A question recently posted on AACC’s chemistry list-serve involved correcting the serum or plasma sodium concentration for the patient’s degree of hyperglycemia in the setting of DKA. The proposed formula was: corrected sodium = measured sodium + [1.6 (glucose – 100) / 100]. The laboratory would then report a “corrected” serum or plasma sodium in addition to the measured sodium.
Would you advise the lab to put this policy into place and report “corrected” sodiums?
In general, other than anion gap, eGFR and EAG, I do not recommend providing clinicians with "corrected" or calculated results.
If the lab provides a "corrected" result (e.g., calculated osmolality based upon sodium, glucose and BUN, or total calcium is corrected for changes in albumin, or the sodium is corrected for changes in glucose), the reporting of such a result “validates” the assumptions that were made in determining the correction. However, assumptions are only “assumptions” and it is unknown whether the assumptions really do apply to the case in question. In short, the calculation estimates are not necessarily correct and should not be reported. A good example of how assumptions can be flawed concerns calculating the serum osmolality in the setting of alcohol poisoning where the true osmolality may be considerably higher than the estimated osmolality (using the formula: osmolality = [2 x Na+] + [BUN/ 2.8] +[ glucose / 18]).
If the lab reports a “corrected” sodium, the clinician then assumes that the calculated sodium is the “true” sodium. However if 2 sodiums are reported on the same sample (measured and “corrected”), there is likely to be confusion in the interpretation of the result(s).
If the clinician wants to "correct" the sodium, that is fine, and they take the responsibility for the assumption of how the sodium changes with glucose. However the lab is then not responsible for a potentially erroneous assumption.
One other very important point: Hyponatremia in the setting of hyperglycemia is not an artifact. It is real. However when the glucose is reduced in DKA through hydration and insulin, and the plasma glucose concentration is reduced, water leaves the extracellular space entering the cellular space raising the extracellular sodium concentration.