Effect of insulin-optimized therapy on stress hyperglycemia and inflammation related factors in patients with severe craniocerebral trauma

doi:10.3877/cma.j.issn.2095-9141.2019.04.005

Abstract

Abstract:

Objective

To observe the therapeutic effect of insulin-optimized therapy on stress hyperglycemia in severe craniocerebral trauma and its influence on inflammation-related factors.

Methods

A total of 274 patients with severe craniocerebral trauma who were enrolled from June 2017 to December 2018 in Department of Critical Care Medicine, Huangshi Central Hospital, Edong Healthcare Group (Affiliated Hospital of Hubei Polytechnic University), they were randomly divided into the observation group and the control group with 137 patients in each group. The observation group was treated with insulin-optimized therapy, while the control group was treated with conventional insulin therapy. The control of stress hyperglycemia in patients with severe craniocerebral trauma was observed by two different treatment schemes.

Results

The tumor necrosis factor-α, C reactive protein, tumor necrosis factor receptor Ⅰ, tumor necrosis factor receptor Ⅱ levels in the observation group after treatment were significantly lower than those in the control group, the difference was statistically significant (P<0.05). There was no significant difference in incidence of hypoglycemia and surgical wound infection between the observation group and the control group (P>0.05), the incidence of respiratory and urinary system infection in the observation group was significantly lower than that in the control group, the difference was statistically significant (P<0.05). The GCS score in the observation group was significantly lower than that in the control group (P<0.05).

Conclusion

Insulin-optimized therapy can reduce the incidence of postoperative infection in patients with severe craniocerebral trauma, reduce the patient’s inflammatory response and improve the prognosis of patients. It can be widely used in clinical practice.

Key words: Insulin-optimized therapy, Stress-induced hyperglycemia, Tumor necrosis factor receptor, C reactive protein

Xiping Mei, Kun Zheng. Effect of insulin-optimized therapy on stress hyperglycemia and inflammation related factors in patients with severe craniocerebral trauma[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2019, 05(04): 210-213.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhsjcswkdzzz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.2095-9141.2019.04.005

https://zhsjcswkdzzz.cma-cmc.com.cn/EN/Y2019/V05/I04/210

Figures/Tables 4

References 17

[1]	Hirsch IB, Buse JB, Leahy J, et al. Options for prandial glucose management in type 2 diabetes patients using basal insulin: addition of a short-acting GLP-1 analogue versus progression to basal-bolus therapy[J]. Diabetes Obes Metab, 2014, 16(3): 206-214.
[2]	Abd El-Wahab EW, Mikheal A, Sidkey F, et al. Insulin resistance as a predictor of early virologic response to HCV therapy among chronic HCV Egyptian patients[J]. J Med Virol, 2015, 87(3): 428-440.
[3]	Shubrook JH Jr. Insulin therapy for challenging patient cases[J]. J Am Osteopath Assoc, 2013, 113(4 Suppl 2): S17-S28.
[4]	Tuo J, Sun H, Shen D, et al. Optimization of insulin pump therapy based on high order run-to-run control scheme[J]. Comput Methods Programs Biomed, 2015, 120(3): 123-134.
[5]	Warren M, Goodhue W. Cerebral tissue pulmonary embolism after severe head trauma in an infant[J]. Am J Forensic Med Pathol, 2013, 34(1): 9-10.
[6]	Xu G, Hu B, Chen G, et al. Analysis of blood trace elements and biochemical indexes levels in severe craniocerebral trauma adults with Glasgow Coma Scale and injury severity score[J]. Biol Trace Elem Res, 2015, 164(2): 192-197.
[7]	Thomas AG, Hegde SV, Dineen RA, et al. Patterns of accidental craniocerebral injury occurring in early childhood[J]. Arch Dis Child, 2013, 98(10): 787-792.
[8]	Richards JE, Kauffmann RM, Obremskey WT, et al. Stress-induced hyperglycemia as a risk factor for surgical-site infection in nondiabetic orthopedic trauma patients admitted to the intensive care unit[J]. J Orthop Trauma, 2013, 27(1): 16-21.
[9]	Chen Y, Yang X, Meng K, et al. Stress-induced hyperglycemia after hip fracture and the increased risk of acute myocardial infarction in nondiabetic patients[J]. Diabetes Care, 2013, 36(10): 3328-3332.
[10]	Bosarge PL, Shoultz TH, Griffin RL, et al. Stress-induced hyperglycemia is associated with higher mortality in severe traumatic brain injury[J]. J Trauma Acute Care Surg, 2015, 79(2): 289-294.
[11]	Wang JY, Zhu C, Qian T, et al. Extracts of black bean peel and pomegranate peel ameliorate oxidative stress-induced hyperglycemia in mice[J]. Exp Ther Med, 2015, 9(1): 43-48.
[12]	Li L, Ye XP, Lu AZ, et al. Hyperglycemia magnifies bupivacaine-induced cell apoptosis triggered by mitochondria dysfunction and endoplasmic reticulum stress[J]. J Neurosci Res, 2013, 91(6): 786-798.
[13]	Taha H, Arya A, Paydar M, et al. Upregulation of insulin secretion and downregulation of pro-inflammatory cytokines, oxidative stress and hyperglycemia in STZ-nicotinamide-induced type 2 diabetic rats by Pseuduvaria monticola bark extract[J]. Food Chem Toxicol, 2014, 66: 295-306.
[14]	Okamura K, Tsubokawa T, Johshita H, et al. Edaravone, a free radical scavenger, attenuates cerebral infarction and hemorrhagic infarction in rats with hyperglycemia[J]. Neurol Res, 2014, 36(1): 65-69.
[15]	Camara ML, Corrigan F, Jaehne EJ, et al. Tumor necrosis factor alpha and its receptors in behaviour and neurobiology of adult mice, in the absence of an immune challenge[J]. Behav Brain Res, 2015, 290: 51-60.
[16]	Arjuman A, Chandra NC. Differential pro-inflammatory responses of TNF-α receptors (TNFR1 and TNFR2) on LOX-1 signalling[J]. Mol Biol Rep, 2015, 42(6): 1039-1047.
[17]	Teixeira AL, de Sousa RT, Zanetti MV, et al. Increased plasma levels of soluble TNF receptors 1 and 2 in bipolar depression and impact of lithium treatment[J]. Hum Psychopharmacol, 2015, 30(1): 52-56.

