The Role of Bicarbonate Therapy in Diabetic Ketoacidosis: A Systematic Review and Meta-Analysis.

Abstract

<h4>Background</h4>Diabetic ketoacidosis (DKA) is a severe diabetes complication managed with fluids, insulin and electrolyte correction. This review evaluates the debated effectiveness of bicarbonate therapy on DKA outcomes.<h4>Methods</h4>Following PRISMA guidelines, we systematically reviewed studies on bicarbonate therapy in DKA. We searched PubMed, Google Scholar, the Cochrane Library and ClinicalTrials.gov (as of August 2024), including studies on patients with DKA. Meta-analysis was conducted using RevMan. Bias risk was assessed with the Newcastle-Ottawa Scale (NOS) for cohort studies, Cochrane's ROB-2 for RCTs and the Joanna Briggs Institute (JBI) Scale for case series. Prospero ID: CRD42024581810.<h4>Results</h4>Eight studies, including 646 patients, met the inclusion criteria. Participants' mean ages spanned from approximately 9.7 years to 45.8 years. Bicarbonate therapy did not significantly improve pH levels (mean difference = -0.02, 95% CI [-0.13, 0.09], p = 0.7), time to resolution of acidosis (mean difference = 0.09 h, 95% CI [-2.6, 2.79], p = 0.95) or potassium levels (mean difference = -0.10, 95% CI [-0.49, 0.29], p = 0.61). Bicarbonate therapy was associated with a marginally longer duration of hospital stay (mean difference = 13.63 h, 95% CI [0.23, 27.03], p = 0.05), although the overall effect size was small. No significant difference was observed in the incidence of hypoglycemia (odds ratio = 2.62, 95% CI [0.59, 11.63], p = 0.20). High heterogeneity was observed across most outcomes, mainly due to variability in study protocols and patient populations.<h4>Conclusion</h4>Bicarbonate therapy provided no meaningful clinical benefit in the routine management of DKA and was associated with potential harm, including worsened hyperglycemia. Consistent with current guidelines, its use should be restricted to cases of severe acidemia (pH < 6.9). Further high-quality studies are needed to clarify its role in extreme acidosis and to explore alternative buffering strategies.