Making rounds today in the ICU, we found this electrolyte panel
| Electrolyte panel | |||||
|---|---|---|---|---|---|
| Na | 138 | Cl | 109 | BUN | 58 |
| K | 4.2 | HCO3 | 17 | creat | 1.8 |
| Blood Sugar | 206 |
Clinical context – 50 year old woman with known cirrhosis and gram negative sepsis. Her creatinine and BUN are improving with volume expansion.
Explain her decreased HCO3
{ 4 comments… read them below or add one }
First, the patient’s BUN/Cr ratio of ~32 is suggests prerenal azotemia, consistent with renal hypoperfusion from her gram negative septicemia. Such a clinical picture is often associated with a lactic acidosis due to more global hypoperfusion leading to tissue hypoxia. Checking the patient’s anion gap, we only see an AG of 12. However, the history of known cirrhosis might be hiding a true anion gap due to decreased albumin, which (if I remember correctly) has a correction factor of ~3meq per 1g albumin below 4.0. Thus a lactic acidosis in a ICU patient with hypoalbuminemia secondary to cirrhosis yield a normal anion gap acidosis with the decreased bicarb we see in this case.
Metabolic acidosis from aggressive fluid resuscitation with NS?
Hyperchloremic metabolic acidosis secondary to volume expansion with NaCl
An anion-gap acidosis (possibly lactic acidosis in the setting of sepsis) is very likely to be present for the reasons described by Phillip above. Beyond that, no other conclusive statements can be made about the presence of additional disturbances. A “mixed” acid-base condition with an additional primary non-gap metabolic acidosis, and either respiratory alkalosis or acidosis remain possibilities, and such a patient might have good reason for all of these additional derangements. The serum albumin (to calculate a corrected delta gap) and at least the pCO2 or pH are required for a more definitive answer.