G., et al. "Potassium balance during treatment of diabetic ketoacidosis with special reference to the use of bicarbonate." The Lancet300.7779 (1972): 665-667.

Duhon, Bryson, et al. "Intravenous sodium bicarbonate therapy in severely acidotic diabetic ketoacidosis." Annals of Pharmacotherapy 47.7-8 (2013): 970-975.

Okuda, Y. U. K. I. C. H. I., et al. "Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis." The Journal of Clinical Endocrinology & Metabolism 81.1 (1996): 314-320.