- Email: [email protected]
Analysis on the risk factors of intracranial infection secondary to traumatic brain injury
Accepted Manuscript Analysis on the risk factors of intracranial infection secondary to traumatic brain injury Chao Lin, Xin Zhao, Haichen Sun PII:
S1008-1275(15)00044-9
DOI:
10.1016/j.cjtee.2014.10.007
Reference:
CJTEE 30
To appear in:
Chinese Journal of Traumatology
Received Date: 22 July 2014 Revised Date:
8 August 2014
Accepted Date: 28 October 2014
Please cite this article as: Lin C, Zhao X, Sun H, Analysis on the risk factors of intracranial infection secondary to traumatic brain injury, Chinese Journal of Traumatology (2015), doi: 10.1016/ j.cjtee.2014.10.007. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Original article
Chao Lin, Xin Zhao, Haichen Sun * Department of Neurosurgery, Jinling Hospital, Nanjing University
RI PT
Analysis on the risk factors of intracranial infection secondary to traumatic brain injury
SC
*Corresponding author: Tel: 86- 025-80860110, Email: [email protected]
M AN U
Received 22 Jul 2014 Revised 08 Aug 2014 Accepted 28 Oct 2014
TE D
Abstract
Objective: To discuss the characteristics and risk factors for intracranial infection post traumatic brain injury to prevent and better the clinical care.
Methods: Retrospective study of 520 patients with traumatic brain injury were included, 308 male
EP
and 212 female. The risky factors of intracranial infection were identified. Results: Thirty two cases (6.54%, 32/520) of intracranial infection were diagnosed. Intracranial
AC C
infection most likely happened 4 to 10 days after injury. Cerebrospinal fluid leakage, drainage, multiple craniotomies were significant related to intracranial infection. Logistic regression predicted cerebrospinal fluid leakage and drainage as independent factors. Conclusion: Intracranial infection is a serious complication after traumatic brain injury. Patients with drainage or cerebrospinal fluid leakage are more risky for intracranial infection. Aggressively precaution should be taken to better outcome. Key words: traumatic brain injury; complication; intracranial infection; risky factor 1. Introduction
ACCEPTED MANUSCRIPT
Traumatic brain injury (TBI) is a global public health issue.1 Intracranial infection, such as meningitis, encephalitis, and brain abscesses, is a relatively uncommon complication in the aftermath of traumatic brain injury, but is often related to poor neurologic prognosis and cognitive disorder after TBI.2-6 Infection-related mortality rates may be as high as 28%.7 Besides the significant financial
RI PT
burden and loss of life, this study aimed to assess the incidence of intracranial infection in patients with TBI and investigate the risk factors for the development of intracranial infection after TBI. 2. Methods 2.1Participants
SC
Retrospectively, patients with TBI admitted to our hospital from January 2011 to December 2013 were investigated. Total 520 patients with TBI were included for the study. Demographic data
M AN U
including age and gender, mechanism of injury, concomitant injuries, treatments, complications, and recovery were collected and reviewed. Patients with concomitant conditions were excluded. To prevent vitiation from interfering factors, patients who died during the course of analysis, or had intracranial infection before their injury were also excluded from the study. The ages of participants were from 14 to 85 years (40.22±8.46 years), including 308 (59.23%) male patients and 212 (40.77%) female. The causes of injury included motor vehicle crashes (MVC), fall,
TE D
assault, and others. The most common cause of trauma was MVC, accounting for 71.15% (370/520). The causes of head injury, Glasgow coma score (GCS) and CT scan findings were listed in Table 1. Patients were evaluated and treated according to clinical principles and guidelines.8 2.2 Definition of Intracranial infection
EP
Intracranial infection was diagnosed if (a) microorganisms were cultured and identified from the cerebrospinal fluid (CSF); and (b) diagnosis was made by the attending physician with at least one
AC C
of the following: increased white cells, elevated protein or decreased glucose on CSF examination, microorganisms seen on Gram stain of CSF, microorganisms cultured from blood or positive antigen test of CSF, blood or urine.5,9 2.3 Statistical analysis
The relationships between predictor variables were explored by using X2 tests and Fisher exact tests. All variables were candidates in a multivariate logistic regression model to assess which variable was independently associated with intracranial infection. In the final multivariate logistic regression model, p values less than 0.05 were considered statistically different. The statistical package used for analyses was SAS 9.2.
