Dear Editor, We read with great interest the recent publication of the BICARICU-2 trial, which investigated the use of intravenous sodium bicarbonate (NaHCO₃) in critically ill patients presenting with both, severe metabolic acidaemia potential of hydrogen (pH) ≤7.20 and moderate-to-severe acute kidney injury (AKI).1,2 The trial’s finding may not fully capture the benefit of NaHCO₃ therapy. The infusion of NaHCO₃ did not significantly reduce the 90-day all-cause mortality in this high-risk subgroup, despite reducing the need for renal replacement therapy (RRT), necessitating a clarification of the conceptual role of this therapy for your broad readership. The results of BICARICU-2 confirm a core principle of critical care pathophysiology: NaHCO₃ functions as a supportive, “bridging” therapy that addresses the effect (the low pH) without modifying the cause (the underlying disease, such as septic shock or multi-organ failure).3 Mortality is often cause-specific. The trial reinforces the hypothesis that mortality in critical illness is inextricably linked to the primary disease process. Infusing an exogenous buffer does not treat the source of lactate overproduction, the inflammatory cascade, or the ultimate organ damage that determines survival.4 Therefore, while mortality is an apposite but rigorous endpoint, it may be relatively insensitive to the effects of supportive therapies such as NaHCO₃ which do not directly modify the underlying disease process. The trial did, however, validate the intended bridging utility of NaHCO₃. The significant reduction in the need for RRT demonstrates that NaHCO₃ is highly effective at: a) Physiological stabilisation: Correcting the acute, severe acidaemia that often serves as a trigger for urgent RRT initiation;5 b) Delaying/avoiding intervention: Buying valuable time for the patient’s own renal function to potentially recover, thus avoiding the inherent risks, resource utilisation, and costs associated with RRT itself. The most crucial message for clinicians is that the neutral mortality finding should not lead to the abandonment of NaHCO₃ as a supportive tool. Instead, it should refine our expectations and indications. A) Avoid routine use: NaHCO₃ should not be administered routinely, expecting improved survival, especially given the risks of fluid/sodium overload, hypernatraemia, and paradoxical intracellular acidosis. B) Targeted use for physiological rescue: Intravenous NaHCO₃ should be reserved for selected situations of profound, life-threatening acidaemia (typically pH < 7.15), when the low pH itself is directly causing acute, correctable physiological derangements, such as impaired myocardial contractility, vasopressor-refractory hypotension, or severe hyperkalaemia, or to adjourn RRT while awaiting access or stabilisation, as demonstrated by the BICARICU-2 results. In these scenarios, bicarbonate functions as a temporary stabilising measure to correct pH-dependent physiological derangements while definitive treatment of the underlying cause is pursued. In conclusion, the BICARICU-2 trial provides critical evidence that NaHCO₃ is a powerful and successful physiological buffer and a valuable bridge to definitive care, but it is not an outcome-modifying drug. Clinicians should continue to use it strategically and selectively to manage the acute, dangerous consequences of acidaemia, recognising that the patient’s ultimate prognosis depends on the efficacy of treatments directed at the underlying cause of their critical illness. Disclosure of use of artificial intelligence (AI)-assistive or generative tools No artificial intelligence (AI) assistive or generative tools were used. Declaration of use of permitted tools We declare that we have not used any permitted tools. Author contributions PKB Concept. LB Write up. TK Literature search. All the authors have participated in the review, drafting and final approval of the manuscript. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
Bhattacharya et al. (Sun,) studied this question.