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Stewart Versus Traditional Approach to Acid-Base Disorders

Emmett, Michael MD

doi: 10.1213/ANE.0000000000001457
Letters to the Editor: Letter to the Editor

Department of Internal Medicine, Baylor University Medical Center, Dallas, Texas,

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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:

  1. pH = 7.20, this defines acidemia. The HCO3 is reduced—therefore, this patient has metabolic acidosis.
  2. 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.
  3. 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, MDDepartment of Internal MedicineBaylor University Medical CenterDallas,

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1. Story DA. Stewart acid-base: a simplified bedside approach. Anesth Analg. 2016;123:511515.
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;268:13821388.
3. Narins RG, Emmett M. Simple and mixed acid-base disorders: a practical approach. Medicine (Baltimore). 1980;59:161187.
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