نوع مقاله : مقاله پژوهشی

نویسندگان

1 دکترای پرستاری، استادیار، مرکز تحقیقات سلامت سالمندان، دانشگاه علوم پزشکی سبزوار، سبزوار، ایران.

2 دانشجوی کارشناس ارشد، پرستاری مراقبت‌های ویژه، دانشگاه علوم پزشکی سبزوار، سبزوار، ایران.

3 استادیار، دانشکده پزشکی، دپارتمان بیهوشی و مراقبت‌های ویژه، دانشگاه علوم پزشکی سبزوار، سبزوار، ایران.

چکیده

مقدمه: اختلالات الکترولیتی و تغییرات سطح هوشیاری از جمله پیامدهای شایع در آسیب‌های تروماتیک مغز هستند که تأثیر جدی بر روند بهبودی بیماران دارند. مطالعه حاضر به‌منظور درک بهتر شیوع اختلالات الکترولیتی و ارتباط آن‌ها با افت سطح هوشیاری در بیماران مبتلابه آسیب‌های تروماتیک مغز انجام‌شده است.
مواد و روش­ها: این مطالعه توصیفی-تحلیلی بر روی ۳۰۰ بیمار بستری در بخش مراقبت‌های ویژه با تشخیص آسیب تروماتیک مغزی از سال 1401 تا 1404 انجام شد. نمونه‌های خون (شامل سدیم، منیزیم، پتاسیم و کلسیم) در بدو پذیرش جمع‌آوری و با استفاده از دستگاه الکترولیت آنالیزر Easy Lyte آنالیز و تحلیل داده‌ها با استفاده از نرم‌افزار SPSS نسخه 24 صورت گرفت.
یافته­ها: اختلال الکترولیتی تقریباً در تمامی انواع آسیب‌های تروماتیک مغز اتفاق افتاد. تمام بیماران با DAI، ICH و IVH نمره GCS کمتر از 8 داشتند. ارتباط آماری معنی‌داری بین سطح سدیم (0.029= p) و منیزیم (0.047= p) با افت سطح هوشیاری وجود دارد؛ اما ازلحاظ پتاسیم (0.182= p) و کلسیم (0.660= p) ارتباط معناداری با افت سطح هوشیاری وجود نداشت.
نتیجه‌گیری: یافته‌های این مطالعه حاکی از آن است که اختلالات الکترولیتی، در بیماران مبتلابه آسیب مغزی تروماتیک شایع هستند. نوسانات در سطح سدیم و منیزیم تأثیر قابل‌توجهی بر سطح هوشیاری بیماران دارند که شناسایی زودهنگام این اختلالات می‌تواند سبب کاهش عوارض و مرگ‌ومیر شود.

تازه های تحقیق

https://scholar.google.com/citations?user=CsdzE0IAAAAJ&hl=en

https://pubmed.ncbi.nlm.nih.gov/?term=ali+asghar+jesmi%5bAuthor%5d&sort

https://scholar.google.com/citations?user=z6xxD74AAAAJ&hl=fa

https://pubmed.ncbi.nlm.nih.gov/?term=maedeh+hamrah%5bAuthor+-+First%5d&sort=

https://scholar.google.com/citations?hl=en&user=wftYotsAAAAJ

https://pubmed.ncbi.nlm.nih.gov/28250601/

 

کلیدواژه‌ها

موضوعات

عنوان مقاله [English]

Prevalence of Electrolyte Disorders and Their Association with Decreased Level of Consciousness in Patients with Traumatic Brain Injury

نویسندگان [English]

  • Ali asghar Jesmi 1
  • Maedeh Hamrah Siyani 2
  • Shakiba Mozari 3

1 Ph.D. in nursing, Assistant professor, Iranian research center on healthy aging, Sabzevar University of Medical Sciences, sabzevar, Iran.

2 MSc. Student in Critical care Nursing, Sabzavar University of Medical Sciences, sabzevar, Iran.

3 Assistant Professor of critical care medicine, department of Anesthesiology, School of Medicine, Sabzavar University of Medical Sciences, Sabzevar, Iran.

چکیده [English]

Introduction: Electrolyte imbalances and altered consciousness are common complications of traumatic brain injury (TBI) that significantly impact patient recovery. This study aimed to determine the prevalence of electrolyte disturbances and their association with decreased consciousness in TBI patients.
Materials and Methods: This descriptive-analytical study included 300 ICU patients with TBI from 2022 to 2025. Blood samples (sodium, magnesium, potassium, calcium) were measured using an EasyLyte analyzer. Data were analyzed with SPSS 24.
Results: Electrolyte disturbances occurred in types of traumatic brain injury. All patients with diffuse axonal injury (DAI), intracerebral hemorrhage (ICH), and intraventricular hemorrhage (IVH) had a Glasgow Coma Scale (GCS) score <8. A statistically significant association was observed between serum sodium (p = 0.029) and magnesium levels (p = 0.047) with decreased levels of consciousness. However, no significant relationship was found between potassium (p = 0.182) and calcium levels (p = 0.660) and reduced consciousness.
Conclusion: Electrolyte disturbances, particularly hypokalemia and hypocalcemia, are prevalent in TBI patients. Early detection and correction may reduce complications and mortality.

