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Department of Anesthesiology, University of South Florida College of Medicine, Tampa, FL
To the Editor:
I was surprised to read in the article by Waters et al. (1) that the iatrogenic acidosis after normal saline administration was treated with bicarbonate dosed using an arterial blood base deficit measurement. Substantial research indicates bicarbonate administration is not efficacious and is potentially harmful in patients with a moderate acidosis (2–7). Prospective awareness that patients receiving large amounts of normal saline likely will become acidotic is the norm. Thus, I wonder if the choice to treat with bicarbonate came from a review board perception that to allow the study to continue, the acidosis had to be treated in some way, effective or ineffective. Clinically, I doubt that many would choose to employ a technique of rescue-bicarbonate at a base deficit level of -5 mEq/L, and I wonder how that number was determined given the concern for intracellular acidosis, hypernatremia, and other adverse effects ascribed to bicarbonate therapy.
References
Department of General Anesthesiology, Cleveland Clinic Foundation, Cleveland, OH Department of Anesthesiology, Mayo Clinic, Rochester, MN
In Response:
I would like to thank Dr. Soto for showing such a detailed interest in our recent study (1). Our study attempted to determine if any differences in outcome could be detected in patients undergoing aortic aneurysm repair when lactated Ringer’s solution or normal saline solution was used as the primary crystalloid solution. One of the outcome end points assessed was the amount of sodium bicarbonate used to treat acidosis. Dr. Soto correctly assumes that the choice of a base deficit of -5 mEq/L as a trigger for bicarbonate treatment was chosen as a compromise end point; however, the compromise was not to satisfy our IRB but rather the perspective of our surgeons and anesthesiologists who feel that tight maintenance of acid-base and electrolyte homeostasis is important during aortic cross-clamping. It is difficult to argue with their perspective because there is conflicting data regarding the intracellular acidosis to which Dr. Soto refers. The title of a recent editorial in Critical Care Medicine, "Sodium bicarbonate and intracellular acidosis: Myth or reality?" (2) alludes to this debate.
In any study protocol, one needs to establish a trigger for therapeutic intervention, and that is what we did in our study. We agree with Dr. Soto that in many situations, we would not treat an acidosis with a base deficit of -5 mmol/L. In the studied clinical scenario, aortic aneurysm repair where an aortic cross-clamp is applied for a prolonged period of time, a base deficit of -5 mmol/L is only one point on a downward trend. Thus, we felt that it represented a legitimate therapeutic treatment point. We agree that the potential value of therapy in the treatment of severe acidemia remains an important issue, but further studies are required to fully delineate the scope and efficacy of bicarbonate treatment.
References
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