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PloS one
Par Broman ME et Forsal I.
Contenu en anglais
Hyperglycemia causes compensatory decrease of plasma sodium concentration by an influx of water from the cellular compartment. When the glucose level is corrected, the sodium concentration will follow and increase to its original level.
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A complex MATLAB script incorporating the Katz and Hillier correction formulas was developed to evaluate the impact of hyperglycemia on sodium levels and to analyze sodium shifts in 9,863 patients across 297,714 paired sodium-glucose measurements. Intensive care unit (ICU) mortality and morbidity data were extracted for the full cohort to assess outcomes.
95.3% of the glucose values (283,686) implied a correction factor for the measured sodium levels in the cohort. Correction of all sodium values for hyperglycemia did not change the adjusted ICU mortalities. Increased maximum sodium shift/24 h starting from 4.00-5.99 mmol/L was related to increased independent ICU mortality. Correction of sodium levels by using Katz and Hillier formulas for hyperglycemia did not change the adjusted ICU mortalities. 602/9,863 (6.1%) patients showed a sodium shift more than 8 mmol/L/24 h. 31 patients (5.1%) were missed without correction for hyperglycemia by the Katz formula and 54 patients (9.0%) were missed without correction by the Hillier formula.
Failure to correct sodium for hyperglycemia misses 5-9% of patients with large sodium shifts (>8 mmol/L per 24 hours). Additionally, a sodium shift as low as 4.00-5.99 mmol/L per 24 hours is an independent risk factor for increased ICU mortality.
Publié dans PloS one. Le résumé est reproduit tel qu’il a été publié et reste l’œuvre de ses auteurs ; lisez l’article complet à la source.
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