کلیدواژه‌ها [English]

  • Traumatic Brain Injuries
  • Electrolyte disturbances
  • Consciousness Disorders
  • Critical Care
  1. Centers for Disease Control and Prevention (CDC). Traumatic Brain Injury (TBI): What is TBI? 2025/July/5.Available from: https://www.cdc.gov/traumaticbraininjury/about.html.
  2. Tagliaferri F, Compagnone C, Korsic M, Servadei F, Kraus J. A systematic review of brain injury epidemiology in Europe. Acta Neurochir (Wien). 2006;148(3):255-68; discussion 68.doi: 10.1007/s00701-005-0651-y.
  3. Mauritz W, Wilbacher I, Majdan M, Leitgeb J, Janciak I, Brazinova A, et al. Epidemiology, treatment and outcome of patients after severe traumatic brain injury in European regions with different economic status. Eur J Public Health. 2008;18(6):575-80.doi: 10.1093/eurpub/ckn079.
  4. Majdan M, Mauritz W, Brazinova A, Rusnak M, Leitgeb J, Janciak I, et al. Severity and outcome of traumatic brain injuries (TBI) with different causes of injury. Brain Inj. 2011;25(9):797-805.doi: 10.3109/02699052.2011.581642
  5. Demass TB, Guadie AG, Mengistu TB, Belay ZA, Melese AA, Berneh AA, et al. The magnitude of mortality and its predictors among adult patients admitted to the Intensive care unit in Amhara Regional State, Northwest Ethiopia. Sci Rep. 2023;13(1):12010.doi: 10.1038/s41598-023-39190-7.
  6. Andersen BJ, Marmarou A. Functional compartmentalization of energy production in neural tissue. Brain Res. 1992;585(1-2):190-5.doi: 10.1016/0006-8993(92)91206-t.
  7. Dey S, Kumar R, Tarat A. Evaluation of Electrolyte Imbalance in Patients With Traumatic Brain Injury Admitted in the Central ICU of a Tertiary Care Centre: A Prospective Observational Study. Cureus. 2021;13(8):e17517. doi: 10.7759/cureus.17517.
  8. Deveduthras N, Balakrishna Y, Muckart D, Harrichandparsad R, Hardcastle T. The prevalence of sodium abnormalities in moderate to severe traumatic brain injury patients in a level 1 Trauma unit in Durban. S Afr J Surg. 2019;57(2):62.10.17159/2078-5151/2019/v57n2a2823 9.
  9. Suman S KN, Singh Y, Kumar V, Yadav G, et al. Evaluation of serum electrolytes in traumatic brain injury patients: prospective randomized observational study. Journal of Anesthesia & Critical Care: Open Access. 2016;5(3):00184. DOI: 15406/jaccoa.2016.05.00184
  10. von Reyn CR, Spaethling JM, Mesfin MN, Ma M, Neumar RW, Smith DH, et al. Calpain mediates proteolysis of the voltage-gated sodium channel alpha-subunit. J 2009;29(33):10350-6 doi: 10.1523/JNEUROSCI.2339-09.2009.
  11. Jin D, Jin S, Liu B, Ding Y, Zhou F, Jin Y. Association between serum sodium and in-hospital mortality among critically ill patients with spontaneous subarachnoid hemorrhage. Frontiers in Neurology. 2022;Volume 13 - 2022.doi: 10.3389/fneur.2022.1025808.
  12. Eisinger RS, Sorrentino ZA, Lucke-Wold B, Zhou S, Barlow B, Hoh B, et al. Severe headache trajectory following aneurysmal subarachnoid hemorrhage: the association with lower sodium levels. Brain Inj. 2022;36(4):579-85.doi: 10.1080/02699052.2022.2055146.
  13. von Reyn CR, Mott RE, Siman R, Smith DH, Meaney DF. Mechanisms of calpain mediated proteolysis of voltage gated sodium channel α-subunits following in vitro dynamic stretch injury. J Neurochem. 2012;121(5):793-805.doi: 10.1111/j.1471-4159.2012.07735.x.
  14. Li T, Zhuang D, Cai S, Ding F, Tian F, Huang M, et al. Low serum calcium is a novel predictor of unfavorable prognosis after traumatic brain injury. Heliyon. 2023;9(8):e18475.
  15. Can A, Du R. Calcium, magnesium, and subarachnoid hemorrhage. Aging (Albany NY). 2018;10(9):2212-3.doi: 10.1016/j.heliyon.2023.e18475.