组别	例数	TNF-α（μg/L）		CRP（mg/L）
组别	例数	治疗前	治疗后	治疗前	治疗后
观察组	137	13.37±7.51	6.32±3.67^a	107.25±21.96	81.56±8.95^a
对照组	137	14.29±6.84	10.25±3.09^a	110.71±20.05	93.82±9.86^a
t值	?	1.060	9.588	1.362	7.865
P值	?	0.290	0.000	0.174	0.000

组别	例数	TNF-α（μg/L）		CRP（mg/L）
组别	例数	治疗前	治疗后	治疗前	治疗后
观察组	137	13.37±7.51	6.32±3.67^a	107.25±21.96	81.56±8.95^a
对照组	137	14.29±6.84	10.25±3.09^a	110.71±20.05	93.82±9.86^a
t值	?	1.060	9.588	1.362	7.865
P值	?	0.290	0.000	0.174	0.000

组别	例数	TNFRⅠ		TNFRⅡ
组别	例数	治疗前	治疗后	治疗前	治疗后
观察组	137	1903.54±247.51	1163.32±193.67^a	3107.25±261.96	1053.82±272.36^a
对照组	137	1864.29±216.84	1350.25±203.09^a	3140.71±250.05	1271.56±245.95^a
t值	?	0.416	4.588	1.739	7.532
P值	?	0.687	0.000	0.131	0.000

组别	例数	TNFRⅠ		TNFRⅡ
组别	例数	治疗前	治疗后	治疗前	治疗后
观察组	137	1903.54±247.51	1163.32±193.67^a	3107.25±261.96	1053.82±272.36^a
对照组	137	1864.29±216.84	1350.25±203.09^a	3140.71±250.05	1271.56±245.95^a
t值	?	0.416	4.588	1.739	7.532
P值	?	0.687	0.000	0.131	0.000

组别	例数	术后低血糖	术后感染部位
组别	例数	术后低血糖	伤口切口	呼吸系统	泌尿系统
观察组	137	34（24.82）	45（32.85）	56（40.88）	23（16.79）
对照组	137	27（19.71）	51（37.23）	74（54.01）	47（34.31）
χ²值	?	1.033	0.577	4.742	11.052
P值	?	0.309	0.447	0.029	0.000

Please choose a citation manager

Content to export