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Objective: The Fencl-Stewart approach to acid-base physiology allows detailed, quantitative insights into acid-base disorders. We tested the hypothesis that this type of analysis would reveal complex acid-base changes in patients after liver transplantation that differed from those in a general intensive care unit population., Methods: Data were collected retrospectively on patients on admission to the ICU after liver transplantation between 2001 and 2003 and prospectively on a convenience group of general ICU patients in 2001., Results: Data were collected from 100 ICU patients and 83 liver transplant patients. Values for most clinical chemistry variables differed between the two groups, with considerable variation within the groups. All acid- base variables differed between the control and transplant groups (P < 0.005). Overall, the transplant group had metabolic acidosis (mean base excess +/-SD, -4.5 +/-3.1mmol/L) due to both a sodium chloride effect on base excess (-4.0 +/-4.1 mmol/L) and an other ion effect on base excess (-6.3 +/-4.2 mmol/L). The sodium chloride effect was mainly due to increased chloride concentration. All estimates of other anions (anion gap, corrected anion gap, strong ion gap, and the other ion effect on base excess) suggested that other anions play an important role in the acid-base status of patients after liver transplantation. These effects on base excess were partly offset by a greater metabolic alkalosis in the transplant group caused by a marked effect of decreased albumin on base excess (5.8 +/-1.5 mmol/L)., Conclusions: The Fencl-Stewart approach allowed us to quantitatively assess the factors contributing to patients' acid-base status. We found complex acid-base changes in patients immediately after liver transplantation.

The bicarbonate centered approach to acid-base physiology involves complex explanations for the metabolic acidosis associated with chronic renal failure. We used the alternate Stewart approach to acid-base physiology to quantify the acid-base chemistry of patients with chronic renal failure. We examined the plasma and urine chemistry of 19 patients with chronic renal failure who were predialysis and 20 healthy volunteers. We compared the plasma strong-ion-difference due to sodium,potassium,and chloride ions as well as the weak acids albumin and phosphate. We used a simplified Fencl-Stewart approach to quantify the effects of sodium-chloride, albumin, and unmeasured ions on base-excess. The chronic renal failure group had a greater metabolic acidosis, with a base-excess that differed from the healthy group by a mean of -2.7 mmol/L, p = 0.04. This was associated with a strong ion acidosis due to both increased chloride and decreased sodium. The anion gap, strong-ion-gap, and base-excess effect of unmeasured ions were similar in both groups suggesting that unmeasured ions had only a minor role in the acid-base status in this group of patients.

The history of assessing the acid-base equilibrium and associated disorders is intertwined with the evolution of the definition of an acid. In the 1950s clinical chemists combined the Henderson-Hasselbalch equation and the Bronsted-Lowry definition of an acid to produce the current bicarbonate ion-centred approach to metabolic acid-base disorders. Stewart repackaged pre-1950 ideas of acid-base in the late 1970s, including the Van Slyke definition of an acid. Stewart also used laws of physical chemistry to produce a new acid-base approach. This approach, using the strong ion difference (particularly the sodium chloride difference) and the concentration of weak acids (particularly albumin), pushes bicarbonate into a minor role as an acid-base indicator rather than as an important mechanism. The Stewart approach may offer new insights into acid-base disorders and therapies.