DIFFERENTIATED HYPEROSMOLARY THERAPY IN CEREBRAL EDEMA IN PATIENTS WITH CRANIOCEREBRAL INJURY
Murotov Temur Malik Nizomovich , Phd, Associate Professor, Department Of Anesthesiology And Resuscitation Of The Tashkent Medical Academy, Tashkent, Republic Of Uzbekistan Mi'rzambetov Dastan Qi'uani'shbaevich , Master Of The Department Of Anesthesiology And Resuscitation Of The Tashkent Medical Academy, Tashkent, Republic Of UzbekistanAbstract
to study the pathophysiological aspects of cerebral edema and compare the effectiveness of using 15% mannitol solution and hypertonic 3.5%, 7%, 10% sodium chloride solution in the complex treatment of patients with head injury. Material and methods: 90 patients from 18 years old to 68 years old with various traumatic brain injuries and inhibition of consciousness level from 4 to 13 points on the Glasgow coma scale were examined.
Results: infusion of mannitol at the indicated dosage reduced ICP after 30 minutes by 42, 3%, and after 120 minutes it remained below the initial data by 23.9%. Infusion of a 3.5% NaCl solution already by the 30th minute led to a decrease of ICP by 48.6%, and by the end of 120 minutes the ICP remained below the initial data by 35.9%. Infusion of a 7% NaCl solution already by the 30th minute led to a decrease in ICP by 55.4%, and by the end of 120 minutes the ICP remained below the initial data by 39.9%. Infusion of a 10% NaCl solution already by the 30th minute led to a decrease in ICP by 58.4%, and by the end of 120 minutes the ICP remained below the initial data by 45.9%.
Conclusions: the decrease in ICP within 30 and 120 minutes after the introduction of hyperosmolar solutions is more pronounced with iv administration of 3.5%, 7%, 10% NaCl solution relative to 15% Mannitol in calculated dosages, which should be borne in mind in patients with concomitant cardiac and renal pathology.
Keywords
Traumatic brain injury, hypertonic saline, intracranial pressure
References
Adnan H., Laura W. et al. The role of the complement system in
traumatic brain injury: a review. Journal of Neuroinflammation. 2018. 15:24
Feigin VL.V., Theadom A., et al, and the BIONIC Study Group. / Incidence of traumatic brain injury in New Zealand-a population-based study. // Lancet Neurol 2013; 12: 53-64.
Chauhan, N.B. / Chronic neurodegenerative consequences of traumatic brain injury. // Restor. Neurol. Neurosci. 2014, 32, 337–365.
Sayed I.A., Shafiq U.R. et al, / Nicotinamide Improves Functional Recovery
via Regulation of the RAGE/JNK/NF-κB Signaling Pathway after Brain Injury. //J. Clin. Med. 2019, 8, 271; doi:10.3390/jcm8020271
Johnson, V.E.; Stewart, W.; Smith, D.H. Axonal pathology in traumatic brain injury. Exp. Neurol. 2013, 246, 35–43.
Elizabeth M.R. Kristin M.B. et al. Effect of controlled cortical impact on the passage of pituitary adenylate cyclase activating polypeptide (PACAP) across the
blood-brain barrier. Author manuscript; available in PMC 2019 January 01. 99: 8–13.
Vimala N.B., Duong T.N. et al. Nanoparticle-based therapeutics for brain injury. Author manuscript; available in PMC. 2019 January 01.
Maas A.I.R., Menon D.K. et al. / Traumatic brain injury- integrated approaches to improve prevention, clinical care, and research. // Lancet Neurology. 2017; 16 (12). pp. 987-1048. ISSN 1474-4422.
Acosta S.A., Tajiri N., et al. Alpha-Synuclein as a pathological link between chronic traumatic brain injury and parkinson’s disease. J Cell Physiol. 2015; 230:1024–32
Briana I.M., Sarah E.S. Current trends in biomarker discovery and
analysis tools for traumatic brain injury. Journal of Biological Engineering. 2019; 13:16
Amira S. D., Sarah M., et al. Stem cells and combination therapy for the treatment of traumatic brain injury. Behavioural Brain Research. 2018; 340. 49–62
Rostami E. Traumatic brain injury models in animals, Methods Mol. Biol. 2016; 1462. 47–59
Jha, R.M., Puccio, A.M., et al. Sulfonylurea Receptor-1: a novel biomarker for cerebral edema in severe traumatic brain injury. Crit. Care Med. 45, 2017. 255–264.
