Abstract: SA-PO1015
Pseudo-Anion-Gap Metabolic Acidosis from Severe Hypertriglyceridemia Corrected by Plasma Exchange: A Case Series
Session Information
- Fellows/Residents Case Reports: Fluid, Electrolytes, Acid Base
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nephrology Education
- 1302 Fellows and Residents Case Reports
Authors
- Ludwig, John Travis, Rush University Medical Center, Chicago, Illinois, United States
- Carag, Charissa Marie R., Rush University Medical Center, Chicago, Illinois, United States
- Behara, Venkata R., NANI (Nephrology Associates of Northern Illinois), Mt. Prospect, Illinois, United States
- Baxi, Pravir V., Rush University Medical Center, Chicago, Illinois, United States
- Gashti, Casey N., Rush University Medical Center, Chicago, Illinois, United States
Background
A link between severe hypertriglyceridemia (H-TG) and falsely low or even unmeasurable serum bicarbonate ([HCO3]), known as pseudo-hypobicarbonatemia, has been reported. This is believed to be due to interference by serum triglycerides (TG) - typically >1000 mg/dL - when the commonly used enzymatic assay is utilized for [HCO3] measurement. When the [HCO3] is calculated using an ABG machine, the value is near normal. Chloride measurements are not affected by the TG level. This could lead to the misdiagnosis of a severe anion-gap metabolic acidosis, resulting in an extensive work-up that would typically include expensive toxicology screening.
Methods
We report a series of 4 pts with pseudo-hypobicarbonatemia associated with severe H-TG (Tab. 1). All TG values were >2000 mg/dl and each pt had lipemic serum. All pts had a measured serum [HCO3] of ≤ 6 mmol/L and an elevated anion gap (AG). The calculated [HCO3] from a simultaneous blood sample run using a blood gas machine was 15-27 mmol/L with a pH in the normal range. 3 of the 4 pts presented with acute pancreatitis from H-TG and received 1-3 membrane based therapeutic plasma exchange (TPE) treatments with immediate improvement in TG levels. The 4th pt had discontinuation of PEG-L-asparaginase, known to cause H-TG, and did not require TPE. In each case the serum [HCO3] normalized after lowering of H-TG with a simultaneous resolution of the elevated AG.
Conclusion
Pseudo-anion-gap metabolic acidosis is a laboratory phenomenon seen when severe H-TG interferes with the normal enzymatic measurement of the [HCO3]. The calculated [HCO3] is not affected when determined using a blood gas analysis machine. While this phenomenon has been previously described, this is the first report to demonstrate immediate resolution of the pseudo-anion-gap metabolic acidosis following aggressive lowering of the TG levels with TPE. Recognition of lipemic serum in the setting of an otherwise unexplained AG metabolic acidosis should prompt the clinician to get an ABG sample for true determination of the acid-base status. Doing so may avoid an extensive and expensive metabolic work-up.
Table 1