Analysis of risk factors for the 28-day neurological outcome in patients with sepsis complicated with consciousness disorder_West China Medical Journal

Authors：

YUAN Zhongxin ^1,2 , YAO Peng ^1,2 , HE Yarong ^1,2 , GU Zhihan ^1,2 , ZHAO Jie ^1,2 , ZHOU Yaxiong ^1,2 ,  CAO Yu ^1,2

1. Emergency Department / Emergency Medical Laboratory, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P. R. China;
2. Disaster Medical Center, Sichuan University, Chengdu, Sichuan 610041, P. R. China;

Corresponding?author：

CAO Yu, Email: yuyuer@126.com

Keywords：

Sepsis; Consciousness disorder; Neurological function; Prognosis

DOI：

10.7507/1002-0179.202011113

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Objective To investigate the risk factors affecting the 28-day neurological outcome after admission of patients with sepsis complicated with consciousness disorder, create a simple scoring system, and evaluate its predictive value for the poor neurological outcome.Methods We retrospectively collected and analyzed the demographic data, clinical data, 28-day survival status and neurologic outcome of patients with sepsis complicated with disturbance of consciousness admitted to the Emergency Department of West China Hospital of Sichuan University between June 1st, 2017 and May 31st, 2018. Independent risk factors for the 28-day neurologic outcome of patients with disturbance of consciousness were obtained through univariate analyses and multiple logistic regression analysis, and then the continuous variables of risk factors were converted to binary variables according to the cut-off values from receiver operating characteristic (ROC) curve analysis, a simple scoring system was established and it’s predictive value for 28-day neurological outcome of patients with sepsis complicated with consciousness disorder was assessed.Results A total of 149 patients with sepsis complicated with consciousness disorder were included in this study, including 103 males (69.1%) and 46 females (30.9%), with an average age of (58.2±18.6) years old. There were 72 patients (48.3%) with poor outcome of neurological function on Day 28 after admission. Multiple logistic regression analysis revealed that total bile acid [odds ratio (OR)=1.040, 95% confidence interval (CI) (1.004, 1.077), P=0.027], blood ammonia [OR=1.014, 95%CI (1.001, 1.027), P=0.030], pulmonary infection [OR=3.255, 95%CI (1.401, 7.566), P=0.006], and Glasgow Coma Score (GCS) [OR=0.837, 95%CI (0.739, 0.949), P=0.005] were independent influencing factors for the poor neurological function in patients with sepsis complicated with consciousness disorder on Day 28 after admission. The area under the ROC curve predicting the 28-day poor neurological function was 0.754 [95%CI (0.676, 0.832)], and the sensitivity and specificity were 79.2% and 63.6%, respectively.Conclusion For emergency patients with sepsis complicated with consciousness disorder, a simple scoring system based on early GCS, pulmonary infection, serum ammonia, and total bile acid has a favorable predictive value for short-term neurological function.

Citation： YUAN Zhongxin, YAO Peng, HE Yarong, GU Zhihan, ZHAO Jie, ZHOU Yaxiong, CAO Yu. Analysis of risk factors for the 28-day neurological outcome in patients with sepsis complicated with consciousness disorder. West China Medical Journal, 2020, 35(11): 1344-1349. doi: 10.7507/1002-0179.202011113 Copy

