Letters to the Editor: Letter to the Editor
To the Editor:
The title of the article “Stewart Acid-Base: A Simplified Bedside Approach” by Story1 is a paradox. There is nothing simple about the “Stewart Approach.” For years, Stewart advocates have tried, unsuccessfully, to demonstrate that this approach offers a unique mechanistic or pathophysiologic insight into acid-base physiology.
Undoubtedly, the Stewart methodology (and the “base excess” approach) can be used to diagnose metabolic acid-base disorders, but it has no advantage over the classic physiologic methodology advanced by Schwartz and Relman2 and Narins and Emmett.3 The “Stewart Approach” is a more complicated and less-intuitive framework for diagnosing and understanding acid-base physiology/pathophysiology. Dr Story describes an intubated cirrhotic patient (who had received generous intravenous saline expansion) with the following laboratory results: Na: 133; Cl: 110; lactate: 5 (all mmol/L); albumin: 22 g/L; arterial blood gas—pH 7.20; PCO2 40; HCO3 15. Potassium and venous HCO3 (or total CO2) were not reported. The latter can be assumed to be about 16 to 17 mEq/L. Dr Story then uses the Stewart framework to reach his acid-base diagnostic conclusions (with which I agree). I will use the traditional approach to analyze and interpret the patient’s disorder:
- pH = 7.20, this defines acidemia. The HCO3 is reduced—therefore, this patient has metabolic acidosis.
- Metabolic acidosis should generate hyperventilation and reduce the PCO2. How low should it be? The “Winter’s equation [PCO2 = 1.5 (HCO3) + 8] or other rules [PCO2 = HCO3 + 15] can be used. They indicate that the HCO3 should be about 30 mm Hg. But the PCO2 is too high at 40! Therefore, this patient also has respiratory acidosis.
- Whenever a diagnosis of metabolic acidosis is established, determine whether it is an anion gap (AG) acidosis, a hyperchloremic acidosis, or a combination of the 2. The AG is calculated as AG = Na − (Cl + HCO3). In this case, AG = 133 − (110 + 16) = 7 mEq/L. However, an additional step is required when the albumin concentration is reduced. Add 3 mEq/L for each 1 gm% reduction below the normal albumin concentration. Therefore, the “corrected AG” is about 13 mEq/L.
The reduction in HCO3 concentration (or delta HCO3), which is about 8 mEq/L (from a normal baseline of about 25), should be similar to the elevation in the AG, the increase in Cl, or a combination of the 2. In this case, the AG is increased by about 3 mEq/L (normal baseline = about 10), but the HCO3 is reduced by about 8 mEq/L. Therefore, this patient has both AG and hyperchloremic acidosis. The AG acidosis is a lactic acidosis (lactate = 5 mEq/L). The hyperchloremic acidosis was at least partially generated by extra-cellular fluid expansion with normal saline. Large-volume saline expansion invariably generates a hyperchloremic metabolic acidosis because of dilution of extra-cellular fluid HCO3 and other base buffers. The classic traditional approach generates the correct acid-base diagnoses: hyperchloremic (probably NaCl expansion) and AG (lactic) metabolic acidosis and respiratory acidosis. However, it is a simpler, more straightforward and easier to understand methodology than that of Stewart.
Michael Emmett, MD
Department of Internal Medicine
Baylor University Medical Center
1. Story DA. Stewart acid-base: a simplified bedside approach. Anesth Analg. 2016;123:511–515.
2. Schwartz WB, Relman AS. A critique of the parameters used in the evaluation of acid-base disorders. “Whole-blood buffer base” and “standard bicarbonate” compared with blood pH and plasma bicarbonate concentration. N Engl J Med. 1963;268:1382–1388.
3. Narins RG, Emmett M. Simple and mixed acid-base disorders: a practical approach. Medicine (Baltimore). 1980;59:161–187.