ACCEPTED MANUSCRIPT
3. Results Thirty two (6.54%) Of the 520 patients evaluated, developed intracranial infection during study period. X2 tests and Fisher exact tests revealed that there were significant correlations between occurrence of intracranial infection and cerebrospinal fluid leak, drainage (lumbar or ventricular
RI PT
drainage) and multiple craniotomies (more than twice). Gender, age, admission GCS and
prophylactic use of antibiotics did not influence the development of intracranial infection (Table 2). Results of multivariate logistic regression were summarized in Table 3. In this model, cerebrospinal fluid leak (OR, 2.071; P=0.0091) and drains (OR, 1.923; P=0.0165) were independent predictors of
SC
intracranial infection. There was no independent association between intracranial infection and admission GCS, prophylactic use of antibiotics, or multiple craniotomy.
the fourteenth day after injury (Figure 1). 4. Discussion
M AN U
Intracranial infections developed within 4-10 days after TBI. In our study, the latest case occurred at
Intracranial infection is uncommon after TBI, but the outcome would be severe, both mortality and morbidity would increase.4,9,10 Of the 520 patients with TBI in this study, intracranial infection rate was 6.54%. Logistic regression indicated that cerebrospinal fluid leak and drainage were risk factors
TE D
for intracranial infection. There was no correlation between intracranial infection and admission GCS, prophylactic use of antibiotics, or multiple craniotomies. The low GCS indicates a severe head injury. Major TBI may result in immune paralysis and greater infection susceptibility. But in our study, severity of brain injury did not increase the rate of
EP
intracranial infection. The efficacy of antibiotic prophylaxis, especially during the perioperative period, in patients after TBI remains unclear.11 The risks of antibiotic use, including drug resistances
AC C
and economic burden, require clinical assessments to antibiotic administration.5,12-14 Although significant correlation between intracranial infection and multiple craniotomies, logistic regression analysis showed that the multiple craniotomies was not a risk factor for intracranial infection.
The drainage of lumbar and ventricular drainage was an independent risk factor for intracranial infection in our study. Ventricular drainage is associated with the meningitis in prospective and retrospective studies.5,15-17 The duration of the drainage seems to increase the risk of intracranial infection, especially if the drainage exceeds 3 days.9,18 Definite conclusions may not be drawn from our study, but it would be prudent to suggest the earlier removal of the drainage. The development
ACCEPTED MANUSCRIPT
of intracranial infection carried an independent association with CSF leak, in agreement with previous results.19, 20 Patients with CSF leak should be treated as soon as possible. There are some limitations in this study. First, this is a retrospective, nonrandomized trial, which may produce bias regarding to patient and data collection and analysis. However, we believe our data be
RI PT
useful, as we used strict inclusion criteria for TBI and standard infection definitions. Secondly, in modern intensive care units, intracranial pressure (ICP) monitor in the severe head injury patient is recommended by all guidelines based on available clinical evidence.21-23 ICP monitor may be one of risk factors in the development of intracranial infection.21,24,25 Due to the lack of relevant data, we did not analyze this factor. Finally, our regression analysis only revealed statistical associations, not
SC
cause and effect.
In conclusion, the results of this study indicate that intracranial infection is not common in patients
M AN U
with TBI. The communication of the CSF with the environment is an independent risk factor for intracranial infection after brain injury. Early and effective treatment of this targeted population is important to the prevention of intracranial infection. Further prospective studies using a comparative effectiveness approach may be employed to investigate whether varying infection prevention and
TE D
management strategies impacts the outcome.
References
1. Hyder AA, Wunderlich CA, Puvanachandra P, et al. The impact of traumatic brain injuries: a global perspective. Neuro Rehabilitation. 2007;22:341-353.