1.	Kempker JA, Martin GS. The changing epidemiology and definitions of sepsis. Clin Chest Med, 2016, 37(2): 165-179.
2.	Hawiger J, Veach RA, Zienkiewicz J. New paradigms in sepsis: from prevention to protection of failing microcirculation. J Thromb Haemost, 2015, 13(10): 1743-1756.
3.	Sweis R, Ortiz J, Biller J. Neurology of sepsis. Curr Neurol Neurosci Rep, 2016, 16(3): 21.
4.	Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 2016, 315(8): 801-810.
5.	Edgren E, Hedstrand U, Kelsey S, et al. Assessment of neurological prognosis in comatose survivors of cardiac arrest. BRCT I Study Group. Lancet, 1994, 343(8905): 1055-1059.
6.	Karinch AM, Pan M, Lin CM, et al. Glutamine metabolism in sepsis and infection. J Nutr, 2001, 131(9 Suppl): 2535S-2538S; discussion 2550S-2551S.
7.	Ghatak T, Azim A, Mahindra S, et al. Can Klebsiella sepsis lead to hyperammonemic encephalopathy with normal liver function?. J Anaesthesiol Clin Pharmacol, 2013, 29(3): 415-416.
8.	G?rg B, Wettstein M, Metzger S, et al. Lipopolysaccharide-induced tyrosine nitration and inactivation of hepatic glutamine synthetase in the rat. Hepatology, 2005, 41(5): 1065-1073.
9.	Brusilow SW, Koehler RC, Traystman RJ, et al. Astrocyte glutamine synthetase: importance in hyperammonemic syndromes and potential target for therapy. Neurotherapeutics, 2010, 7(4): 452-470.
10.	Rose CF. Ammonia-lowering strategies for the treatment of hepatic encephalopathy. Clin Pharmacol Ther, 2012, 92(3): 321-331.
11.	Gonzalez-Usano A, Cauli O, Agusti A, et al. Hyperammonemia alters the modulation by different neurosteroids of the glutamate-nitric oxide-cyclic GMP pathway through NMDA-GABAA-or sigma receptors in cerebellum in vivo. J Neurochem, 2013, 125(1): 133-143.
12.	Lee JM, Trauner M, Soroka CJ, et al. Expression of the bile salt export pump is maintained after chronic cholestasis in the rat. Gastroenterology, 2000, 118(1): 163-172.
13.	Trauner M, Arrese M, Soroka CJ, et al. The rat canalicular conjugate export pump (Mrp2) is down-regulated in intrahepatic and obstructive cholestasis. Gastroenterology, 1997, 113(1): 255-264.
14.	Dufour JF, Turner TJ, Arias IM. Nitric oxide blocks bile canalicular contraction by inhibiting inositol trisphosphate-dependent calcium mobilization. Gastroenterology, 1995, 108(3): 841-849.
15.	Spirlì C, Nathanson MH, Fiorotto R, et al. Proinflammatory cytokines inhibit secretion in rat bile duct epithelium. Gastroenterology, 2001, 121(1): 156-169.
16.	Spirlì C, Fabris L, Duner E, et al. Cytokine-stimulated nitric oxide production inhibits adenylyl cyclase and cAMP-dependent secretion in cholangiocytes. Gastroenterology, 2003, 124(3): 737-753.
17.	Dhainaut JF, Marin N, Mignon A, et al. Hepatic response to sepsis: interaction between coagulation and inflammatory processes. Crit Care Med, 2001, 29(7 Suppl): S42-S47.
18.	Seymour CW, Liu VX, Iwashyna TJ, et al. Assessment of clinical criteria for sepsis: for the third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA, 2016, 315(8): 762-774.
19.	Guo J, Cheng Y, Wang Q, et al. Changes of rScO₂ and ScvO₂ in children with sepsis-related encephalopathy with different prognoses and clinical features. Exp Ther Med, 2019, 17(5): 3943-3948.
20.	Maiti P, Singh SB, Sharma AK, et al. Hypobaric hypoxia induces oxidative stress in rat brain. Neurochem Int, 2006, 49(8): 709-716.
21.	Margaill I, Plotkine M, Lerouet D. Antioxidant strategies in the treatment of stroke. Free Radic Biol Med, 2005, 39(4): 429-443.
22.	Niizuma K, Endo H, Chan PH. Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival. J Neurochem, 2009, 109(Suppl 1): 133-138.
23.	Ramanathan L, Gozal D, Siegel JM. Antioxidant responses to chronic hypoxia in the rat cerebellum and pons. J Neurochem, 2005, 93(1): 47-52.
24.	Adam-Vizi V. Production of reactive oxygen species in brain mitochondria: contribution by electron transport chain and non-electron transport chain sources. Antioxid Redox Signal, 2005, 7(9/10): 1140-1149.
25.	Degracia DJ, Kumar R, Owen CR, et al. Molecular pathways of protein synthesis inhibition during brain reperfusion: implications for neuronal survival or death. J Cereb Blood Flow Metab, 2002, 22(2): 127-141.

