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Hyperchloremic Acidosis

Wilkes, Nicholas J.; Mallett, Susan V.; Mythen, Michael G.

doi: 10.1097/00000539-200212000-00076
LETTERS TO THE EDITOR: Letters & Announcements
Free

Centre for Anaesthesia

Royal Free and University College Medical School

London, United Kingdom

In Response:

The development of hyperchloremic metabolic acidosis after infusion of sufficiently large volumes of saline or saline-based colloid solutions is reproducible and perhaps not surprising.

Dr. Parekh’s letter lends support to the suggestion that the diagnosis of hyperchloremic acidosis may result in undesirable intervention. This may be the inappropriate administration of further intravenous fluids with a high chloride content, aggravating rather than improving the condition.

The diagnosis of hyperchloremic metabolic acidosis, of course, constitutes a biochemical finding. It is fair play to ask whether this type of acidosis is benign and self-limiting, or whether it is clinically relevant and should be treated or—better yet—prevented. Evidence for improved primary or secondary outcome variables in the absence of hyperchloremic metabolic acidosis is now emerging. In our study, the administration of crystalloids and colloids of more balanced composition resulted in better gastrointestinal perfusion than infusion of saline-based fluids (1). Such a finding has been related to better outcome in another study (2). Improved gut perfusion may also contribute to the prevention of postoperative nausea and vomiting, thus providing a better quality of anesthesia (3). The intraoperative urine output was larger in patients in the balanced fluid group of our study than in the saline group, but the difference did not reach statistical significance.

Metabolic acidosis, whatever its origin, can depress myocardial contractility, reduce cardiac output, and impair renal and intestinal blood flow. Acidemia and cellular acidosis have the capacity to inactivate membrane calcium channels and to inhibit the release of norepinephrine from sympathetic nerve fibers. Such metabolic vasodilatation and neuromodulation may result in the redistribution of cardiac output away from internal organs.

Plasma chloride levels affect afferent arteriolar tone through calcium activated chloride channels and modulate the release of renin. Hyperchloremia can reduce renal blood flow and glomerular filtration rate (4,5).

Current evidence suggests that hyperchloremic metabolic acidosis is clinically relevant. As a solution for large-volume intraoperative infusions, we prefer crystalloids and colloids with a more balanced composition.

Nicholas J. Wilkes

Susan V. Mallett

Michael G. Mythen

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References

1. Wilkes NJ, Woolf R, Mutch M, et al. The effects of balanced versus saline-based hetastarch and crystalloid solutions on acid base and electrolyte status and gastric mucosal perfusion in elderly surgical patients. Anesth Analg 2001; 93: 811–6.
2. Mythen MG, Webb AR. Perioperative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg 1995; 130: 423–9.
3. Gan TJ, Mythen MG, Glass PSA. Intraoperative gut hypoperfusion may be a risk factor for postoperative nausea and vomiting. Brit J Anaesth 1997; 78: 476.
4. Wilcox CS. Regulation of renal blood flow by plasma chloride. J Clin Invest 1983; 71: 726–35.
5. Hansen PB, Jensen BL, Skott O. Chloride regulates afferent arteriolar contraction in response to depolarization. Hypertension 1998; 32: 1066–70.
© 2002 International Anesthesia Research Society