EP
2. Prasad K, Rai NK, Kumar A. Use of corticosteroids and other adjunct therapies for acute bacterial meningitis in adults. Curr Infect Dis Rep. 2012;14:445-453
AC C
3. Grimwood K, Anderson P, Anderson V, et al. Twelve year outcomes following bacterial meningitis: further evidence for persisting effects. Arch Dis Child. 2000;83:111-116. 4.Boque MC, Bodi M, Rello J. Trauma, head injury, and neurosurgery infections. Semin Respir Infect. 2000;15:280-286.
5.Kourbeti IS, Jacobs AV, Koslow M, et al. Risk factors associated with postcraniotomy meningitis. Neurosurgery 2007;60:317-25; discussion 325-326. 6.Park P, Garton HJ, Kocan MJ, et al. Risk of infection with prolonged ventricular catheterization. Neurosurgery. 2004;55:594-9; discussion 599-601.
ACCEPTED MANUSCRIPT
7.Harrison-Felix C, Whiteneck G, Devivo MJ, et al. Causes of death following 1 year postinjury among individuals with traumatic brain injury. J Head Trauma Rehabil. 2006;21:22-33. 8.Carney NA, Ghajar J. Guidelines for the management of severe traumatic brain injury. Introduction
RI PT
. J Neurotrauma. 2007;24 Suppl 1:S1-2. 9.Kourbeti IS, Vakis AF, Papadakis JA, et al. Infections in traumatic brain injury patient. Clin Microbiol Infect. 2012;18:359-364.
10.Briggs S, Ellis-Pegler R, Raymond N, et al. Gram-negative bacillary meningitis after cranial
SC
surgery or trauma in adults. Scand J Infect Dis. 2004;36:165-173.
11.Bellamy JL, Molendijk J, Reddy SK, et al. Severe infectious complications following frontal sinus fracture: the impact of operative delay and perioperative antibiotic use. Plast Reconstr Surg
M AN U
2013;132:154-162.
12.Park M, Markus P, Matesic D, et al. Safety and effectiveness of a preoperative allergy clinic in decreasing vancomycin use in patients with a history of penicillin allergy. Ann Allergy Asthma Immunol.2006;97:681-687.
13.Pitout JD, Sanders CC, Sanders WE Jr. Antimicrobial resistance with focus on beta-lactam
TE D
resistance in gram-negative bacilli. Am J Med.1997;103:51-59.
14.Antimicrobial prophylaxis in neurosurgery and after head injury. Infection in Neurosurgery Working Party of the British Society for Antimicrobial Chemotherapy. Lancet.1994;344:1547-1551. 15.Mayhall CG, Archer NH, Lamb VA, et al. Ventriculostomy-related infections. A prospective
EP
epidemiologic study. N Engl J Med. 1984;310:553-559. 16. Bota DP, Lefranc F, Vilallobos HR, et al. Ventriculostomy-related infections in critically ill
AC C
patients: a 6-year experience. J Neurosurg. 2005;103:468-472. 17.Lozier AP, Sciacca RR, Romagnoli MF, et al. Ventriculostomy-related infections: a critical review of the literature. Neurosurgery. 2002;51:170-181; discussion 181-182. 18.Lyke KE, Obasanjo OO, Williams MA, et al. Ventriculitis complicating use of intraventricular catheters in adult neurosurgical patients. Clin Infect Dis . 2001;33:2028-2033. 19.Mollman HD, Haines SJ. Risk factors for postoperative neurosurgical wound infection. A casecontrol study. J Neurosurg 1986;64:902-6.
ACCEPTED MANUSCRIPT
20.Alharfi IM, Stewart TC, Helali IA, et al. Infection Rates, Fevers, and Associated Factors in Pediatric Severe Traumatic Brain Injury. J Neurotrauma. 2014;31:452-458. 21. Morton R, Lucas TH 2nd, Ko A, et al. Intracerebral abscess associated with the Camino intracranial pressure monitor: case report and review of the literature. Neurosurgery. 2012;71:E193-
RI PT
198.
