Pseudometabolic Acidosis in Patient with Severe Hypertriglyceridemia
Presentation Number: SAT 510
Date of Presentation: April 1st, 2017
Christopher Bowman*1, Joesph Wiencek1, Craig Richard Sussman1, Brad Adams2, Gregory Sephel2, Jennifer Colby2, James Nichols2 and Alison Woodworth2
1Vanderbilt University Medical Center, Nashville, TN, 2Vanderbilt University Medical Center
Background: Lipemia is a common interference in clinical laboratory testing.
Clinical case: A 62-year male with past medical history of type 2 diabetes mellitus, CAD, and hypertriglyceridemia presented to pre-op clinic for routine evaluation prior to carpal tunnel surgery. A basic metabolic panel (reference interval in parentheses) showed a sodium 124 mmol/L (136-144), potassium 4.3 mmol/L (3.3-4.8), Chloride 92 mmol/L (98-107), CO2 6 mmol/L (23-31), and glucose 392 mg/dl (70-99). Patient was admitted for DKA and treated with an insulin infusion and IV fluids. Urinalysis was negative for ketones, lactic acid was mildly elevated at 2.6 mEq/L, and urine drug screen was negative. The lipid panel (mg/dL) showed triglycerides >5680 (<149), HDL 17 (>40), LDL 47 (1-129), and cholesterol 814 (0-199). Lipase was within the reference interval. Patient denied any nausea, vomiting, or shortness of breath. He was treated with insulin infusion, fenofibrate, fish oil, and rosuvastatin. Review of previous discharge summary showed a routine office visit with asymptomatic serum CO2 <5 mmol/L leading to a hospital admission. He was treated for DKA over 4 days and metformin was discontinued. Of note, during both admissions, his venous blood gases showed pH 7.39-7.43 (7.35-7.45) with serum HCO3 24-26 mmol/L (21-28). The discordant results between serum basic metabolic panel and blood gas analysis were further investigated in our laboratory. To determine the amount of lipemia needed to interfere with the CO2 assay, hyperlipidemic specimens from a patient with severe hypertriglyceridemia (triglycerides >3,500 mg/dL) were titrated into normolipidemic plasma pool at various percent concentrations. Samples with increasing lipid concentrations of 0, 5, 15, 25, 35, 50, and 100% were analyzed by either the Abbott Architect or Ortho Vitros enzymatic CO2 assays. Differences were noted between expected (calculated via linear regression analysis) and observed CO2 concentrations with both assays, with the highest difference present on the current assay (Abbott) used at Vanderbilt University hospital. At triglyceride concentrations of 1000 mg/dL, 2000 mg/dL and 3500 mg/dL the negative bias was 23%, 42% and 65%, respectively. This pseudometabolic acidosis is due to severe hypertriglyceridemia interference within the spectrophotometric method leading to falsely low CO2 concentrations.
Conclusion: Pseudometabolic acidosis from hypertriglyceridemia can lead to unintended clinical management decisions and possibly unnecessary hospital admissions. It is important to interpret CO2 results in the context of clinical symptoms and other laboratory results in patients with hypertriglyceridemia.
Nothing to Disclose: CB, JW, CRS, BA, GS, JC, JN, AW