Subscribe to RSS

DOI: 10.1055/s-0045-1808246
A Comparative Study on the Trends of Blood Glucose, Serum Triglycerides, and CRP-Based Levels in Correlation with GCS among Patients with Traumatic Head Injury

Abstract
Background
Traumatic head injury, which has a high mortality rate, can present as mild contusions, hemorrhages (subdural, extradural, intraparenchymal), diffuse axonal injuries, or direct penetrating injuries. Glasgow Coma Scale (GCS) is used to assess the severity of head injury. Stress-induced hyperglycemia associated with traumatic brain injury has high mortality compared with hyperglycemia in diabetic patients. Stress-induced hyperglycemia not only occurs due to head injury but also serves as a predictor of its outcome. C-reactive protein (CRP) levels are also associated with severity of head injury. Triglyceride levels are said to correlate with neuroinflammation and apoptosis, thus pivotal with severity of traumatic brain injury. With this background, this study aims to compare the levels of blood glucose, CRP, and serum triglycerides in patients with traumatic head injury according to their level of consciousness.
Objectives
This article compares the levels of blood glucose, CRP, and serum triglyceride in traumatic head injury patients according to their GCS and assesses their trends.
Materials and Methods
Patients were divided into two groups (patients with GCS ≤ 8 as group 1 and patients with GCS > 8 as group 2). Blood was collected in these patients at admission, 24 hours after admission, and 48 hours after admission. Glucose was estimated at admission, 24 hours, and 48 hours after admission. CRP and triglycerides were estimated after 24 and 48 hours after admission. The levels were compared between groups and also their trends were assessed.
Statistics
Mean and standard deviation were calculated for the above parameters using Excel. Statistical analysis was done using SPSS software version 26. Statistical significance was assessed using “t-test” and “analysis of variance.” A p-value of < 0.05 was considered statistically significant.
Result
Group 1 showed increased levels of glucose after 24 and 48 hours compared with group 2. CRP showed increased levels in group 1 compared with group 2. There was no significant difference in triglyceride levels between the two groups. Levels of blood glucose showed decreasing trends in group 2. CRP showed increasing trend in group 1. Triglyceride levels showed increasing trend in both the groups.
Conclusion
The decreasing trend in glucose levels in group 2 and increasing trend in CRP levels in group 1 are due to the same pathogenesis, which is associated with the severity of head injury. Increased trends in triglyceride levels were seen in both the groups. Since the association of levels of these parameters and their trends with severity of head injury, regular and serial monitoring of these analytes may be used as prognostic marker.
Keywords
C-reactive protein - Glasgow Coma Scale - glucose - stress induced hyperglycemia - traumatic brain injury - triglyceridePublication History
Article published online:
07 May 2025
© 2025. Asian Congress of Neurological Surgeons. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)
Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India
-
References
- 1 Demlie TA, Alemu MT, Messelu MA, Wagnew F, Mekonen EG. Incidence and predictors of mortality among traumatic brain injury patients admitted to Amhara region Comprehensive Specialized Hospitals, northwest Ethiopia, 2022. BMC Emerg Med 2023; 23 (01) 55
- 2 Bosarge PL, Shoultz TH, Griffin RL, Kerby JD. Stress-induced hyperglycemia is associated with higher mortality in severe traumatic brain injury. J Trauma Acute Care Surg 2015; 79 (02) 289-294
- 3 Liu Y, Yang P, Liu HC, Sun S, Zhang JL, Kang J. The significance of the detection of serum lactate dehydrogenase, hypersensitive C-reactive protein, and N-terminal pro-brain natriuretic peptide for the evaluation of the severity and progression of pediatric patients with traumatic brain injury. Curr Neurovasc Res 2022; 19 (02) 219-224
- 4 Carabias CS, Gomez PA, Panero I. et al; i+12 Neurotraumatology Group Collaborators. Chitinase-3-like protein 1, serum amyloid A1, C-reactive protein, and procalcitonin are promising biomarkers for intracranial severity assessment of traumatic brain injury: relationship with Glasgow Coma Scale and computed tomography volumetry. World Neurosurg 2020; 134: e120-e143
- 5 Rovlias A, Kotsou S. The influence of hyperglycemia on neurological outcome in patients with severe head injury. Neurosurgery 2000; 46 (02) 335-342 , discussion 342–343
- 6 Salehpour F, Bazzazi AM, Aghazadeh J, Abbasivash R, Forouhideh Y, Mirzaei F. et al. Can serum glucose level in early admission predict outcome in patients with severe head trauma?. World Neurosurg 2016; 87: 132-135
- 7 Introduction - Evaluation of the Disability Determination Process for Traumatic Brain Injury in Veterans - NCBI Bookshelf. Accessed August 6, 2024 at: https://www.ncbi.nlm.nih.gov/books/NBK542605/
- 8 Werner C, Engelhard K. Pathophysiology of traumatic brain injury. Br J Anaesth 2007; 99 (01) 4-9
- 9 Tsai YC, Wu SC, Hsieh TM. et al. Association of stress-induced hyperglycemia and diabetic hyperglycemia with mortality in patients with traumatic brain injury: analysis of a propensity score-matched population. Int J Environ Res Public Health 2020; 17 (12) 1-11
- 10 Ng SY, Lee AYW. Traumatic brain injuries: pathophysiology and potential therapeutic targets. Front Cell Neurosci 2019; 13: 528
- 11 Vedantam D, Poman DS, Motwani L, Asif N, Patel A, Anne KK. Stress-induced hyperglycemia: consequences and management. Cureus 2022; 14 (07) e26714
- 12 Kajbaf F, Mojtahedzadeh M, Abdollahi M. Mechanisms underlying stress-induced hyperglycemia in critically ill patients. Therapy 2007; 4 (01) 97-106
- 13 Beishuizen A, Thijs LG. The immunoneuroendocrine axis in critical illness: beneficial adaptation or neuroendocrine exhaustion?. Curr Opin Crit Care 2004; 10 (06) 461-467
- 14 Andreelli F, Jacquier D, Troy S. Molecular aspects of insulin therapy in critically ill patients. Curr Opin Clin Nutr Metab Care 2006; 9 (02) 124-130
- 15 Besedovsky HO, del Rey A. Feed-back interactions between immunological cells and the hypothalamus-pituitary-adrenal axis. Neth J Med 1991; 39 (3-4): 274-280
- 16 Sandi C, Castro-Alamancos MA, Cambronero JC, Bailón C, Guaza C, Borrel J. Interacciones entre el sistema inmunitario y el sistema neuroendocrino. Implicaciones del eje hipotálamo-hipófisis-adrenal [Interactions between the immune system and the neuroendocrine system. Implications of the hypothalamo-hypophyseal-adrenal axis]. Arch Neurobiol (Madr) 1989; 52 (06) 277-286
- 17 Bateman A, Singh A, Kral T, Solomon S. The immune-hypothalamic-pituitary-adrenal axis. Endocr Rev 1989; 10 (01) 92-112
- 18 Khani S, Tayek JA. Cortisol increases gluconeogenesis in humans: its role in the metabolic syndrome. Clin Sci (Lond) 2001; 101 (06) 739-747
- 19 Hanson RW, Reshef L. Regulation of phosphoenolpyruvate carboxykinase (GTP) gene expression. Annu Rev Biochem 1997; 66: 581-611
- 20 Gustavson SM, Chu CA, Nishizawa M. et al. Interaction of glucagon and epinephrine in the control of hepatic glucose production in the conscious dog. Am J Physiol Endocrinol Metab 2003; 284 (04) E695-E707
- 21 Pepys MB, Hirschfield GM. C-reactive protein: a critical update. J Clin Invest 2003; 111 (12) 1805-1812
- 22 Pepys MB, Baltz ML. Acute phase proteins with special reference to C-reactive protein and related proteins (pentaxins) and serum amyloid A protein. Adv Immunol 1983; 34 (C): 141-212
- 23 Clapp BR, Hirschfield GM, Storry C. et al. Inflammation and endothelial function: direct vascular effects of human C-reactive protein on nitric oxide bioavailability. Circulation 2005; 111 (12) 1530-1536
- 24 Ballou SP, Lozanski G. Induction of inflammatory cytokine release from cultured human monocytes by C-reactive protein. Cytokine 1992; 4 (05) 361-368
- 25 Xu L, Korley F, Puccio A. et al. High-sensitivity C-reactive protein as a prognostic biomarker for traumatic brain injury (TBI): A TRACK-TBI Study (1550). Neurology 2020;94(15_Supplement)
- 26 Shetty T, Erdemir GA, Nguyen JT. High-sensitivity C-reactive protein (hsCRP): retrospective study of potential blood biomarker of inflammation in acute mild traumatic brain injury (mTBI) (P3-14.020). Neurology. 2024;102(7_Supplement_1)
- 27 Su SH, Xu W, Li M. et al. Elevated C-reactive protein levels may be a predictor of persistent unfavourable symptoms in patients with mild traumatic brain injury: a preliminary study. Brain Behav Immun 2014; 38: 111-117
- 28 Kuo JR, Lim SW, Zheng HX. et al. Triglyceride is a good biomarker of increased injury severity on a high fat diet rat after traumatic brain injury. Neurochem Res 2020; 45 (07) 1536-1550