Comments on: AMS – an acid-base problem II

By: Pro Nephros

Pro Nephros — Sat, 20 Jun 2009 04:30:22 +0000

First ABG and SMA-7 disagree with regard to bicarb – calculated bicarb with given pH and pCO2 from ABG would be 29, yielding total CO2 of about 31. If we assume that the bicarb from the SMA-7 was erroneous (usually the case when there’s significant discrepancy with the ABG) and true total CO2 was about 31, there’s not much of an anion gap. All of the electrolytes have been diluted by the osmotic effect of the severe hyperglycemia – but the chloride is proportionally lower than the sodium. The primary disturbance at presentation then appears to have been chloride depletion metabolic alkalosis, and I don’t think one has to invoke a ketoacidosis or lactic acidosis or come up with a fancy triple disturbance at that point.

Two days later the chloride deficit has been repaired, and the impact of hyperglycemia on sodium is much less – but the pCO2 is still high. Evidently the patient has baseline respiratory acidosis – presumably due to his CNS problem. At least now the calculated and measured bicarbonate agree. In retrospect, his original metabolic alkalosis may have been more completely “compensated” than expected…

By: Rahul

Rahul — Sat, 20 Jun 2009 00:17:01 +0000

Nice one, SIR

By: cory

cory — Fri, 19 Jun 2009 14:13:06 +0000

I’m going to say we have a patient with a chronic compensated respiratory acidosis, more likely than not an obstructive sleep apnea or moderate obstructive airway obstruction.
This is the primary problem (r/o hypothyroidism), He now develops glucose intolerance, probably as a result of type II DM with elevated glucose. He is volume depleted, probably mild to moderate hypokalemia with glucosuria and kaliuresis. he compensates by drinking water to give him a low serum sodium and chloride that is actually normal when corrected for the elevated blood glucose (total body free water normal). His osmolarity is not markedly abnormal. There is no or minimal ketoacidosis (? serum/urine ketones – I’m guessing trace to negative) so his pH is a result of the compensation for respiratory acidosis and some metabolic alkalosis due to mild hypokalemia. With volume replacement, potassium replacement and insulin he reverts to his primary problem.
so my guess is primary respiratory acidosis, secondary metabolic alkalosis (compensation), tertiary metabolic alkalosis secondary to volume depletion and total body hypokalemia. Little or no free water deficit.