Treatment of acute non-anion gap metabolic acidosis

Abstract

Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acid–base disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide might be less frequent than in high anion gap metabolic acidosis because of better tissue perfusion and the ability to eliminate carbon dioxide. Further basic and clinical research is needed to facilitate development of evidence-based guidelines for therapy of this important and increasingly common acid–base disorder.

Metabolic acidosis during parenteral nutrition: Pathophysiological mechanisms

“…However, when there is a strong indication for TPN administration, the use of newer solutions could reduce the incidence of MA because they contain a higher concentration of organic acid anions (potential base). [ 36 ] Nonetheless, MA represents a potentially dangerous problem in those patients receiving TPN and presenting with conditions as diarrhea or proximal renal tubular acidosis due to increased bicarbonate loss, acute or chronic renal failure due to decrease acid excretion and various forms of shock due to lactic accumulation. Therefore, close monitoring of parameters that are evolved in the assessment of acid-base balance disturbance is necessary in order to achieve the early correction of MA.…”

Removal of urea by electro-oxidation in a miniature dialysis device: a study in awake goats

“…This reduction in plasma bicarbonate concentration was accompanied by an increase in plasma chloride of a similar magnitude. The most likely explanation for this combination (hyperchloremic metabolic acidosis) is the intravenous infusion of solutions that exclusively contained chloride as an anion (16), although minor chloride release across the dialyzer (only in experiments with 2 units) probably related to the exchange of phosphate and organic acids for chloride in the FeOOH beads, may have played a role. No influence on pH was observed, which was due to a coinciding decrease in arterial PCO 2 , probably because of stress-induced hyperventilation which increased during the experiment while the effect of the sedatives wore off.…”

Etiology and Management of Acute Metabolic Acidosis: An Update

“…Firstly, increased CO 2 production requires ventilatory compensation. Secondly, bicarbonate administration lowers the intracellular pH [43], most likely as a result of increased CO 2 transfer into the intracellular compartment. Finally, bicarbonate infusion has been shown to even elevate systemic lactate levels [44].…”