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Sodium acetate infusion in critically ill trauma patients for hyperchloremic acidosis

INTRODUCTION: Sodium acetate has been shown to cause hemodynamic instability when used as a hemodialysis buffer. The pattern of hemodynamic response to injury will be evaluated between those who received sodium acetate and those who did not. The primary purpose of the study is to analyze the effect...

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Autores principales: McCague, Andrew, Dermendjieva, Mira, Hutchinson, Ryan, Wong, David T, Dao, Nguyen
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087685/
https://www.ncbi.nlm.nih.gov/pubmed/21486493
http://dx.doi.org/10.1186/1757-7241-19-24
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author McCague, Andrew
Dermendjieva, Mira
Hutchinson, Ryan
Wong, David T
Dao, Nguyen
author_facet McCague, Andrew
Dermendjieva, Mira
Hutchinson, Ryan
Wong, David T
Dao, Nguyen
author_sort McCague, Andrew
collection PubMed
description INTRODUCTION: Sodium acetate has been shown to cause hemodynamic instability when used as a hemodialysis buffer. The pattern of hemodynamic response to injury will be evaluated between those who received sodium acetate and those who did not. The primary purpose of the study is to analyze the effect of sodium acetate on hemodynamic parameters. Secondarily we looked at the effects on prevention and treatment of hyperchloremic metabolic acidosis. METHODS: The study arm was comprised of patients who had received sodium acetate infusions in place of normal saline between March 2005 and December 2009. A control arm was created based on matching three pre-treatment variables: injury severity score (ISS), pH (+/- 0.03) and base deficit (+/- 3). A retrospective chart review was performed for patients in both arms. Blood pressure, arterial blood gas data and chemistry values were recorded for the time points of -6, -1, 0, 1, 6, 12, 24, 48, and 72 hours from start of sodium acetate infusion. Patients were excluded based on the following criteria: patients who were given sodium bicarbonate within 48 hours of starting sodium acetate, those given sodium acetate as a bolus, non-trauma patients, burn patients, patients who expired within 24 hours of arrival to the ICU, patients diagnosed with rhabdomyolysis and patients whose medical record could not be obtained. RESULTS: A total of 78 patients were included in the study, 39 in the study arm and 39 in the control arm. There were no statistically significant drops in blood pressure within either group. The median pH between the two groups at the start of infusion was equal. Both groups trended towards normal pH with the study arm improving faster than the control arm. The median serum bicarbonate at start of sodium acetate infusion was 19 mmol/L and 20 mmol/L at time zero for the study and control arms respectively with both trending upward during the study period. Chloride trended up initially in both groups but the study arm began to correct sooner at 24 hours compared to 48 hours for the control arm. CONCLUSION: We analyzed the use of sodium acetate as an alternative to normal saline or lactated ringers during resuscitation of critically ill trauma patients at a single center. Our data shows that the hemodynamic profile remained favorable, without evidence of instability at any point during the study period. Normalization of hyperchloremia and metabolic acidosis occurred faster in the patients who received sodium acetate.
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spelling pubmed-30876852011-05-05 Sodium acetate infusion in critically ill trauma patients for hyperchloremic acidosis McCague, Andrew Dermendjieva, Mira Hutchinson, Ryan Wong, David T Dao, Nguyen Scand J Trauma Resusc Emerg Med Original Research INTRODUCTION: Sodium acetate has been shown to cause hemodynamic instability when used as a hemodialysis buffer. The pattern of hemodynamic response to injury will be evaluated between those who received sodium acetate and those who did not. The primary purpose of the study is to analyze the effect of sodium acetate on hemodynamic parameters. Secondarily we looked at the effects on prevention and treatment of hyperchloremic metabolic acidosis. METHODS: The study arm was comprised of patients who had received sodium acetate infusions in place of normal saline between March 2005 and December 2009. A control arm was created based on matching three pre-treatment variables: injury severity score (ISS), pH (+/- 0.03) and base deficit (+/- 3). A retrospective chart review was performed for patients in both arms. Blood pressure, arterial blood gas data and chemistry values were recorded for the time points of -6, -1, 0, 1, 6, 12, 24, 48, and 72 hours from start of sodium acetate infusion. Patients were excluded based on the following criteria: patients who were given sodium bicarbonate within 48 hours of starting sodium acetate, those given sodium acetate as a bolus, non-trauma patients, burn patients, patients who expired within 24 hours of arrival to the ICU, patients diagnosed with rhabdomyolysis and patients whose medical record could not be obtained. RESULTS: A total of 78 patients were included in the study, 39 in the study arm and 39 in the control arm. There were no statistically significant drops in blood pressure within either group. The median pH between the two groups at the start of infusion was equal. Both groups trended towards normal pH with the study arm improving faster than the control arm. The median serum bicarbonate at start of sodium acetate infusion was 19 mmol/L and 20 mmol/L at time zero for the study and control arms respectively with both trending upward during the study period. Chloride trended up initially in both groups but the study arm began to correct sooner at 24 hours compared to 48 hours for the control arm. CONCLUSION: We analyzed the use of sodium acetate as an alternative to normal saline or lactated ringers during resuscitation of critically ill trauma patients at a single center. Our data shows that the hemodynamic profile remained favorable, without evidence of instability at any point during the study period. Normalization of hyperchloremia and metabolic acidosis occurred faster in the patients who received sodium acetate. BioMed Central 2011-04-13 /pmc/articles/PMC3087685/ /pubmed/21486493 http://dx.doi.org/10.1186/1757-7241-19-24 Text en Copyright ©2011 McCague et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
McCague, Andrew
Dermendjieva, Mira
Hutchinson, Ryan
Wong, David T
Dao, Nguyen
Sodium acetate infusion in critically ill trauma patients for hyperchloremic acidosis
title Sodium acetate infusion in critically ill trauma patients for hyperchloremic acidosis
title_full Sodium acetate infusion in critically ill trauma patients for hyperchloremic acidosis
title_fullStr Sodium acetate infusion in critically ill trauma patients for hyperchloremic acidosis
title_full_unstemmed Sodium acetate infusion in critically ill trauma patients for hyperchloremic acidosis
title_short Sodium acetate infusion in critically ill trauma patients for hyperchloremic acidosis
title_sort sodium acetate infusion in critically ill trauma patients for hyperchloremic acidosis
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087685/
https://www.ncbi.nlm.nih.gov/pubmed/21486493
http://dx.doi.org/10.1186/1757-7241-19-24
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