To the Editor:-Mathes et al.,  in their case report titled “Dilutional Acidosis: Is it a Real Clinical Entity?” have reported a case of metabolic acidosis that they believe is due to dilutional acidosis developing as a direct result of infusion of a large volume of isotonic saline. Although we agree that dilutional acidosis can occur when the plasma bicarbonate concentration is decreased by extracellular fluid expansion, we disagree with the authors on the following issues:
1. This case report is not a true example of “dilutional acidosis.” Dilutional acidosis occurs when the plasma bicarbonate concentration decreases as a result of volume expansion with solutions that contain neither acid nor alkali.  The intraoperative metabolic acidosis that occurred in this case may not be the direct result of giving a large volume of isotonic saline. Instead, the following factors may have significantly contributed to the generation of this metabolic acidosis:
- Bicarbonate loss in conjunction with 3.5-l blood loss
- Bicarbonate loss due to electrolyte exchange from the normal saline that was used to moisten laparotomy sponges and to irrigate the surgical field
- Decreased “buffer power” of blood due to blood loss
- Accumulation of fixed acids
Fixed acids are responsible for the formation of 50–100 mmol of hydrogen ions per day. In the acute setting, the magnitude of contribution of the kidney to the pH homeostasis may be insignificant. In this case, however, the operative procedure lasted longer than 8 h, and this length of time cannot be regarded as an acute situation. Accumulation of fixed acids during this extended period of time can contribute significantly to this metabolic acidosis. To rule out the possibility of fixed acids playing a role in the metabolic acidosis, the authors emphasized the presence of nonanion gap metabolic acidosis in this patient. Although increased anion gap may be used as a criterion to differentiate the various causes of metabolic acidosis, the possibility of nonanion gap or even decreased anion gap (as compared with baseline anion gap) exists in the presence of organic acid acidosis in conjunction with extreme hyperchloremia. In this patient, the chloride increased from 90 to 128 mEq/l.
2. Discrepancy in the proposed treatment of metabolic acidosis: The treatment of acidosis depends on its severity, any associated electrolyte/hemodynamic disturbance, and the judgment of the clinician. Although the authors state that there is no need to manage dilutional metabolic acidosis with bicarbonate, yet their patient was treated with bicarbonate dialysate in the ICU. We are in agreement in this therapy. We believe that the correction of metabolic acidosis that followed the dialysis in this case is in part be due to the removal of the unmeasured fixed acids.
Arjang Khorasani, M.D.
Assistant Professor; Department of Anesthesiology; Rush University Medical College; Chairman, Division of Critical Care Anesthesiology; Department of Anesthesiology & Pain Management; Cook County Hospital; Chicago, Illinois
Samuel K. Appavu, M.D.
Assistant Professor of Surgery; Department of Surgery; University of Illinois College of Medicine at Chicago; Chairman, Division of Surgical Critical Care; Cook County Hospital; Chicago, Illinois
Simin Saatee, M.D.
Assistant Professor; Department of Anesthesiology; Rush University Medical College; Department of Anesthesiology & Pain Management; Cook County Hospital; Chicago, Illinois