Abstract: SA-PO0601
Discordant Bicarbonate Unmasking Severe Hypertriglyceridemia: Pseudohypobicarbonatemia Mimicking Toxic Alcohol-Associated Metabolic Acidosis
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Khan, Noorelle, MedStar Washington Hospital Center, Washington, District of Columbia, United States
- Thach, Lonnie, MedStar Washington Hospital Center, Washington, District of Columbia, United States
- Schiller, Patrick T., Nephrology Associates, Chicago, Illinois, United States
Introduction
High anion gap metabolic acidosis (HAGMA) with an elevated osmolar gap often triggers empiric treatment for toxic alcohol ingestion. However, assay interference can produce misleading biochemical profiles. Pseudohypobicarbonatemia due to severe hypertriglyceridemia is an underrecognized cause that may lead to unnecessary antidote use and escalation of care.
Case Description
A man in his 30s with alcohol use disorder presented with nausea, vomiting, and abdominal pain. Laboratory evaluation demonstrated sodium 125 mEq/L, bicarbonate 14 mEq/L, anion gap 23, creatinine 0.43 mg/dL, and BUN 6 mg/dL. Measured serum osmolality was 355 mOsm/kg with an osmolar gap of 37, raising concern for toxic alcohol ingestion; however, lactate was 1.8 mmol/L.Venous blood gas revealed pH 7.45, pCO2 40 mmHg, and bicarbonate 28 mEq/L, inconsistent with metabolic acidosis. This marked discordance between serum and blood gas bicarbonate raised concern for assay interference rather than true acidemia. Empiric therapy with fomepizole and bicarbonate infusion was deferred. Toxic alcohol levels later returned as negative.Further evaluation revealed severe hypertriglyceridemia (triglycerides 5076 mg/dL). With initiation of lipid-lowering therapy, triglyceride levels declined in parallel with normalization of serum bicarbonate, confirming pseudohypobicarbonatemia.
Discussion
Severe hypertriglyceridemia interferes with spectrophotometric measurement of serum total bicarbonate, producing falsely low bicarbonate levels due to light scattering. In contrast, blood gas analyzers derive bicarbonate using the Henderson–Hasselbalch equation and are not affected by lipemia. This discrepancy can mimic HAGMA with an elevated osmolar gap and lead to inappropriate evaluation and empiric therapy for toxic alcohol ingestion. A key diagnostic clue is a normal or alkalemic pH despite a low serum bicarbonate, which should prompt evaluation for assay interference.
Conclusion: Pseudohypobicarbonatemia should be considered in patients with apparent HAGMA and elevated osmolar gap when clinical and blood gas findings are discordant. Early recognition of this laboratory artifact can prevent unnecessary toxicologic interventions and guide appropriate management.