2026, Number 3
<< Back Next >>
Med Crit 2026; 40 (3)
Association between 48-hours sodium variation and mortality in patients with traumatic brain injury in the Intensive Care Unit
Castro CVH, Jiménez CC
Language: Spanish
References: 17
Page: 172-176
PDF size: 679.64 Kb.
ABSTRACT
Introduction: traumatic brain injury (TBI) is a major public health problem with high incidence and mortality. Sodium plays a key role in osmotic balance and intracranial hypertension management. Dysnatremias are frequent and have been associated with mortality rates up to 86%, partly due to complications such as diabetes insipidus.
Objective: to determine the relationship between 48-hour serum sodium variation and mortality in patients with TBI admitted to the intensive care unit.
Material and methods: observational, descriptive, retrospective, and analytical study in patients with TBI admitted to the Intensive Care Unit of High Specialty Medical Unit, Specialty Hospital No. 1, Bajío National Medical Center, Mexican Social Security Institute. Serum sodium levels was recorded at admission and after 48 hours, as well as clinical outcome (survival or death). All consecutive cases between September 2023 and March 2025 was included. Statistical analysis will be performed using SPSS v25.
Results: a total of 95 patients with severe TBI were included (mean age 40.9 years, 70.3% male), with an overall survival of 89% and hospital mortality of 11%. The 48-hour sodium delta was higher in non-survivors (7.5 vs 2.67 mEq/L; p = 0.02), with an AUC of 0.72 and a cutoff of 7.0 mEq/L (sensitivity 70%, specificity 75.3%). A delta ≥ 6.0 mEq/L was associated with acute kidney injury (AUC 0.72; sensitivity 83.3%, specificity 67.4%). Non-survivors had greater use of hypertonic solutions, more acute kidney injury (AKI) cases, poorer oxygenation, and higher rates of hepatic failure and thrombocytopenia. They also showed worse scores in SOFA, APACHE II, and Marshall scales, and lower initial Glasgow scores. Neurological functional outcomes at 30 days were significantly better in survivors according to Rankin and GOSE scales.
Conclusions: the 48-hour sodium delta was identified as an early dynamic biomarker associated with mortality and acute kidney injury in patients with severe TBI. Close monitoring and controlled correction of sodium may optimize management and improve survival and functional outcomes.
REFERENCES
Carney N, Totten AM, O’Reilly C, et al. Guidelines for themanagement of severe traumatic brain injury, fourth edition.Neurosurgery. 2017;80(1):6-15.
Maas AIR, Menon DK, Manley GT, et al. Traumatic braininjury: progress and challenges in prevention, clinical care, andresearch. Lancet Neurol. 2022;21(11):1004-1060.
Carrillo-Esper R, Meza-Márquez JM, et al. Traumacraneoencefálico. Rev Mex Anest. 2026;49(2):S433-S434.
Khellaf A, Khan DZ, Helmy A. Recent advances in traumaticbrain injury. J Neurol. 2019;266(11):2878-2889. doi: 10.1007/s00415-019-09541-4.
Sarkar C, Zhao Z, Aungst S, Sabirzhanov B, Faden AI, LipinskiMM. Impaired autophagy flux is associated with neuronal celldeath after traumatic brain injury. Autophagy. 2014;10(12):2208-2222. doi: 10.4161/15548627.2014.981787.
Pin-On P, Saringkarinkul A, Punjasawadwong Y, KachaS, Wilairat D. Serum electrolyte imbalance and prognosticfactors of postoperative death in adult traumatic brain injurypatients: a prospective cohort study. Medicine (Baltimore).2018;97(45):e13081. doi: 10.1097/MD.0000000000013081.
Li M, Hu YH, Chen G. Hypernatremia severity and the risk ofdeath after traumatic brain injury. Injury. 2013;44(9):1213-1218.doi: 10.1016/j.injury.2012.05.021.
Ngatuvai M, Martinez B, Sauder M, Beeton G, Andrade R, MakaP, et al. Traumatic brain injury, electrolyte levels, and associatedoutcomes: a systematic review. J Surg Res. 2023;289:106-115.doi: 10.1016/j.jss.2023.03.029.
Roquilly A, Moyer JD, Huet O, et al. Effect of continuous infusionof hypertonic saline vs standard care on 6-month neurologicaloutcomes in patients with traumatic brain injury: the COBIrandomized clinical trial. JAMA. 2021;325(20):2056-2066.
Estrada RF, Morales GJ, Tabla RE, Solís LB, NavarroAHA, Martínez VM, et al. Neuroprotección y traumatismocraneoencefálico. Rev Fac Med (Méx.). 2012;55(4):16-29.
Okidi R, Ogwang DM, Okello TR, et al. Factors affecting mortalityafter traumatic brain injury in a resource-poor setting. BJS Open.2020;4(2):320-325. doi: 10.1002/bjs5.50243.
Wu H, Bai M, Li X, Xing Y, Sun S. Diagnosis and treatmentof brain injury complicated by hypernatremia. Front Neurol.2022;13:1026540. doi: 10.3389/fneur.2022.1026540.
Wang X, Li X, Sun J, Wang M, Lang W, Xu X. Relationshipbetween sodium level and in-hospital mortality in traumaticbrain injury patients of MIMIC IV database. Front Neurol.2024;15:1349710. doi:10.3389/fneur.2024.1349710.
Zaragoza JJ, Gómez-Fregoso JA, Hernández-Barajas EM, etal. Acute kidney injury with hypernatremia and major adversekidney events. Clin Kidney J. 2024;18(2):sfae419. doi: 10.1093/ckj/sfae419.
Anteneh ZA, Kebede SK, Azene AG. Incidence and predictorsof acute kidney injury among traumatic brain injury patients inNorthwest Ethiopia: a cohort study using survival analysis. BMCNephrol. 2025;26(1):96. doi: 10.1186/s12882-025-04024-3.
Barea-Mendoza JA, Chico-Fernández M, Quintana-Díaz M,et al. Traumatic brain injury and acute kidney injury-outcomesand associated risk factors. J Clin Med. 2022;11(23):7216. doi:10.3390/jcm11237216.
Ranson J, Magnus BE, Temkin N, et al. Diagnosing theGOSE: structural and psychometric properties using itemresponse theory, a TRACK-TBI pilot study. J Neurotrauma.2019;36(17):2493-2505. doi: 10.1089/neu.2018.5998.