The Bedside Stewart Approach in the Emergency Department

The management of complex acid-base disorders in the Emergency Department (ED) requires a precise understanding of metabolic derangements that traditional bicarbonate-centered models often fail to capture. The physicochemical model, or Stewart approach, provides a mechanistic framework for analyzing these disturbances by identifying independent variables that control pH: partial pressure of carbon dioxide (PCO_2), strong ion difference (SID), and the total concentration of weak acids (A_{TOT}) [1,3].

In clinical practice, a Simplified Stewart Approach (also known as the Bedside Stewart) is used to quantify metabolic acid-base status by partitioning the Standard Base Excess (SBE) into actionable components [2,3].

The SALT Equation: A Practical Framework

The SALT mnemonic, developed to assist bedside clinicians, categorizes the metabolic drivers of acid-base status. The equation allows clinicians to determine the specific milliequivalent (mEq/L) effect of each component on the patient’s overall SBE [2].

The SALT Equation: \text{Standard Base Excess (SBE)} = S + A + L + T

Component	Element	Formula / Calculation
S	Sodium-Chloride Effect	[Na^+] - [Cl^-] - 35 (mEq/L)
A	Albumin Effect	0.25 \times (42 - \text{measured Albumin in g/L})
L	Lactate Effect	1.0 - \text{measured Lactate}
T	Trash (Other) Ions	SBE - (S + A + L)

Normal Reference Points

To apply this model, clinicians assume a "normal point" of pH 7.40, PCO_2 40 mmHg, Sodium 140 mM, Chloride 105 mM, Lactate 1.0 mM, and Albumin 42 g/L [2].

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Acidosis: Causes and Interpretation

Metabolic acidosis occurs when the SID decreases, weak acids increase, or unmeasured "trash" ions accumulate.

Negative SID and Strong Ion Effects (Acidifying)

A decrease in the difference between strong cations (Sodium) and strong anions (Chloride and Lactate) results in an acidifying effect.

Hyperchloremia: This is the primary cause of a negative Sodium-Chloride effect. It is frequently iatrogenic, caused by large volumes of 0.9% saline resuscitation. Because saline has a SID of 0, it decreases the plasma SID as chloride levels rise faster than sodium [2,3].
Lactic Acidosis: Increased lactate acts as a strong anion. As lactate concentration rises above the reference 1.0 mM, it narrows the SID, contributing directly to acidosis. High lactate is a critical prognostic marker for mortality in shock and sepsis [1,2].

Negative Excess Ions (Trash/Other Ions)

The "Trash" (T) component represents unmeasured ions that contribute to a narrowed SID and a widened anion gap. These include:

Ketones: Significant in diabetic ketoacidosis (DKA) or euglycemic ketoacidosis associated with SGLT2 inhibitors [2].
Organic Acids and Toxins: Accumulated in renal failure or exogenous poisoning [1].
Inorganic Phosphate and Sulfate: Often elevated in critical illness and organ dysfunction [1,2].

High Albumin (Acidosis Effect)

Though rare in the ED compared to hypoalbuminemia, hyperalbuminemia (e.g., following concentrated 5% albumin therapy) increases the total concentration of weak acids, which exerts an acidifying effect on the plasma [2].

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Alkalosis: Causes and Interpretation

Metabolic alkalosis occurs when the SID increases or the concentration of weak acids (primarily albumin) decreases.

High SID and Positive Strong Ion Effects (Alkalising)

An increase in the SID exerts an alkalising effect on the SBE.

Relative Hypochloremia: When chloride levels are low relative to sodium, the SID widens. This can occur in volume depletion or following certain therapies [2].
Sodium Bicarbonate Therapy: Administering sodium bicarbonate is effectively an infusion of sodium (a strong cation) without a strong anion. This increases the SID, thereby raising the pH [2].
Balanced Solutions: Fluids like Ringer’s Lactate or Plasma-Lyte contain strong anions (lactate, acetate, gluconate) that are rapidly metabolized. Once cleared, they leave behind the sodium cation, widening the SID and exerting an alkalising effect [2].

Low Albumin (Alkalising Effect)

Hypoalbuminemia is ubiquitous in critically ill patients and acts as a primary driver of metabolic alkalosis. Because albumin is a weak acid, its absence reduces the total acid load in the plasma [1,2].

Masking Effect: A low albumin can mask an underlying acidosis. For every 10 g/L decrease in albumin below the 42 g/L reference, the SBE increases by approximately 2.5 mEq/L. Consequently, a patient may have a "normal" pH or SBE despite significant lactic or hyperchloremic acidosis because the alkalising effect of hypoalbuminemia is offsetting the acidifying components [2].

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Clinical Application in the ED

Integrating the Bedside Stewart approach allows ED doctors to differentiate between iatrogenic causes (saline-induced hyperchloremia) and pathological causes (lactic acidosis or unmeasured anions).

Practical Steps for ED Analysis:

Assess Respiratory Status: Use PCO_2 as the primary respiratory metric.
Quantify SBE: Obtain the overall metabolic status from the blood gas.
Calculate the SALT Components:
- Determine if the acidosis is driven by Chloride (S), Lactate (L), or "Trash" ions (T).
- Adjust the assessment for the "Alkalosis" effect of low Albumin (A).
Targeted Intervention:
- If S is highly negative: Switch from saline to balanced crystalloids to mitigate hyperchloremic acidosis [1].
- If A is low: Recognize that the true metabolic derangement is more severe than the SBE suggests [2].
- If T is high: Investigate for ketones, renal failure, or toxins [2].

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References

Reis GH, Viana LM, Guillarducci VT, Delgado MA. A simplified physicochemical approach to acid-base disorders: perioperative practical application. Acute Crit Care. 2025;40(3):509-511.
Story DA. Acid–Base Analysis in the Operating Room: A Bedside Stewart Approach. Anesthesia Experts. 2023 Dec 19. Available from: https://anesthesiaexperts.com/
Story DA. Stewart acid-base: a simplified bedside approach. Anesth Analg. 2016;123:511-5.
Magder S, Emami A. Practical approach to physical-chemical acid-base management: Stewart at the bedside. Ann Am Thorac Soc. 2015;12:111-7.
Gomez H, Kellum JA. Understanding acid base disorders. Crit Care Clin. 2015;31:849-60.
Dos Passos MG, Blaya LB, Boniatti MM. Comparison of a modified Story approach to traditional evaluation of acid-base disturbances in patients with shock: a cohort study. J Clin Monit Comput. 2022;36:817-22.
Story DA, Morimatsu H, Bellomo R. Strong ions, weak acids and base excess: a simplified Fencl-Stewart approach to clinical acid-base disorders. Br J Anaesth. 2004;92(1):54-60.

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