1. Kempker JA, Martin GS. The changing epidemiology and definitions of sepsis. Clin Chest Med, 2016, 37(2): 165-179.
2. Hawiger J, Veach RA, Zienkiewicz J. New paradigms in sepsis: from prevention to protection of failing microcirculation. J Thromb Haemost, 2015, 13(10): 1743-1756.
3. Sweis R, Ortiz J, Biller J. Neurology of sepsis. Curr Neurol Neurosci Rep, 2016, 16(3): 21.
4. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 2016, 315(8): 801-810.
5. Edgren E, Hedstrand U, Kelsey S, et al. Assessment of neurological prognosis in comatose survivors of cardiac arrest. BRCT I Study Group. Lancet, 1994, 343(8905): 1055-1059.
6. Karinch AM, Pan M, Lin CM, et al. Glutamine metabolism in sepsis and infection. J Nutr, 2001, 131(9 Suppl): 2535S-2538S; discussion 2550S-2551S.
7. Ghatak T, Azim A, Mahindra S, et al. Can Klebsiella sepsis lead to hyperammonemic encephalopathy with normal liver function?. J Anaesthesiol Clin Pharmacol, 2013, 29(3): 415-416.
8. G?rg B, Wettstein M, Metzger S, et al. Lipopolysaccharide-induced tyrosine nitration and inactivation of hepatic glutamine synthetase in the rat. Hepatology, 2005, 41(5): 1065-1073.
9. Brusilow SW, Koehler RC, Traystman RJ, et al. Astrocyte glutamine synthetase: importance in hyperammonemic syndromes and potential target for therapy. Neurotherapeutics, 2010, 7(4): 452-470.
10. Rose CF. Ammonia-lowering strategies for the treatment of hepatic encephalopathy. Clin Pharmacol Ther, 2012, 92(3): 321-331.
11. Gonzalez-Usano A, Cauli O, Agusti A, et al. Hyperammonemia alters the modulation by different neurosteroids of the glutamate-nitric oxide-cyclic GMP pathway through NMDA-GABAA-or sigma receptors in cerebellum in vivo. J Neurochem, 2013, 125(1): 133-143.
12. Lee JM, Trauner M, Soroka CJ, et al. Expression of the bile salt export pump is maintained after chronic cholestasis in the rat. Gastroenterology, 2000, 118(1): 163-172.
13. Trauner M, Arrese M, Soroka CJ, et al. The rat canalicular conjugate export pump (Mrp2) is down-regulated in intrahepatic and obstructive cholestasis. Gastroenterology, 1997, 113(1): 255-264.
14. Dufour JF, Turner TJ, Arias IM. Nitric oxide blocks bile canalicular contraction by inhibiting inositol trisphosphate-dependent calcium mobilization. Gastroenterology, 1995, 108(3): 841-849.
15. Spirlì C, Nathanson MH, Fiorotto R, et al. Proinflammatory cytokines inhibit secretion in rat bile duct epithelium. Gastroenterology, 2001, 121(1): 156-169.
16. Spirlì C, Fabris L, Duner E, et al. Cytokine-stimulated nitric oxide production inhibits adenylyl cyclase and cAMP-dependent secretion in cholangiocytes. Gastroenterology, 2003, 124(3): 737-753.
17. Dhainaut JF, Marin N, Mignon A, et al. Hepatic response to sepsis: interaction between coagulation and inflammatory processes. Crit Care Med, 2001, 29(7 Suppl): S42-S47.
18. Seymour CW, Liu VX, Iwashyna TJ, et al. Assessment of clinical criteria for sepsis: for the third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA, 2016, 315(8): 762-774.
19. Guo J, Cheng Y, Wang Q, et al. Changes of rScO₂ and ScvO₂ in children with sepsis-related encephalopathy with different prognoses and clinical features. Exp Ther Med, 2019, 17(5): 3943-3948.
20. Maiti P, Singh SB, Sharma AK, et al. Hypobaric hypoxia induces oxidative stress in rat brain. Neurochem Int, 2006, 49(8): 709-716.
21. Margaill I, Plotkine M, Lerouet D. Antioxidant strategies in the treatment of stroke. Free Radic Biol Med, 2005, 39(4): 429-443.
22. Niizuma K, Endo H, Chan PH. Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival. J Neurochem, 2009, 109(Suppl 1): 133-138.
23. Ramanathan L, Gozal D, Siegel JM. Antioxidant responses to chronic hypoxia in the rat cerebellum and pons. J Neurochem, 2005, 93(1): 47-52.
24. Adam-Vizi V. Production of reactive oxygen species in brain mitochondria: contribution by electron transport chain and non-electron transport chain sources. Antioxid Redox Signal, 2005, 7(9/10): 1140-1149.
25. Degracia DJ, Kumar R, Owen CR, et al. Molecular pathways of protein synthesis inhibition during brain reperfusion: implications for neuronal survival or death. J Cereb Blood Flow Metab, 2002, 22(2): 127-141.

West China Medical Journal

Analysis of risk factors for the 28-day neurological outcome in patients with sepsis complicated with consciousness disorder

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