22.Gelabert-Gonzalez M, Ginesta-Galan V, Sernamito-Garcia R, et al. The Camino intracranial pressure device in clinical practice. Assessment in a 1000 cases. Acta Neurochir (Wien) .2006;148:435-441.
SC
23.Gambardella G, Zaccone C, Cardia E, et al. Intracranial pressure monitoring in children: comparison of external ventricular device with the fiberoptic system. Childs Nerv Syst. 1993;9:470-
M AN U
473.
24.Shapiro S, Bowman R, Callahan J, et al. The fiberoptic intraparenchymal cerebral pressure monitor in 244 patients. Surg Neurol. 1996;45:278-82.
25.Martinez-Manas RM, Santamarta D, de Campos JM, et al. Camino intracranial pressure monitor:
TE D
prospective study of accuracy and complications . J Neurol Neurosurg Psychiatry. 2000;69:82-86.
Characteristic
Male
AC C
Gender
EP
Table 1. Demographic information of patients with TBI.
Female
No. of patients
308 212
Injury Mechanism
Motor vehicle accident
370
Fall
78
ACCEPTED MANUSCRIPT
Assaultive
32
Others
40
127
6-8
225
9-12
112
13-15
56
SC
3-5
RI PT
GCS
Admission CT imaging Epidural hematoma
M AN U
78
Subdural hematoma
198
Intracerebral hematoma
298
Diffuse axonal injury
EP
TE D
65
AC C
Table 2. Risky factors for intracranial infection in the patients with TBI Factors
No. of patients
intracranial infection (%)
308
20 (6.49%)
212
12(5.66%)
168
6(3.57%)
P
Gender Male
Female Age (year)
0.853
ACCEPTED MANUSCRIPT
232
16(6.90%)
120
10(8.33%)
3-5
127
8(6.30%)
6-8
225
16(7.11%)
9-12
112
6(5.36%)
13-15
56
2(3.57%)
25 25-50
0.207
positive
137
negative
383
without Drainage with
AC C
without
0.770
20(14.60%) 12(3.13%)
228
15(6.58%)
292
17(5.82%)
EP
with
TE D
Prophylactic use of antibiotics
M AN U
Cerebrospinal fluid leak
SC
Admission GCS
RI PT
50
118
14(11.86%)
402
18(4.48%)
54
7(12.96%)
466
25(5.36%)
0.001
0.718
0.007
Multiple craniotomies ( 2) with
without
0.038
ACCEPTED MANUSCRIPT
Table 3. Multivariate logistic regression analysis of the association between risk factors and intracranial infection Factors
OR value
95% CI
Admission GCS scores
1.724.
0.725-3.326
Cerebrospinal fluid leak
2.071
1.636-4.378
Prophylactic use of antibiotics
0.988
0.133-2.135
Drainage
1.923
1.122-3.335
0.0165
Multiple craniotomies
1.542
0.763-3.375
0.3151
RI PT
P
0.0091
0.9169
SC
M AN U
Figure legends
0.8755
AC C
EP
TE D
Figure 1. The time of occurring intracranial infection in the patients with TBI.
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
S1008-1275(15)00044-9
DOI:
10.1016/j.cjtee.2014.10.007
Reference:
CJTEE 30
To appear in:
Chinese Journal of Traumatology
Received Date: 22 July 2014 Revised Date:
8 August 2014
Accepted Date: 28 October 2014
Please cite this article as: Lin C, Zhao X, Sun H, Analysis on the risk factors of intracranial infection secondary to traumatic brain injury, Chinese Journal of Traumatology (2015), doi: 10.1016/ j.cjtee.2014.10.007. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Original article
Chao Lin, Xin Zhao, Haichen Sun * Department of Neurosurgery, Jinling Hospital, Nanjing University
RI PT
Analysis on the risk factors of intracranial infection secondary to traumatic brain injury
SC
*Corresponding author: Tel: 86- 025-80860110, Email: [email protected]
M AN U
Received 22 Jul 2014 Revised 08 Aug 2014 Accepted 28 Oct 2014
TE D
Abstract
Objective: To discuss the characteristics and risk factors for intracranial infection post traumatic brain injury to prevent and better the clinical care.
