Severe Metabolic Acidosis in Intensive Care: Implications for Acute Kidney Injury, Bicarbonate, and Renal Replacement Therapy

Severe metabolic acidosis is a frequent finding in the intensive care unit (ICU) and a critical marker of clinical severity and organ dysfunction, closely linked to acute kidney injury (AKI) due to shared physiological mechanisms and the loss of the kidney’s ability to maintain acid-base homeostasis. Therefore, it represents the biochemical expression of heterogeneous pathophysiological mechanisms related to acid-base balance. These include tissue hypoperfusion, sepsis, mitochondrial dysfunction, accumulation of unmeasured anions, bicarbonate loss, and reduced renal excretion of the acid load. Its presence is associated with increased mortality, greater vasopressor and mechanical ventilation requirements, prolonged ICU stay, and a higher likelihood of renal replacement therapy (RRT). However, pH correction alone does not guarantee clinical improvement. Therefore, contemporary management prioritizes the etiology, severity of the acidemia, and hemodynamic status. In this context, sodium bicarbonate plays a limited and selective role, particularly in severe acidemia with advanced AKI or hyperkalemia, or as temporary supportive therapy while the underlying cause is corrected or extracorporeal support is arranged. Similarly, RRT should be reserved for refractory cases and should not be initiated based solely on isolated pH thresholds. This review analyzes the definition, epidemiology, clinical implications, pathophysiology, and therapeutic strategies for severe metabolic acidosis in critically ill patients, with emphasis on its interaction with AKI, the rational use of bicarbonate, and the timing of RRT initiation.