Unterberg AW, Stover J, et al. Edema and brain trauma. Neuroscience. 2004; 129:1019–1027.
Shah S, Kimberly WT. Today’s approach to treating brain swelling in the neuro intensive care unit. Semin Neurol 2016; 36:502–7.
Lykke K., Assentoft M., et. all. Evaluating the involvement of cerebral microvascular endothelial Na(+)/K(+)-ATPase and Na(+)- K(+)-2Cl(-) co-transporter in electrolyte fuxes in an in vitro blood–brain
barrier model of dehydration. J Cereb Blood Flow Metab. 2017.
Nicholas A. P., Lane B. F, et. all. Hyperosmolar Therapy for the Treatment of Cerebral Edema. U.S. Pharmacist, January 19.2018
Raimondas J. Vaiva H. Pathophysiology of severe traumatic brain injury and
management of intracranial hypertension. Lietuvos chirurgija. 2019, vol. 18(2), pp. 62–71
Carney N., Totten A.M., et. all. Guidelines for the Management of Severe
Traumatic Brain Injury, Fourth Edition. Neurosurgery 2017; 80(1): 6–15.
20. Diringer M.N. New trends in hyperosmolar therapy? Current opinion in critical care 2013;19(2):77–82.
21. Tongrong C., Kong N., et. all. Current Purpose and Practice of Hypertonic Saline in Neurosurgery: A Review of the Literature. World Neurosurgery 2014; 82(6): 1307–1318.
22. Wen‑Xin Z., Yong‑Li H. et. all. Hypertonic saline attenuates expression of Notch signaling and proinflammatory mediators in activated microglia in experimentally induced cerebral ischemia and hypoxic BV‑2 microglia. BMC Neurosci (2017) 18:32.
23. Huang L.Q., Zhu G.F., et. all. Hypertonic saline alleviates cerebral edema by inhibiting microglia-derived TNF-alpha and IL-1beta-induced Na–K–Cl cotransporter up-regulation. J Neuroinflammation. 2014;11:102.
24. Chen J., Leong S.Y., et. all. Differential expression of cell fate determinants in neurons and glial cells of adult mouse spinal cord after compression injury. Eur J Neurosci. 2005;22(8):1895–906.
25. Grandbarbe L., Michelucci A., et. all. Notch signaling modulates the activation of microglial cells. Glia. 2007;55(15):1519–30.
26. Neumann H., Kotter M.R., et. all. Debris clearance by microglia: an essential link between degeneration and regeneration. Brain. 2009;132(Pt 2):288–95.
27. Hong-Ke Z., Qiao- Sheng W., et. all. A comparative study on the efficacy of 10% hypertonic saline and equal volume of 20% mannitol in the treatment of experimentally induced cerebral edema in adult rats. Zeng et al. BMC Neuroscience 2010, 11:153.
28. Yang-W.L., Song L. et. all. Neutrophils in traumatic brain injury (TBI):
friend or foe?. Journal of Neuroinflammation (2018) 15:146.
29. Mantovani A., Cassatella M.A., et. all. Neutrophils in the. Activation and regulation of innate and adaptive immunity. Nat Rev. Immunol. 2011; 11:519.
30. Wilson E.H., Weninger W., et. all. Trafficking of immune cells in the
central nervous system. J Clin Invest. 2010; 120:1368–79.
31. Rizoli S.B., Rhind S.G., et al. The immunomodulatory effects of hypertonic saline resuscitation in patients sustaining traumatic hemorrhagic shock: a randomized, controlled, double- blinded trial. Ann Surg. 2006; 243:47-57.
32. Hartl R., Medary M., et. all. Hypertonic/hyperoncotic saline attenuates macrocirculatoy disturbances after traumatic brain injury. J Trauma 1997;42: S41-7.
Article Statistics
Copyright License
Copyright (c) 2023 Murotov Temur Malik Nizomovich, Mi'rzambetov Dastan Qi'uani'shbaevich
This work is licensed under a Creative Commons Attribution 4.0 International License.
Authors retain the copyright of their manuscripts, and all Open Access articles are disseminated under the terms of the Creative Commons Attribution License 4.0 (CC-BY), which licenses unrestricted use, distribution, and reproduction in any medium, provided that the original work is appropriately cited. The use of general descriptive names, trade names, trademarks, and so forth in this publication, even if not specifically identified, does not imply that these names are not protected by the relevant laws and regulations.