Question 9.3

Hypoalbuminemia is common in the long-term ICU patient.

a)    How does this finding alter your interpretation of acid-base data?

b)    List two methods of how you would adjust for this.
(40% marks)

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College answer

Not available.

Discussion

This is an excellent stem made surprising only by the fact that we have never seen the like of it in CICM past papers. Certainly, through history, CICM trainees have been asked to adjust their calculations for albumin, but never have they been asked to spell out the exact scenarios where this is necessary, or how they would do it.

Moreover, the question specifically asked for the ways in which hypoalbuminaemia bedevils acid-base interpretation (i.e. mentioning calcium correction would probably not have scored any marks). The longer version of these explanations is available in the short chapter on the sources of error in blood gas analysis. Here, only a brief point-form answer is attempted, commensurate with the modest 40% weighting of the question.

a)    How does hypoalbuminaemia alter your interpretation of acid-base data?

  • Albumin is an anionic protein which, in solution, acts as a weak acid.
  • In the classical Boston interpretation of acid-base disorders, albumin is a major contributor to the unmeasured anions (the "anion gap"), of which about 75% is normally attributable to albumin 
  • In the transatlantic Copenhagen interpretation of acid-base disorders, albumin influences the base excess, as it increases the titratable acidity of the body fluids.
  • In the physicochemical interpretation of acid-base disorders, albumin is one of the components of Atot, the total non-volatile weak acids (the other major contributor being phosphate)
  • Thus, with hypoalbuminaemia,
    • Atot is decreased 
    • Anion gap is decreased
    • Base excess is increased (or, if you prefer, base deficit is decreased)

b)    List two methods of how you would adjust for this.

  • For every 4g/L decrease in serum albumin, the normal expected anion gap decreases by 1. i.e., for every 10 g/L fall in albumin will increase the base excess by 2.5 mEq/L.
  • Alternatively: normal AG = 0.2 ×[albumin] (g/L) + 1.5 × [phosphate] (mmol/L)

For the reader who wants to add more to this answer and who enjoys complex equations, the best single resource which seems to collect them all is Patrick J. Nelligan's chapter on the diagnosis of acid-base disorders from Evidence-Based Practice of Critical Care (2010).

References

Neligan, Patrick J., and Rory O’Donoghue. "56 How Should Acid-Base Disorders Be Diagnosed and Managed?." Clifford S. Deutschman A2MS A2MD A2FCCM, Patrick J. Neligan, MA, MB, FRCARCSI, eds. Evidence-Based Practice of Critical Care. Philadelphia: WB Saunders (2010): 389-396.

Story, David A., Hiroshi Morimatsu, and Rinaldo Bellomo. "Strong ions, weak acids and base excess: a simplified Fencl–Stewart approach to clinical acid–base disorders." British journal of anaesthesia 92.1 (2004): 54-60.

Rossing, T. H., N. Maffeo, and V. Fencl. "Acid-base effects of altering plasma protein concentration in human blood in vitro." Journal of applied physiology 61.6 (1986): 2260-2265.

Berend, Kenrick. "Diagnostic use of base excess in acid–base disorders." New England Journal of Medicine 378.15 (2018): 1419-1428.