  16. Zhuang D, Li T, Wu X, Xie H, Sheng J, Chen X, et al. Low serum calcium promotes traumatic intracerebral hematoma expansion by the response of immune cell: A multicenter retrospective cohort study. Sci Rep. 2025;15(1):8639.doi: 10.1038/s41598-025-93416-4.
  17. Yekefallah L, Mohammadi S, Yaghoubi S, Mafi M. Assessment the relationship between sodium and potassium, serum level in Admission time with clinical outcome in head trauma patients. Critical Care Nursing. 2019;12(3):25-32.
  18. Reinert M, Khaldi A, Zauner A, Doppenberg E, Choi S, Bullock R. High extracellular potassium and its correlates after severe head injury: relationship to high intracranial pressure. Neurosurg Focus. 2000;8(1):e10.doi: 10.3171/foc.2000.8.1.2027.
  19. Katayama Y, Becker DP, Tamura T, Hovda DA. Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury. J Neurosurg. 1990;73(6):889-900.doi: 10.3171/jns.1990.73.6.0889.
  20. Yekefallah L, Mohammadi S, Yaghoubi S, Mafi M. Assessment the relationship between phosphorus and magnesium, serum level with clinical outcome in head trauma patients. The Journal of Qazvin University of Medical Sciences. 2019;23(5):396-405.
  21. Wang R, Xu J, He M. Abnormal serum Magnesium Level is Associated with the Coagulopathy in Traumatic Brain Injury Patients. Clin Appl Thromb Hemost. 2024;30: doi: 10.1177/10760296241280919.
  22. Wang R, He M, Xu J. Initial Serum Magnesium Level Is Associated with Mortality Risk in Traumatic Brain Injury Patients. Nutrients. 2022;14-1.doi: 10.3390/nu14194174.
  23. Rafiq MFA, Ahmed N, Khan AA. SERUM ELECTROLYTE DERANGEMENTS IN PATIENTS WITH TRAUMATIC BRAIN INJURY. Journal of Ayub Medical College Abbottabad. 2013;25(1-2):162-4.doi: 10.1080/02699052.2025.2512785.
  24. Tam CW, Shum HP, Yan WW. Impact of Dysnatremia and Dyskalemia on Prognosis in Patients with Aneurysmal Subarachnoid Hemorrhage: A Retrospective Study. Indian J Crit Care Med. 2019;23(12):562-7. doi: 10.5005/jp-journals-10071-23292.
  25. Kocik VI, April MD, Rizzo JA, Dengler BA, Schauer SG. A Review of Electrolyte, Mineral, and Vitamin Changes After Traumatic Brain Injury. Mil Med. 2024;189(1-2):e101-e9.doi: 10.1093/milmed/usad112.
  26. Jabalameli m, taheri s. Evaluation of plasma Sodium, Potassium and osmolarity level in patients with head trauma in neurosurgery ICU. scientific magazine yafte. 2011;13(1):90-8.Doi:10.4103/abr.abr_393_21 .
  27. Mekkodathil A, El-Menyar A, Hakim S, Al Jogol H, Parchani A, Peralta R, et al. Initial Serum Levels of Magnesium and Calcium as Predictors of Mortality in Traumatic Brain Injury Patients: A Retrospective Study. Diagnostics (Basel). 2023;13 (6) DOI: 3390/diagnostics13061172
  28. RekhaPhukan R, Medhi G. Study of Serum Sodium and Potassium Levels in Patients with Acute Subarachnoid Haemorrhage.doi: 10.1080/02688697.2016.1181151.
  29. Wu X, Lu X, Lu X, Yu J, Sun Y, Du Z, et al. Prevalence of severe hypokalaemia in patients with traumatic brain injury. Injury. 2015;46(1):35-41.doi: 10.1016/j.injury.2014.08.002.
  30. Fukui S, Katoh H, Tsuzuki N, Ishihara S, Otani N, Uozumi Y, et al. Gender disparities in serum electrolytes levels after subarachnoid hemorrhage. J Clin Neurosci. 2004;11(6):606-9. DOI: 1016/j.jocn.2003.02.016
  31. Wang GH, Yan Y, Shen HP, Chu Z. The Clinical Characteristics of Electrolyte Disturbance in Patients with Moderate and Severe Traumatic Brain Injury Who Underwent Craniotomy and Its Influence on Prognosis. J Korean Neurosurg Soc. 2023;66(3):332-9 doi: 10.3340/jkns.2022.0078.
