Sean K R Tan1, Leif Kolmodin1, Mypinder S Sekhon2, Lu Qiao1, Jie Zou1, William R Henderson2, Donald E G Griesdale3,4,5,6. 1. Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada. 2. Division of Critical Care Medicine, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. 3. Division of Critical Care Medicine, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. donald.griesdale@vch.ca. 4. Department of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, BC, Canada. donald.griesdale@vch.ca. 5. Centre for Clinical Epidemiology and Evaluation, Vancouver Coastal Health Research Institute, Vancouver, BC, Canada. donald.griesdale@vch.ca. 6. Critical Care Medicine, Vancouver General Hospital, Room 2438, Jim Pattison Pavilion, 2nd Floor, 855 West 12th Avenue, Vancouver, BC, V5Z 1M9, Canada. donald.griesdale@vch.ca.
Abstract
PURPOSE: Hypertonic saline (HTS) is used to control intracranial pressure (ICP) in patients with traumatic brain injury (TBI); however, in prior studies, the resultant hypernatremia has been associated with increased mortality. We aimed to study the effect of HTS on ICP and mortality in patients with severe TBI. METHODS: We performed a retrospective cohort study of 231 patients with severe TBI (Glasgow Coma Scale [GCS] ≤ 8) admitted to two neurotrauma units from 2006-2012. We recorded daily HTS, ICP, and serum sodium (Na) concentration. We used Cox proportional regression modelling for hospital mortality and incorporated the following time-dependent variables: use of HTS, hypernatremia, and desmopressin administration. RESULTS: The mean [standard deviation (SD)] age of patients was 34 (17) and the median (interquartile range [IQR]) GCS was 6 [3-8]. Hypertonic saline was administered as a continuous infusion in 124 of 231 (54%) patients over 788 of 2,968 (27%) patient-days. Hypernatremia (Na > 145 mmol·L(-1)) developed in 151 of 231 (65%) patients over 717 of 2,968 (24%) patients-days. In patients who developed hypernatremia, the median [IQR] Na was 146 [142-147] mmol·L(-1). Overall hospital mortality was 26% (59 of 231 patients). After adjusting for baseline covariates, neither HTS (hazard ratio [HR], 1.07; 95% confidence interval [CI], 0.56 to 2.05; P = 0.84) nor hypernatremia (HR, 1.31; 95% CI, 0.68 to 2.55; P = 0.42) was associated with hospital mortality. There was no effect modification by either HTS or hypernatremia on each another. Patients who received HTS observed a significant decrease in ICP during their ICU stay compared with those who did not receive HTS (4 mmHg; 95% CI, 2 to 6; P < 0.001 vs 2 mmHg; 95% CI, -1 to 5; P = 0.14). CONCLUSIONS: Hypertonic saline and hypernatremia are not associated with hospital mortality in patients with severe TBI.
PURPOSE:Hypertonic saline (HTS) is used to control intracranial pressure (ICP) in patients with traumatic brain injury (TBI); however, in prior studies, the resultant hypernatremia has been associated with increased mortality. We aimed to study the effect of HTS on ICP and mortality in patients with severe TBI. METHODS: We performed a retrospective cohort study of 231 patients with severe TBI (Glasgow Coma Scale [GCS] ≤ 8) admitted to two neurotrauma units from 2006-2012. We recorded daily HTS, ICP, and serum sodium (Na) concentration. We used Cox proportional regression modelling for hospital mortality and incorporated the following time-dependent variables: use of HTS, hypernatremia, and desmopressin administration. RESULTS: The mean [standard deviation (SD)] age of patients was 34 (17) and the median (interquartile range [IQR]) GCS was 6 [3-8]. Hypertonic saline was administered as a continuous infusion in 124 of 231 (54%) patients over 788 of 2,968 (27%) patient-days. Hypernatremia (Na > 145 mmol·L(-1)) developed in 151 of 231 (65%) patients over 717 of 2,968 (24%) patients-days. In patients who developed hypernatremia, the median [IQR] Na was 146 [142-147] mmol·L(-1). Overall hospital mortality was 26% (59 of 231 patients). After adjusting for baseline covariates, neither HTS (hazard ratio [HR], 1.07; 95% confidence interval [CI], 0.56 to 2.05; P = 0.84) nor hypernatremia (HR, 1.31; 95% CI, 0.68 to 2.55; P = 0.42) was associated with hospital mortality. There was no effect modification by either HTS or hypernatremia on each another. Patients who received HTS observed a significant decrease in ICP during their ICU stay compared with those who did not receive HTS (4 mmHg; 95% CI, 2 to 6; P < 0.001 vs 2 mmHg; 95% CI, -1 to 5; P = 0.14). CONCLUSIONS:Hypertonic saline and hypernatremia are not associated with hospital mortality in patients with severe TBI.
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