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Department of Critical Care & Anaesthesia, New Cross Hospital, Wolverhampton, United Kingdom
To the Editor:
The recent editorial (1) and original article (2) on hyperchloremic acidosis made interesting reading.
In the past, hyperchloremic acidosis contributed to misdiagnosis in one of our patients, leading to unnecessary laparotomy and initiation of dopexamine infusion. In view of this occurrence and recent publications on the subject (1,2), an audit of this biochemical abnormality was initiated. The audit period was 6 weeks. We collected the data on demographics, APACHE II, type and amount of intravenous fluid received before admission to critical care unit, analysis of arterial blood gases, electrolytes, serum lactate, total intake, and urine output in the first 24 hours. A total of 24 patients were studied. Sixteen patients had BE > -2.0 (range, -2.1 to -10.2 mEg/L). Serum chloride was increased in 23 patients (range, 109–133 mmols/dL), and serum lactate was normal (ref value <1.78 mEg/L) in 12 patients, seven of which had BE > -2.0 (range, -2.1 to -8.8 mEg/l) and pH <7.35.
In this small study, we saw hyperchloremic acidosis in 29% (7 of 24) cases. Normal saline (0.9%) was the predominant intravenous fluid given to these patients. The audit has increased awareness of this entity among trainee doctors and nurses in our unit. Whether this will change the anesthetic practice or not remains to be seen. I have changed mine.
References
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.
References
This article has been cited by other articles:
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  R. G. Craig and J. M. Hunter Recent developments in the perioperative management of adult patients with chronic kidney disease Br. J. Anaesth., September 1, 2008; 101(3): 296 - 310. [Abstract] [Full Text] [PDF]
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