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Correspondence  |   February 2000
Saline Infusion, Acidosis, and the Stewart Approach
Author Notes
  • Staff Anaesthetist
  • Department of Anaesthesia
  • davids@austin.unimelb.edu.au
  • Staff Anaesthetist
  • Department of Anaesthesia
  • Associate Professor
  • Intensivist and Director of Research
  • Department of Intensive Care
  • Austin and Repatriation Medical Centre
  • Austin Hospital
  • Heidelberg
  • Melbourne, Victoria 3084, Australia
Article Information
Correspondence
Correspondence   |   February 2000
Saline Infusion, Acidosis, and the Stewart Approach
Anesthesiology 2 2000, Vol.92, 624. doi:
Anesthesiology 2 2000, Vol.92, 624. doi:
To the Editor:—
The report by Scheingraber et al.  1 highlights the phenomenon of acidemia after infusion of 0.9% saline in the perioperative period. The accompanying editorial 2 discusses several relevant points; however, we are disappointed that neither the article nor the editorial addresses the central issue of the relative merits of the Stewart approach 3 in describing acid–base physiology and pathophysiology.
Compared with the Henderson-Hasselbalch approach, the Stewart approach has a number of appealing features. (1) The control of acid–base and water homeostasis can be explained in terms of both sodium and chloride regulation. (2) Acid–base status is partly controlled by a number of plasma electrolytes, notably sodium and chloride. These electrolytes can be manipulated in the clinical setting to optimize acid-base status. (3) The factors controlling acid–base status are independent. Criticisms of the Henderson-Haselbalch approach include a lack of independence between carbon dioxide and bicarbonate. 4 (4) The Henderson-Hasselbalch approach does not allow assessment of nonvolatile buffers, whereas the Stewart approach explicitly includes assessment of weak acids. 4 
Comparison of the Stewart and Henderson-Hasselbalch approaches is complicated by the fact that both approaches adequately describe the acid–base end point, as Scheingraber et al.  demonstrate. 1 Further study is required to determine which approach better describes the mechanisms of acid–base physiology.
Previous animal studies 5 have suggested that the alkalinizing effect of lactate-containing solutions in acute resuscitation is time dependent, which underscores the concept of lactate as a strong ion. The removal of lactate from the circulation will increase the strong ion difference and reduce acidosis. 3 This effect may be supplemented by further increases in the strong ion difference associated with lactate metabolism 6; in contrast, added chloride ions appear to persist longer in the circulation. Subsequently, a smaller strong ion difference is maintained along with greater acidosis, as seen in the report by Scheingraber et al.  1 
References
Scheingraber S, Rehm M, Sehmisch C, Finsterer U: Rapid saline infusion produces hyperchloremic acidosis in patients undergoing gynecologic surgery. A NESTHESIOLOGY 1999; 90:1265–70Scheingraber, S Rehm, M Sehmisch, C Finsterer, U
Prough DS, Bidani A: Hyperchloremic metabolic acidosis is a predictable consequence of intraoperative infusion of 0.9% saline (editorial). A NESTHESIOLOGY 1999; 90:1247–9Prough, DS Bidani, A
Stewart PA: Modern quantitative acid-base chemistry. Can J Physiol Pharmacol 1983; 61:1444–61Stewart, PA
Fencl V, Leith DE: Stewart’s quantitative acid-base chemistry: Applications in biology and medicine. Respir Physiol 1993; 91:1–16Fencl, V Leith, DE
Traverso LW, Lee WP, Langford MJ: Fluid resuscitation after an otherwise fatal hemorrhage: I Crystalloid solutions. J Trauma 1986; 26:168–75Traverso, LW Lee, WP Langford, MJ
White SA, Goldhill DR: Is Hartmann’s the solution? Anaesthesia 1997; 52:422–7.White, SA Goldhill, DR