To explore the effect of 23.4% hypertonic saline for management of elevated intracranial pressure in children admitted to our institution for severe traumatic brain injury.
Single-center, retrospective medical chart analysis.
A PICU at a level 1 pediatric trauma center in the United States.
Children admitted for severe traumatic brain injury from 2006 to 2016 who received 23.4% hypertonic saline and whose intracranial pressures were measured within 5 hours of receiving 23.4% hypertonic saline.
Over the 10-year period, 1,587 children were admitted for traumatic brain injury, 155 of whom were deemed severe per this study’s criteria. Forty of these children received at least one dose of hypertonic saline, but 14 were excluded for insufficient intracranial pressure data. Among the remaining 26 children, one hundred one 23.4% hypertonic saline boluses were used in the analysis. Use of 23.4% hypertonic saline was associated with a decrease in intracranial pressure of approximately 7 mm Hg at both within 1 hour after the bolus (p < 0.01) and 4 hours after the bolus (p < 0.01) when compared with the intracranial pressure measured within 1 hour before the hypertonic saline bolus. These effects remained significant after adjusting for Functional Status Scale score and CT Marshall scores. There was no statistically significant association between adjunctive therapies, such as antiepileptics and analgesics, and changes in intracranial pressure. There was no laboratory evidence of hyperkalemia or renal injury after use of 23.4% hypertonic saline. Across all hospitalizations, 65% of the study population demonstrated an abnormally elevated creatinine at least once, but only three episodes of acute kidney injury occurred in total, all before hypertonic saline administration. Eight of the 26 children in this analysis died during their hospitalization. The Functional Status Scale scores ranged from 6 to 26 with a mean of 12.2 and SD of 5.7.
Use of 23.4% hypertonic saline with children admitted for severe traumatic brain injury is associated with a statistically significant decrease in intracranial pressure within 1 hour of use.
1Department of Pediatrics, University of Minnesota, Minneapolis, MN.
2Department of Neurosurgery, Hennepin Healthcare, Minneapolis, MN.
3Department of Pediatrics, Hennepin Healthcare, Minneapolis, MN.
4Biostatistical Design and Analysis Center, Clinical and Translational Science Institute, University of Minnesota, Minneapolis, MN.
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Supported, in part, by the National Center for Advancing Translational Sciences of the National Institutes of Health Award Number UL1TR002494.
Dr. Wu’s institution received funding from National Center for Advancing Translational Sciences (NCATS) of the National Institutes of Health (NIH), and he disclosed that the NIH/NCATS funding was used to support the work of the statistician, Lei Zhang, who is employed by the Clinical and Translational Science Institute at the University of Minnesota, and her statistical services are supported by the NIH/NCATS grant mentioned above. Dr. Samadani received funding from Abbott Diagnostic Laboratories (grant, consultant), Continuing Legal Education in Minnesota, New York (speaking honorarium), Integra Corporation (grant, speaking honorarium), Islamic Medical Association of North America (speaking honorarium), Medtronic (speaking honorarium, consultant), Minnesota Brain Injury Alliance (speaking honorarium), National Football League (consultant), National Neurotrauma Society (speaking honorarium), North American Brain Injury Society (speaking honorarium), Oculogica (equity), Texas, Minnesota, and Wisconsin High School Coaches Associations (speaking honorarium), U.S. Veterans Administration and Office of Research and Development (research grant), and USA Football (speaking honorarium). Ms. Zhang received support for article research from the NIH. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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