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Should bicarbonate be used to treat metabolic acidosis? A study examining the evidence
Summarized from Fujii T, Udy A, Licari E et al. Sodium bicarbonate therapy for critically ill patients with metabolic acidosis: a scoping and systematic review. J Critical Care 2019; 51: 184-191
Metabolic acidosis – defined as a decrease in blood pH consequent on primary reduction in plasma bicarbonate concentration – is diagnosed by the following findings on arterial blood gas analysis: reduced pH, reduced bicarbonate and increased base deficit; compensatory decrease in pCO2 may also be a feature.
This disturbance of acid-base balance is a frequent finding among the critically ill; common causes include sepsis, lactic acidosis and diabetic ketoacidosis.
It is common practice to administer replacement bicarbonate buffer in the form of intravenous sodium bicarbonate to critically ill patients with metabolic acidosis on the assumption that the intended restoration of blood pH is therapeutically beneficial. Despite its relatively widespread use, the role of exogenous sodium bicarbonate therapy in the generality of critically ill patients with metabolic acidosis is controversial. This recently published literature review study addresses that controversy.
The stated aim of study was to “assess the biochemical and physiological effects, clinical efficacy, and safety of sodium bicarbonate therapy in critically ill patients with acute metabolic acidosis”.
Study investigators adopted two literature review searching strategies: a scoping review to assess the biochemical and physiological effects of sodium bicarbonate administration; and a systematic review to assess its clinical efficacy.
Extensive library research of the voluminous body of published studies on the use of sodium bicarbonate in metabolic acidosis revealed 12 studies that fulfilled the investigators eligibility criteria for assessment of biological and physiological effects of sodium bicarbonate administration; and two clinical trials that fulfilled their eligibility criteria for assessment of its clinical efficacy.
Analysis of the 12 studies used to asses biological and physiological effects revealed that sodium bicarbonate administration results in increase in pH, serum bicarbonate, base excess, pCO2 and serum sodium, along with concomitant reduction in serum potassium and anion gap. Seven of the studies provided data that allowed calculation of the rate of increase in pH (0.04 pH units/hr) and base excess (1.6 mmol/L/hr).
Limited, somewhat conflicting, data relating to change of three other biochemical parameters (serum chloride, ionized calcium and pO2) is presented graphically in the study report along with the more robust data relating to the previously mentioned biochemical parameters.
Just two randomized controlled trials were judged eligible for assessment of the efficacy of sodium bicarbonate therapy. The first, published in 2005, involving just 18 patients who were randomized to receive either a single dose of 1 mol/L sodium bicarbonate over a period of 1 hour or alternative buffer treatment (0.3 mmol/mL THAM acetate). The second, published in 2018, involved 400 patients randomized to receive either repeated doses of 0.5 mol/L sodium bicarbonate over 30 minutes or no treatment.
Since only the second of these two trials reported their predefined outcomes, the authors were unable to perform pooled analysis. The relative risk for all-cause mortality in the second trial was 0.83 (95 % confidence interval, 0.68, 1.02) and renal replacement therapy was used less frequently in the bicarbonate group. These two broadly positive efficacy findings of the trial, however, are negated somewhat by the finding that bicarbonate therapy was associated with increased risk of hypocalcemia and hypokalemia requiring treatment (respective relative risks, 1.65 and 1.14). Data relating to any efficacious or deleterious effect on hemodynamic parameters was lacking. Overall statistical analysis revealed that certainty of the clinical efficacy of sodium bicarbonate was low.
In discussion of their study, the authors provide some detail of some of the many other studies of bicarbonate therapy in metabolic acidosis that did not meet their eligibility criteria.
Overall the authors of this study conclude that they found limited data to assess the biochemical and physiological effect of sodium bicarbonate therapy and that the lack of robust randomized trials prevents any conclusion regarding its clinical efficacy. They suggest that further research is justified and necessary, given the continued widespread use of the therapy. Apparently, the controversy remains unresolved.
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