To the Editor:--Several points in the case report "Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation" merit further discussion.
We do not believe that the transient perioperative hyperchloremic metabolic acidosis in this patient required the presence of the ileal bladder augmentation. We accept that prolonged contact of urine with bowel mucosa will allow for water reabsorption, passive chloride reabsorption, and active HCO3sup - secretion, leading to a net HCO sub 3 sup - loss and metabolic acidosis. In this patient, an indwelling urinary catheter was placed preoperatively, and although the catheter was transiently obstructed at the initiation of surgery, the decreased time of contact between the urine and bowel mucosa inherent with bladder drainage mitigates the importance of the ileal augmented bladder.
In our opinion, the principal reason for the acidosis was the large chloride load infused into this 13-kg patient. Although the authors admit that administration of a large amount of normal saline has been reported to result in a dilutional hyperchloremic acidosis, they also believed that this occurrence is an unusual clinical event and "that other factors were involved." We acknowledge that the literature concerning hyperchloremic metabolic acidosis after normal saline infusion is sparse. However, there are data associated with the use of hypertonic saline that describe the development of hyperchloremic acidosis. [2,3]These data suggest that less concentrated normal saline may cause hyperchloremic acidosis if administered in large quantities, as was done in this case.
The importance of hyperchloremia is emphasized by Stewart's mathematically based approach to acid-base balance. [4,5]According to Stewart, the major determinant of Hydrogen sup + concentration is the strong ion difference (SID) in the body. In a solution containing any collection of strong electrolytes, the Hydrogen sup + concentration is determined by the difference between the positively charged and negatively charged strong ions (molecules that completely dissociate in water). In the body, the SID is equal to the difference between the sum of the Sodium sup + and Potassium sup + concentration and the Chlorine sup - concentration (SID = Sodium sup + + Potassium sup + - Chlorine sup -) A decrease in SID is associated with a metabolic acidosis, and an increase in SID is associated with a metabolic alkalosis. Change in Chlorine sup - concentration is the major anionic contributor to change in Hydrogen sup + homeostasis. The development of significant hyperchloremia with large volumes of saline for fluid resuscitation would result in a decrease in SID and metabolic acidosis. Furthermore, the Stewart model is able to quantify the effect that electrolyte change has on base deficit. Using this methodology, the expected base deficit effect from hyperchloremia in this patient would have sufficiently explained the observed base deficit.
We urge anesthesiologists to consider the importance of hyperchloremic acidosis during prolonged surgical procedures in which large volumes of saline are used for volume replacement. Because many still believe that the cause of metabolic acidosis in the surgical patient is the result of tissue hypoperfusion and cellular hypoxemia, the clinician attempts to maximize tissue perfusion with liberal volume infusions to support cardiac output. The common practice of treating acidemia with fluid may be worsening the acidemia rather than correcting it. We commend the authors in recognizing this interesting acid-base problem and encourage anesthesiologists to consider the role of fluids in acid-base change.
Lawrence R. Miller, M.D., Jonathan H. Waters, M.D.,, Charlton Provost, Department of Anesthesiology FHP, Inc., Fountain Valley, California, Department of Anesthesiology, University of California, Irvine Medical Center, 101 City Drive South, Route 81A, Orange, California 92668.