  32. Dooling E, Winkelman C. Hyponatremia in the patient with subarachnoid hemorrhage. J Neurosci Nurs. 2004;36(3):130-5. doi: 10.1097/01376517-200406000-00003.
  33. Hoffman H, Ziechmann R, Gould G, Chin LS. The Impact of Aneurysm Location on Incidence and Etiology of Hyponatremia Following Subarachnoid Hemorrhage. World Neurosurg. 2018;110:e621-e6 doi: 10.1016/j.wneu.2017.11.058.
  34. Sajadieh A, Binici Z, Mouridsen MR, Nielsen OW, Hansen JF, Haugaard SB. Mild hyponatremia carries a poor prognosis in community subjects. Am J Med. 2009;122(7):679-86.doi: 10.1016/j.amjmed.2008.11.033.
  35. Mekkodathil A, El-Menyar A, Hakim S, Al Jogol H, Parchani A, Peralta R, et al. Initial serum levels of magnesium and calcium as predictors of mortality in traumatic brain injury patients: a retrospective study. Diagnostics. 2023;13(6):1172 doi: 10.3390/diagnostics13061172.
  36. Kocik VI, April MD, Rizzo JA, Dengler BA, Schauer SG. A review of electrolyte, mineral, and vitamin changes after traumatic brain injury. Military medicine. 2024;189(1-2):e101-e9.
  37. Wolf JA, Stys PK, Lusardi T, Meaney D, Smith DH. Traumatic axonal injury induces calcium influx modulated by tetrodotoxin-sensitive sodium channels. J Neurosci. 2001;21(6):1923-30 doi: 10.1523/JNEUROSCI.21-06-01923.2001.
  38. Song H, McEwan PP, Ameen-Ali KE, Tomasevich A, Kennedy-Dietrich C, Palma A, et al. Concussion leads to widespread axonal sodium channel loss and disruption of the node of Ranvier. Acta Neuropathol. 2022;144(5):967-85. doi: 10.1007/s00401-022-02498-1
  39. Iwata A, Stys PK, Wolf JA, Chen XH, Taylor AG, Meaney DF, et al. Traumatic axonal injury induces proteolytic cleavage of the voltage-gated sodium channels modulated by tetrodotoxin and protease inhibitors. J Neurosci. 2004;24(19):4605-13. doi: 10.1523/JNEUROSCI.0515-03.2004.
  40. Vinas-Rios JM, Sanchez-Aguilar M, Sanchez-Rodriguez JJ, Gonzalez-Aguirre D, Heinen C, Meyer F, et al. Hypocalcaemia as a prognostic factor of early mortality in moderate and severe traumatic brain injury. Neurol Res. 2014;36(2):102-6.doi: 10.1179/1743132813Y.0000000272
  41. Chang JJ, Armonda R, Goyal N, Arthur AS. Magnesium: Pathophysiological mechanisms and potential therapeutic roles in intracerebral hemorrhage. Neural Regen Res. 2019;14(7):1116-21.
  42. Sen AP, Gulati A. Use of magnesium in traumatic brain injury. Neurotherapeutics. 2010;7(1):91-9. doi: 10.4103/1673-5374.251189.
  43. McDonald JW, Silverstein FS, Johnston MV. Magnesium reduces N-methyl-D-aspartate (NMDA)-mediated brain injury in perinatal rats. Neurosci Lett. 1990;109(1-2):234-8. DOI: 1016/0304-3940(90)90569-u
  44. Liotta EM, Karmarkar A, Batra A, Kim M, Prabhakaran S, Naidech AM, et al. Magnesium and Hemorrhage Volume in Patients With Aneurysmal Subarachnoid Hemorrhage. Crit Care Med. 2020;48(1):104-10. doi: 10.1097/CCM.0000000000004079.
  45. Cheng Z, Huang X, Muse FM, Xia L, Zhan Z, Lin X, et al. Low Serum Magnesium Levels Are Associated With Hemorrhagic Transformation After Thrombolysis in Acute Ischemic Stroke. Front Neurol. 2020;11:962 doi: 10.3389/fneur.2020.00962.
  46. Goyal N, Tsivgoulis G, Malhotra K, Houck AL, Khorchid YM, Pandhi A, et al. Serum Magnesium Levels and Outcomes in Patients With Acute Spontaneous Intracerebral Hemorrhage. J Am Heart Assoc. 2018;7(8).doi: 10.1161/JAHA.118.008698.
  47. Stippler M, Fischer MR, Puccio AM, Wisniewski SR, Carson-Walter EB, Dixon CE, et al. Serum and cerebrospinal fluid magnesium in severe traumatic brain injury outcome. J Neurotrauma. 2007;24(8):1347-54. doi/pdf/10.1089/neu.2007.0277