naa a22 4500 510799825 CHVBK 20180411083350.0 cr unu---uuuuu 180411e20130201xx s 000 0 eng 10.1007/s12028-012-9794-x doi (NATIONALLICENCE)springer-10.1007/s12028-012-9794-x Falsely Elevated Sodium Levels During Thiopental Treatment in the ICU: Technical Interference on a Laboratory Device with Important Clinical Relevance [Elektronische Daten] [Bart Feyen, Dries Coenen, Philippe Jorens, Kristien Wouters, Andrew Maas, Viviane Van Hoof, Walter Verbrugghe] Introduction: Thiopental is a cornerstone in the treatment of refractory status epilepticus and intractable intracranial hypertension. In our center we observed that thiopental might cause falsely elevated serum sodium levels. Methods: Triggered by a recent case experience of extremely elevated serum sodium levels during thiopental treatment, we retrospectively identified 53 patients treated with thiopental in our intensive care unit between 2007 and 2011 and evaluated electrolyte changes. We differentiated the analysis before and after introduction of a new device for sodium assays (Dimension Vista, Siemens) in the central laboratory in April 2010. Standardized in vitro laboratory tests were performed to study the effect of thiopental on sodium analysis. Results: Before April 2010, serum sodium levels determined in the central laboratory showed a good agreement with the bedside point-of-care (POC) device during thiopental therapy with [sodium]laboratory−[sodium]POC of only 1.08mmol/L (P=.0517). After April 2010, a strong discrepancy between laboratory values and POC values was observed with [sodium]laboratory−[sodium]POC=11.57mmol/L (P<.0001). Standardized in vitro testing confirmed that thiopental induced a dose-dependent false hypernatremia (P=.002). Conclusions: Thiopental treatment can result in falsely elevated serum sodium. This is a critical finding since high sodium levels preclude administrating mannitol or hypertonic saline for the treatment of elevated intracranial pressure. Moreover, a false high sodium level might lead to the inappropriate administration of hypotonic fluids potentially resulting in increased brain edema and even higher intracranial pressure. To our knowledge, this is the first paper describing this clinically relevant phenomenon. Springer Science+Business Media New York, 2012 Thiopental nationallicence Barbiturate(s) nationallicence Sodium nationallicence Hypernatremia nationallicence False elevation nationallicence Drug interference nationallicence Neurocritical care nationallicence Na : Sodium nationallicence POC : Bedside point-of-care laboratory device nationallicence Rapidlab : POC device nationallicence Dimension Vista : Central laboratory auto analyzer nationallicence Vitros : Central laboratory auto analyzer nationallicence ICP : Intracranial pressure nationallicence Feyen Bart Department of Neurosurgery, Antwerp University Hospital, University of Antwerp, Wilrijkstraat 10, 2650, Edegem, Belgium aut Coenen Dries Department of Clinical Chemistry, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut Jorens Philippe Department of Critical Care Medicine, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut Wouters Kristien Department of Scientific Coordination and Biostatistics, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut Maas Andrew Department of Neurosurgery, Antwerp University Hospital, University of Antwerp, Wilrijkstraat 10, 2650, Edegem, Belgium aut Van Hoof Viviane Department of Clinical Chemistry, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut Verbrugghe Walter Department of Critical Care Medicine, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut Neurocritical Care Humana Press Inc 18/1(2013-02-01), 64-69 1541-6933 18:1<64 2013 18 12028 https://doi.org/10.1007/s12028-012-9794-x text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s12028-012-9794-x text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Feyen Bart Department of Neurosurgery, Antwerp University Hospital, University of Antwerp, Wilrijkstraat 10, 2650, Edegem, Belgium aut NATIONALLICENCE 700 1- Coenen Dries Department of Clinical Chemistry, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut NATIONALLICENCE 700 1- Jorens Philippe Department of Critical Care Medicine, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut NATIONALLICENCE 700 1- Wouters Kristien Department of Scientific Coordination and Biostatistics, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut NATIONALLICENCE 700 1- Maas Andrew Department of Neurosurgery, Antwerp University Hospital, University of Antwerp, Wilrijkstraat 10, 2650, Edegem, Belgium aut NATIONALLICENCE 700 1- Van Hoof Viviane Department of Clinical Chemistry, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut NATIONALLICENCE 700 1- Verbrugghe Walter Department of Critical Care Medicine, Antwerp University Hospital, University of Antwerp, Edegem, Belgium aut NATIONALLICENCE 773 0- Neurocritical Care Humana Press Inc 18/1(2013-02-01), 64-69 1541-6933 18:1<64 2013 18 12028 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer