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 - triglyceride

Introduction

Traumatic head injury has a high mortality rate.[1] Head injuries can present as mild contusions, hemorrhages (subdural, extradural, intraparenchymal), diffuse axonal injuries, or direct penetrating injuries. Stress-induced hyperglycemia is known to been associated with increased mortality in traumatic brain injury (TBI) patients.[2] Interestingly, stress-induced hyperglycemia is linked to higher mortality compared with hyperglycemia in diabetic patients with head injuries.[3] C-reactive protein (CRP), an inflammatory marker, has also been associated with the severity of head injuries.[3] [4] Notably, stress-induced hyperglycemia not only occurs due to head injury but also serves as a predictor of its outcome.[5] Several studies have identified the role of stress-induced hyperglycemia secondary to TBI and similarly the role of CRP and triglycerides. There is limited literature regarding their correlation to Glasgow Coma Scale (GCS) and severity of head injury especially in the patients of this region. In our study, we have compared trends in blood glucose levels and CRP among traumatic head injury patients based on their GCS scores, which is used to assess the severity of head injury based on patient's level of consciousness.

Aim

This article measures the levels of serum glucose, CRP, and triglyceride in patients with traumatic head injury.

This article also compares the levels of serum glucose, CRP, and triglyceride between patients with GCS ≤ 8 and GCS > 8. It also observes the trends in the above parameters in both the groups.

Materials and Methods

Institutional ethical committee approval was obtained dated on October 3, 2021. Informed consent from patients or from their attender was obtained after explaining about the study in Government Stanley Medical College, Chennai, Tamil Nadu, India. Note that 5 mL of sample was collected from the patients along with short history and clinical examination, with GCS. Sample size was calculated using the formula Z (1–×)2 SD2/C2 = (1.96*1.96*76.03*76.03)/(18.7*18.7) = 64 (mean = 187.98, standard deviation [SD] = 76.03), mean and SD are taken from Salehpour et al.[6] The calculated sample size was n = 64.

Inclusion criteria: Traumatic head injury patients of age 18 to 60 years.

Exclusion criteria: Patients with other autoimmune disease like rheumatic arthritis.

Patients with history of diabetes mellitus or other systemic illness.

Then, the patients were divided into two groups according to their GCS (patients with GCS ≤ 8 as group 1 and patients with GCS > 8 as group 2). Samples were collected during admission to the hospital, 24 hours after admission to the hospital, and 48 hours after admission to the hospital. In 24 hours, blood glucose was measured in samples collected at admission and 24 and 48 hours after admission. CRP and triglycerides were measured in samples collected after 24 and 48 hours after admission. Levels of glucose, CRP, and triglycerides were compared between the two groups. Also, trends of glucose, CRP, and triglycerides were assessed in both the groups.

Statistics

The values of glucose, triglyceride, and CRP along with patient age and GCS were entered in Excel. Patients were categorized according to GCS as group 1 and group2.

• Total patients = 75

• Group 1: Patients with GCS ≤ 8 (n = 33)

• Group 2: Patients with GCS > 8 (n = 42)

Laboratory results for glucose values at 0 hours, after 24 hours, and after 48 hours were obtained. For triglyceride, after 24 and 48 hours values were obtained. For CRP, after 24 and 48 hours values were obtained. Mean and SD 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.

The difference in means of glucose, CRP, and triglycerides were calculated between two groups at admission, after 24 hours, and after 48 hours. The difference in the mean value at admission, after 24 hours, and after 48 hours was calculated for the same analyte to find out the trends in glucose, triglyceride, and CRP.

Result

The characteristic of the two groups shows that there is no significant difference in age between the two groups. Age of the two groups, 37.88 ± 11.99 and 32.93 ± 10.01, respectively, with p-value = 0.061, as given in [Table 1].

Table 1 Comparison of age, glucose, CRP, and triglycerides between the two groups

Parameters	Time of investigation	Group 1 GCS ≤ 8 (n = 33)	Group 2 GCS > 8 (n = 42)	p-Value
Age (in years)		37.88 ± 11.99	32.93 ± 10.01	0.061
Glucose (mg/dL)	At 0 h	136.73 ± 38.26	122.00 ± 23.6	0.058
	After 24 h	136.36 ± 26.84	117.31 ± 16.23	< 0.001
	After 48 h	134.06 ± 31.41	109.74 ± 13.10	< 0.001
CRP (mg/dL)	After 24 h	58.41 ± 14.62	22.19 ± 18.49	< 0.001
	After 48 h	65.81 ± 18.25	22.62 ± 19.16	< 0.001
Triglycerides (mg/dL)	After 24 h	93.33 ± 31.13	109.74 ± 27.09	0.32
	After 48 h	104.88 ± 31.35	107.45 ± 32.07	0.73

Abbreviations: CRP, C-reactive protein; GCS, Glasgow Coma Scale.

Note: Group 1: GCS ≤ 8 and group 2: GCS > 8). p-Value < 0.05 considered statistically significant.

Glucose at admission of group 1 and group 2 were 136.73 ± 38.26 and 122.00 ± 23.6, respectively, with p-value = 0.058 as given in [Table 1]. Glucose after 24 hours of group 1 and group 2 were 136.36 ± 26.84 and 117.31 ± 16.23, respectively, with p-value ≤ 0.001 as given in [Table 1]. Glucose after 48 hours of group 1 and group 2 were 134.06 ± 31.41 and 109.74 ± 13.10, respectively, with p-value ≤ 0.001 as given in [Table 1]. CRP after 24 hours of group 1 and group 2 were 58.41 ± 14.62 and 22.19 ± 18.49, respectively, with p-value ≤ 0.001 as given in [Table 1]. CRP after 48 hours of group 1 and group 2 were 65.81 ± 18.25 and 22.62 ± 19.16, respectively, with p-value ≤ 0.001 as given in [Table 1]. Triglycerides after 24 hours of group 1 and group 2 were 93.33 ± 31.13 and 109.74 ± 27.09, respectively, with p-value = 0.32 as given in [Table 1]. Triglycerides after 48 hours of group 1 and group 2 were 104.88 ± 31.35 and 107.45 ± 32.07, respectively, with p-value = 0.73 as given in [Table 1]. [Fig. 1] shows comparison of serum glucose, at admission, after 24 hours, and after 48 hours between the two groups. [Fig. 1] also shows the difference in CRP levels and triglycerides level between the groups after 24 and 48 hours of admission. No difference in the levels of serum triglycerides between the groups were shown in [Fig. 1].

Fig. 1 Comparing serum glucose, C-reactive protein (CRP), and triglyceride levels at admission, after 24 hours, and after 48 hours between the two groups (group 1: Glasgow Coma Scale [GCS] ≤ 8 and group 2: GCS < 8).

Also, trend of glucose levels in group 1 on admission was 136.72 ± 38.26, after 24 hours was 136.36 ± 26.84, and after 48 hours was 134.06 ± 31.41, with p-value = 0.93 as shown in [Table 2]. The trend of glucose levels in group 2 on admission was 122.00 ± 23.60, after 24 hours was 117.30 ± 16.23, and after 48 hours was 109.74 ± 13.10, with p-value = 0.009 as shown in [Table 2]. The trend of CRP levels in group 1 after 24 and 48 hours were 58.41 ± 14.62 and 65.81 ± 18.25, respectively, with p-value = 0.001 as shown in [Table 2]. The trend of CRP levels in group 2 after 24 and 48 hours were 22.19 ± 18.49 and 22.62 ± 19.16, respectively, with p-value = 0.43 as shown in [Table 2]. The trend of triglycerides levels in group 1 after 24 and 48 hours were 93.33 ± 31.13 and 104.88 ± 31.35, respectively, with p-value ≤ 0.001 as shown in [Table 2]. The trend of triglycerides levels in group 2 after 24 and 48 hours were 100.04 ± 27.09 and 107.45 ± 32.07, respectively, with p-value ≤ 0.001 as shown in [Table 2].

Table 2 Trends in laboratory parameters at admission, after 24 hours, and after 48 hours

Analyte	Group	On admission	After 24 h	After 48 h	p-Value
Glucose	Group 1	136.72 ± 38.26	136.36 ± 26.84	134.06 ± 31.41	0.93
	Group 2	122.00 ± 23.60	117.30 ± 16.23	109.74 ± 13.10	0.009
CRP	Group 1		58.41 ± 14.62	65.81 ± 18.25	0.001
	Group 2		22.19 ± 18.49	22.62 ± 19.16	0.43
Triglycerides	Group 1		93.33 ± 31.13	104.88 ± 31.35	< 0.001
	Group 2		100.04 ± 27.09	107.45 ± 32.07	< 0.001

Abbreviation: CRP, C-reactive protein.

Note: p-Value < 0.05 considered statistically significant.

Discussion

Traumatic head injury or TBI is defined as an insult to the brain from an external force that leads to temporary or permanent impairment of cognitive, physical, or psychosocial function.[7] Traumatic head injury can present with fracture, concussion, hemorrhage (subdural hemorrhage, extradural hemorrhage, intracranial hemorrhage), and brain parenchymal damage. It can be localized or diffuse. The damage caused by TBI may be primary or secondary. Primary injury is caused by direct impact, which is localized. Secondary damage is due to inflammation, which presents later and not at the time of injury, which may disrupt blood–brain barrier (BBB), blood cell infiltration, brain edema, and immune mediators like chemotactic factors and interleukins (ILs).[6] [8] TBI is classified according to the mechanism of injury as focal damage due to contact injury leading to contusion, laceration, or intracranial hemorrhage and diffuse brain damage due to acceleration/deceleration injury, which results in diffuse axonal injury or brain swelling.[2] [3] [9] The biochemical, physiological, and cellular changes that occur during primary brain injury leads to secondary brain injury, which can last from hours to years.[10] Factors contributing to secondary injury are oxidative stress, excitotoxicity, mitochondrial dysfunction, lipid peroxidation, neuroinflammation, axon degeneration, and apoptotic cell death.[10]

Stress-induced hyperglycemia is hyperglycemia in nondiabetic patients, which occurs during illness.[11] Kajbaf et al. reviewed and stated that the main pathogenesis of stress-induced hyperglycemia is due to altered carbohydrate and lipid metabolism.[12] This alteration in metabolism is due to neuroendocrine alteration, counter regulatory hormones, and proinflammatory cytokines. All the above said mechanisms cause insulin resistance, which in turn causes hyperglycemia.[11] The inflammatory changes in critically ill patients alter the function of endocrine system especially the hypothalamus-pituitary-adrenal (HPA) axis. This alteration causes insulin resistance causing hyperglycemia.[13] Insulin treatment given for patients shows better outcome in stress-induced hyperglycemic patients. This result is due to its action on molecular basis probably by activating adenosine mono phosphate (AMP)-activated protein kinase and restores glucose uptake and also by decreasing inflammatory processes.[14] To summarize, in critically ill patients inflammatory changes cause release of cytokines, tumor necrosis factor (TNF), and inflammatory mediators. This release stimulates the HPA axis. This causes insulin resistance, which in turn causes hyperglycemia.[13] [15] [16] [17] Glucose homeostasis is maintained by insulin and counter regulatory hormones. Glucose homeostasis is maintained by metabolic pathways such as gluconeogenesis, glycogenesis, and glycolysis. Phosphoenolpyruvate carboxykinase (PEPCK), which is the key enzyme in gluconeogenesis, is regulated by many hormones like insulin, cortisol, and thyroid hormone. Cortisol administration has shown to increase blood glucose levels.[18] Cortisol and thyroid hormone cause increased activity of PEPCK and insulin inhibits its activity.[19] Glucagon and epinephrine have shown to have a role in increasing blood glucose.[20] TBI leads to increase in counter regulatory hormones. These counter regulatory hormones such as glucagon, cortisol, epinephrine, norepinephrine, thyroid hormone, and growth hormone cause increase in blood glucose levels in different mechanisms[15] [16] [17] [18] [19] [20]

CRP is a pentameric protein with five identical subunits around a central pore. Molecular weight is 120,000 Da. Each subunit contains 208 amino acids with two antiparallel β sheets.[21] CRP is an acute phase reactant.[22] CRP is present in sphingomyelin and phosphatidylcholine is present on the cell membrane of eukaryotic cells. Histone, phosphatidylethanolamine, small nuclear ribonucleoproteins (snRNPs), and lamnin are the ligands with which CRP can bind. CRP can also bind to immunoglobulin receptor. Head of the phospholipids are not available in intact cells to which CRP binds. So, it can bind only to the damaged cells where the head of phospholipids will be freely available for binding.[22] CRP enhances endothelial adhesion and inhibits nitric oxide synthesis.[23] CRP stimulates proinflammatory cytokines such as IL-6, IL-1, and TNF. It also activates plasminogen activator inhibitor-1. This shows the proinflammatory action of CRP.[24] High-sensitivity CRP along with glial fibrillary acidic protein (GFAP) predict disability, which occurs after 6 months.[25] CRP can be used as a biomarker for prognosis of mild TBI, where postconcussion may be a complication and initial prognostic marker may not be available.[26] In mild TBI there was association between CRP and unfavorable symptoms. Since mild TBI patients may recover early or may not have symptoms initially, raise in CRP levels initially will be helpful, which correlated with unfavorable symptoms.[27]

Studies have proven triglyceride levels correlates with neuroinflammation and apoptosis, so it correlates with the severity of TBI.[28] The alteration in hypothalamus-pancreas, hypothalamus-adrenal, and hypothalamus-pituitary axis, which may cause alteration in carbohydrate and lipid metabolism and direct alteration in carbohydrate and lipid metabolism, may be the reason for increase in triglycerides in traumatic head injury. This study did not show increase in the levels of triglycerides in either group. Even though the levels were normal there was increase in levels between 24 and 48 hours. Analyzing the levels of triglycerides for an extended period would give better understanding.

GCS is one of the parameters used to assess the severity of TBI. Patients with TBI are categorized as mild, moderate, and severe according to our GCS. In this study, we have divided our patients into two groups—group 1 (GCS ≤ 8) and group 2 (GCS > 8)—and compared the parameters according to GCS. After TBI, inflammatory changes take place. This inflammatory process leads to edema, disruption of BBB, and neuroinflammation. This causes secondary injury, which presents with late clinical presentation and contributes to mortality and morbidity. The primary injury, which is due to direct impact, cannot be prevented after admission to hospital and it is only treatable. But on the other hand, secondary injury is preventable since it is due to changes that take place after the primary injury.

The same inflammatory processes can also cause increase in blood glucose levels leading to stress-induced hyperglycemia and increased levels of CRP. Hyperglycemia or increased blood glucose levels have an impact on clinical outcome of the patient including mortality and morbidity. TBI severity has an impact of causing stress-induced hyperglycemia.[2] [9] In this study, blood glucose levels were higher in group 1 (GCS ≤ 8) compared with group 2 (GCS > 8) after 24 and 48 hours of admission. Also, there were decreasing trend in blood glucose levels in group 2, which was not there in group 1. CRP levels were higher in group 1 (GCS ≤ 8) compared with group 2 (GCS > 8) after 24 and 48 hours of admission. Also, there was an increasing trend in CRP levels in group 1 and not in group 2. Triglyceride levels did not show any significant difference between both the groups, but there was an increase in trend in triglyceride level in both the groups.

Hyperglycemia at an early stage may be a reliable predictor of the severity of head injury. Patients with severe head injury frequently developed hyperglycemia, and serum glucose level greater than 200 md/dL was associated with worse outcome and higher mortality.[2] Rovlias and Kotsou have also concluded the same. In patients with mild TBI baseline elevated CRP levels may be an independent predictor of persistent postconcussion syndrome, psychological problems, and cognitive impairment.[27]

Limitations

This study was not proceeded after 48 hours and in postsurgery patients. Further continuation of the study in postsurgical patients will help in comparing the outcome with conservatively treated patients and their outcomes.

Conclusion

In this study, there was an increase in blood glucose levels and CRP levels in head injury patients. Levels of blood glucose showed decreasing trends after 24 hours in patients with GCS > 8 compared with patients with GCS ≤ 8. Also, trends in CRP increased after 48 hours compared with values after 24 hours in group 1 but not in group 2 even though the values are increased in group 2, but not as high as group 1. Serum triglyceride levels were not increased more than reference interval in both the groups. But there was an increasing trend with respect to time. Increase in the above analytes was due to brain edema, inflammation, and alteration in neuroendocrine axis, severity of which is associated with severity of head injury. Not only the levels of blood glucose and CRP seem to be associated with severity of head injury, also their trends vary according to the severity of head injury. So, the use of blood glucose levels and CRP levels as a biochemical marker to assess the severity of head injury especially as a serial monitoring is to be considered. As the study outcome was evaluated at 24 and 48 hours, multivariate studies including comparison of postsurgical outcomes and inclusion of more number of patients would add more information to the objective of the study.

Conflict of Interest

None declared.

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Publication History

Article published online:
07 May 2025