NSAID-Augmented Therapy for Cerebral Edema in Severe Traumatic Brain Injury: A Clinical Study
Visolat Khamzaevna Sharipova , Doctor of Medical Sciences, Professor. Scientific Director of the Department of Anesthesiology and Resuscitation at the Republican Scientific Center for Emergency Medical Care. Tashkent, Uzbekistan Temur Khayrullaevich Ashurov , Postgraduate student in the basic doctoral program at the Bukhara State Medical Institute. Bukhara, UzbekistanAbstract
Background: Severe traumatic brain injury (sTBI) is characterized by intense neuroinflammation and progressive cerebral edema, which significantly impact morbidity and mortality. Conventional anti-edema therapies often provide limited control over the inflammatory cascade. This study evaluates the clinical efficacy of augmenting standard treatment with Nimesulide, a non-steroidal anti-inflammatory drug (NSAID), to mitigate cerebral edema and improve neurological recovery.
Methods: A prospective clinical study was conducted on 150 patients with sTBI. Patients were divided into two groups: the Main Group (n=115), receiving standard intensive care supplemented with Nimesulide, and the Control Group (n=35), receiving standard therapy alone. Neurological status was assessed using the Glasgow Coma Scale (GCS) on days 1, 5, and 10. Secondary outcomes included the incidence of complications (pneumonia, seizures), laboratory markers of systemic inflammation (Neutrophil-to-Lymphocyte Ratio - NLR), and neuroimaging dynamics via MSCT and ophthalmoscopy.
Results: On day 1, GCS scores were comparable between groups (9.1±1.2; p>0.05). By day 10, the Main Group showed significantly higher neurological recovery (13.1±1.7) compared to the Control Group (11.5±1.6; p<0.05). NSAID-augmented therapy was associated with a lower incidence of pneumonia (19.1% vs 28.6%) and post-traumatic seizures (14.8% vs 25.7%; p<0.05). Laboratory findings revealed a more rapid normalization of NLR and endotoxicosis markers in the Main Group. MSCT and ophthalmoscopy confirmed accelerated regression of cerebral edema and earlier stabilization of the artery-to-vein ratio (1:1.5) in patients receiving supplemental anti-inflammatory therapy.
Conclusion: Augmenting standard sTBI protocols with Nimesulide significantly accelerates neurological recovery, reduces the volume of cerebral edema, and lowers the frequency of life-threatening complications. These findings suggest that targeting neuroinflammation is a crucial component in optimizing outcomes for patients with severe traumatic brain injury.
Keywords
Severe traumatic brain injury, Cerebral edema, Neuroinflammation
References
Abhay K, et al. Non-mydriatic fundus photography in neurocritical care: A diagnostic tool for intracranial pressure. Neurology India. 2024;72(4):901–908. doi:10.4103/ni.ni_234_24
Bakhos JJ, et al. The role of NSAIDs in neurocritical care: benefits and risks. Journal of Clinical Medicine. 2021;10(4):654. doi:10.3390/jcm10040654
Balkrishna A, et al. Anti-inflammatory and antioxidant activities of Nimesulide in neurodegenerative models. Scientific Reports. 2023;13(1):14231. doi:10.1038/s41598-023-41256-w
Brain Trauma Foundation. Guidelines for the Management of Severe Traumatic Brain Injury, 4th Edition. Neurosurgery. 2020. [Reference Guidelines].
Cederberg D, Siesjö P. What has inflammation to do with traumatic brain injury? Child's Nervous System. 2010;26(4):421–426. doi:10.1007/s00381-009-1029-x
Czosnyka M, Pickard JD. Monitoring and interpretation of intracranial pressure. Journal of Neurology, Neurosurgery & Psychiatry. 2004;75(6):813–821. doi:10.1136/jnnp.2003.033126
Gao H, Chen X, Zhang J. COX-2/PGE2 pathway and blood-brain barrier disruption in traumatic brain injury. Brain Research Bulletin. 2022;183:114–124. doi:10.1016/j.brainresbull.2022.02.022
Haqberdiev T, et al. Dynamics of GCS and NLR in patients with brain edema receiving augmented therapy. Central Asian Medical Journal. 2025;12(3):45–52. [E-pub ahead of print].
Hinson HE, et al. Neuroinflammation in traumatic brain injury: an opportunity for treatment. Current Opinion in Critical Care. 2015;21(2):111–117. doi:10.1097/MCC.0000000000000182
Jassam SA, et al. Neuroinflammation and the blood-brain barrier in traumatic brain injury. Journal of Neuroinflammation. 2017;14(1):84. doi:10.1186/s12974-017-0857-2
Lozano R, et al. Global, regional, and national burden of traumatic brain injury. The Lancet Public Health. 2022;7(1):e23–e35. doi:10.1016/S2468-2667(21)00189-4
Maas AIR, et al. Traumatic brain injury: integrated approaches to improve prevention, clinical care, and research. The Lancet Neurology. 2022;21(5):419–463. doi:10.1016/S1474-4422(22)00009-7
Morganti-Kossmann MC, et al. Role of inflammation in secondary edema and brain injury. Neurotherapeutics. 2019;16(2):309–322. doi:10.1007/s13311-019-00715-3
Sahu JK, et al. Nimesulide as a Neuroprotective Agent: Molecular Mechanisms and Clinical Prospects. Frontiers in Pharmacology. 2023;14:1102453. doi:10.3389/fphar.2023.1102453
Simon DW, et al. The systemic immune response to traumatic brain injury. Nature Reviews Neurology. 2017;13(3):171–184. doi:10.1038/nrneurol.2016.204
Stocchetti N, Maas AI. Traumatic intracranial hypertension. New England Journal of Medicine. 2014;370(22):2121–2130. doi:10.1056/NEJMra1208708
Sulejmanpasic A, Tanovic A. Role of COX-2 Inhibitors in Preventing Secondary Brain Injury: A Systematic Review. Neurocritical Care. 2024;40(2):512–525. doi:10.1007/s12028-023-01844-w
Taneja N, et al. Evaluation of Nimesulide in severe traumatic brain injury: a randomized controlled trial update. Journal of Neurotrauma. 2025;42(1):88–95. doi:10.1089/neu.2024.0412
Vane JR, Botting RM. Mechanism of action of nonsteroidal anti-inflammatory drugs. The American Journal of Medicine. 1998;104(3):2S–8S. doi:10.1016/s0002-9343(98)00032-9
Zeiler FA, et al. Neutrophil-to-Lymphocyte Ratio as a Predictor of Outcomes in Severe Traumatic Brain Injury. World Neurosurgery. 2020;135:e345–e352. doi:10.1016/j.wneu.2019.11.086
Download and View Statistics
Copyright License
Copyright (c) 2026 Visolat Khamzaevna Sharipova, Temur Khayrullaevich Ashurov

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.


Medical Science
| Open Access |
DOI: