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Benefit of point of care testing in patient with major hyperleukocytosis
Guillaume Grzych1, Estelle Roland2, David Beauvais3
1CHU Lille, Service de Biochimie automatisée Protéines, F-59000 Lille, France; INSERM, UMR-1011-European Genomic Institute for Diabetes, Institut Pasteur de Lille, Lille, France.
Insights
Extreme leukocytosis in a child caused falsely high potassium and low sodium levels. Using Clotting Activator/Serum (CAS) tubes corrected these laboratory interferences, ensuring accurate electrolyte measurements.
Area of Science:
- Clinical Chemistry
- Hematology
- Laboratory Medicine
Background:
- Major leukocytosis can cause significant interference in laboratory test results.
- Pseudo-hyperkalemia due to leukocyte lysis is a known phenomenon, particularly with blast cells.
- The mechanism of pseudo-hyponatremia in hyperleukocytosis remains poorly understood.
Purpose of the Study:
- To investigate laboratory interferences in a pediatric case of extreme leukocytosis.
- To identify effective methods for mitigating electrolyte measurement errors caused by hyperleukocytosis.
Main Methods:
- Analysis of blood samples collected in Clotting Activator/Serum (CAS) tubes.
- Comparison of results with point-of-care measurements.
- Evaluation of sample transport methods (human courier).
Main Results:
- CAS tube analysis revealed corrected potassium and sodium levels within the reference range.
- Point-of-care measurements corroborated the corrected electrolyte values.
- Sample transport method did not resolve the observed interferences.
Conclusions:
- Collecting blood in CAS tubes is an effective strategy to suppress electrolyte interferences from hyperleukocytosis.
- Point-of-care testing can provide accurate electrolyte measurements in cases of extreme leukocytosis.
- Centrifugation is a suspected factor in cell lysis leading to these interferences.
Abstract:
We report a case of a child with major leukocytosis (800 × 109/L) leading to a false increase in plasma potassium and an unexpected spurious decrease in sodium. To suppress interferences due to hyperleukocytosis, our laboratory protocol consists of collecting blood on Clotting Activator/Serum tubes (CAS) and/or carrying samples by human courier. CAS tube analysis showed a decreased level of hyperkalemia and sodium within the reference range (consistent with point of care measurements). Pseudo-hyperkalemia caused by extreme hyperleukocytosis has been well documented and is caused by lysis of leukocytes and cell contents release (including potassium) into the plasma, especially regarding blast cells, which are at even higher risk of lysis. Pseudo-hyponatremia mechanism has not yet been described. This interference could be multifactorial; blast lysis could cause intracellular ionic content release, therefore, modifying extracellular fluid ionic ratios. To correct this interference, the hypothesis is that collecting samples on CAS tubes or monitoring patient using point of care analysis are the most efficient solutions, as transport mode did not resolve interference issues. We speculate that cell lysis related to interference is multifactorial but mainly caused by centrifugation. To confirm this, we would have liked to compare ion levels before and after centrifugation.
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