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Rising serum sodium levels are associated with a concurrent development of metabolic alkalosis in critically ill patients

Authors :
Lindner, Gregor
Schwarz, Christoph
Grüssing, Heidelinde
Kneidinger, Nikolaus
Fazekas, Andreas
Funk, Georg-Christian
Lindner, Gregor
Schwarz, Christoph
Grüssing, Heidelinde
Kneidinger, Nikolaus
Fazekas, Andreas
Funk, Georg-Christian
Publication Year :
2018

Abstract

Purpose: Changes in electrolyte homeostasis are important causes of acid-base disorders. While the effects of chloride are well studied, only little is known of the potential contributions of sodium to metabolic acid-base state. Thus, we investigated the effects of intensive care unit (ICU)-acquired hypernatremia on acid-base state. Methods: We included critically ill patients who developed hypernatremia, defined as a serum sodium concentration exceeding 149mmol/L, after ICU admission in this retrospective study. Data on electrolyte and acid-base state in all included patients were gathered in order to analyze the effects of hypernatremia on metabolic acid-base state by use of the physical-chemical approach. Results: A total of 51 patients were included in the study. The time of rising serum sodium and hypernatremia was accompanied by metabolic alkalosis. A transient increase in total base excess (standard base excess from 0.1 to 5.5mmol/L) paralleled by a transient increase in the base excess due to sodium (base excess sodium from 0.7 to 4.1mmol/L) could be observed. The other determinants of metabolic acid-base state remained stable. The increase in base excess was accompanied by a slight increase in overall pH (from 7.392 to 7.429, standard base excess from 0.1 to 5.5mmol/L). Conclusions: Hypernatremia is accompanied by metabolic alkalosis and an increase in pH. Given the high prevalence of hypernatremia, especially in critically ill patients, hypernatremic alkalosis should be part of the differential diagnosis of metabolic acid-base disorders

Details

Database :
OAIster
Notes :
English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1156705548
Document Type :
Electronic Resource