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Abstract: PO1164

Effects of Pseudohyponatremia on the Diagnosis of Severe Metabolic Acidosis

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Raza, Hafiz Muhammad Ali, The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
  • Wall, Barry M., The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States

Pseudohyponatremia is defined as falsely low sodium levels in plasma caused by severe hyperlipidemia or hyperproteinemia. We discuss a case of pseudohyponatremia due to hypertriglyceridemia in a patient admitted with severe metabolic acidosis and acetaminophen induced liver toxicity.

Case Description

43-year-old male with hyperlipidemia, diabetes mellitus, and obesity presented with 4 day-history of abdominal pain, nausea, vomiting, and polydipsia. He had decreased intake and was not taking his insulin for 4 days. Medications include glargine insulin, dulaglutide, empagliflozin, glimepiride, rosuvastatin, fenofibrate and losartan. BP:141/59 mmHg, HR:125 bpm, respirations 28/min, Temperature: 98.7, SpO2. 95% on room air. He appeared clinically volume depleted.
Laboratory testing revealed severely lipemic serum, elevated acetaminophen level 44.1 ug/ml, severely elevated transaminases, arterial pH: 7.03, pCO2 11 mmHg, HCO3 <5 mEq/l. Plasma sodium:109 mEq/L and chloride 81 mEq/l using indirect potentiometry and 131 and 111 mEq/l using direct potentiometry. Serum triglycerides 2951 mg/dl, blood glucose 204 mg/dl, plasma lactate 7.5 mmol/l, and creatinine 0.6 mg/dl. Plasma anion gap was 11 mEq/l using direct potentiometry and could not be calculated using indirect potentiometry, as bicarbonate concentration could not be determined due to lipemia.

Based on severe metabolic acidosis, elevated lactate, and positive urinary ketones, a diagnosis of lactic acidosis and suspected euglycemic DKA was made. Patient was treated with DKA-protocol with insulin and fluid resuscitation, and N- acetylcysteine for acetaminophen induced liver toxicity. Metabolic acidosis markedly improved over the next 72 hours. Hypertriglyceridemia, transaminase elevations, and metabolic acidosis fully resolved during 6 week follow up visit.


Severe hyperlipidemia reduces water content of plasma such that autoanalyzers utilizing indirect potentiometry requiring sample dilution, result in pseudohyponatremia. Direct potentiometry does not require sample dilution and measures true sodium concentration, however, plasma anion gap is reduced due to higher measured chloride concentrations with direct potentiometry. Therefore, physicians must be familiar with the laboratory methods to correctly interpret the plasma anion gap in mangagement of metabolic acidosis when using direct potentiomery measurements.