The urine anion gap: the critical clue to resolve a diagnostic dilemma in a patient with ketoacidosis
The urine anion gap: the critical clue to resolve a diagnostic dilemma in a patient with ketoacidosis. J G Hilton , A C Vandenbroucke , R G Josse , G C Buckley and M L Halperin Abstract Usually, ketoacidosis presents few if any diagnostic or therapeutic problems; in this article, we report a case wh...
Saved in:
Published in: | Diabetes care Vol. 7; no. 5; pp. 486 - 490 |
---|---|
Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
American Diabetes Association
01-09-1984
|
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | The urine anion gap: the critical clue to resolve a diagnostic dilemma in a patient with ketoacidosis.
J G Hilton ,
A C Vandenbroucke ,
R G Josse ,
G C Buckley and
M L Halperin
Abstract
Usually, ketoacidosis presents few if any diagnostic or therapeutic problems; in this article, we report a case where ketoacidosis
was clinically occult and biochemically obscure. The patient presented with acute pancreatitis associated with a modest antecedent
alcohol intake. Metabolic acidosis with a normal anion gap (10 meq/L) was observed together with moderate hyperglycemia and
a 2 + (but not 4 +) test for serum ketones. None of the usual causes of metabolic acidosis with a normal anion gap was identified
nor was there an obvious explanation for a reduction in unmeasured anion gap (e.g., hypoalbuminemia, dysproteinemia, or the
presence of abnormal halides). Despite the initial normal anion gap, ketoacidosis was suspected clinically and this was confirmed
by the elevated serum B-hydroxybutyrate of 8 mmol/L. We deduced that the serum unmeasured anions, which should have been increased
by at least 8 meq/L, were being underestimated because of the effect of hypertriglyceridemia on the serum chloride determination.
When the serum chloride was reestimated by a method not influenced by hyperlipidemia, the value was 102 mmol/L not 112 mmol/L
and, when reevaluated, the anion gap was indeed appropriately elevated. In addition, the urine anion gap (Na + K - Cl) was
103 meq/L in the absence of renal disease. This indicated that the expected large quantity of urinary ammonium must have been
masked by an even greater quantity of unmeasured anion; in this case proven by direct measurement to be B-hydroxybutyrate.
Finally, metabolism of the alcohol ingested, which yields hepatic NADH, could explain, in part, the modest hyperglycemia and
the absence of a 4 + test for serum ketones. |
---|---|
ISSN: | 0149-5992 1935-5548 |
DOI: | 10.2337/diacare.7.5.486 |