Methods: Retrospective study of 520 patients with traumatic brain injury were included, 308 male
EP
and 212 female. The risky factors of intracranial infection were identified. Results: Thirty two cases (6.54%, 32/520) of intracranial infection were diagnosed. Intracranial
AC C
infection most likely happened 4 to 10 days after injury. Cerebrospinal fluid leakage, drainage, multiple craniotomies were significant related to intracranial infection. Logistic regression predicted cerebrospinal fluid leakage and drainage as independent factors. Conclusion: Intracranial infection is a serious complication after traumatic brain injury. Patients with drainage or cerebrospinal fluid leakage are more risky for intracranial infection. Aggressively precaution should be taken to better outcome. Key words: traumatic brain injury; complication; intracranial infection; risky factor 1. Introduction
ACCEPTED MANUSCRIPT
Traumatic brain injury (TBI) is a global public health issue.1 Intracranial infection, such as meningitis, encephalitis, and brain abscesses, is a relatively uncommon complication in the aftermath of traumatic brain injury, but is often related to poor neurologic prognosis and cognitive disorder after TBI.2-6 Infection-related mortality rates may be as high as 28%.7 Besides the significant financial
RI PT
burden and loss of life, this study aimed to assess the incidence of intracranial infection in patients with TBI and investigate the risk factors for the development of intracranial infection after TBI. 2. Methods 2.1Participants
SC
Retrospectively, patients with TBI admitted to our hospital from January 2011 to December 2013 were investigated. Total 520 patients with TBI were included for the study. Demographic data
M AN U
including age and gender, mechanism of injury, concomitant injuries, treatments, complications, and recovery were collected and reviewed. Patients with concomitant conditions were excluded. To prevent vitiation from interfering factors, patients who died during the course of analysis, or had intracranial infection before their injury were also excluded from the study. The ages of participants were from 14 to 85 years (40.22±8.46 years), including 308 (59.23%) male patients and 212 (40.77%) female. The causes of injury included motor vehicle crashes (MVC), fall,
TE D
assault, and others. The most common cause of trauma was MVC, accounting for 71.15% (370/520). The causes of head injury, Glasgow coma score (GCS) and CT scan findings were listed in Table 1. Patients were evaluated and treated according to clinical principles and guidelines.8 2.2 Definition of Intracranial infection
EP
Intracranial infection was diagnosed if (a) microorganisms were cultured and identified from the cerebrospinal fluid (CSF); and (b) diagnosis was made by the attending physician with at least one
AC C
of the following: increased white cells, elevated protein or decreased glucose on CSF examination, microorganisms seen on Gram stain of CSF, microorganisms cultured from blood or positive antigen test of CSF, blood or urine.5,9 2.3 Statistical analysis
The relationships between predictor variables were explored by using X2 tests and Fisher exact tests. All variables were candidates in a multivariate logistic regression model to assess which variable was independently associated with intracranial infection. In the final multivariate logistic regression model, p values less than 0.05 were considered statistically different. The statistical package used for analyses was SAS 9.2.
ACCEPTED MANUSCRIPT
3. Results Thirty two (6.54%) Of the 520 patients evaluated, developed intracranial infection during study period. X2 tests and Fisher exact tests revealed that there were significant correlations between occurrence of intracranial infection and cerebrospinal fluid leak, drainage (lumbar or ventricular
RI PT
drainage) and multiple craniotomies (more than twice). Gender, age, admission GCS and
prophylactic use of antibiotics did not influence the development of intracranial infection (Table 2). Results of multivariate logistic regression were summarized in Table 3. In this model, cerebrospinal fluid leak (OR, 2.071; P=0.0091) and drains (OR, 1.923; P=0.0165) were independent predictors of
SC
intracranial infection. There was no independent association between intracranial infection and admission GCS, prophylactic use of antibiotics, or multiple craniotomy.
the fourteenth day after injury (Figure 1). 4. Discussion
M AN U
Intracranial infections developed within 4-10 days after TBI. In our study, the latest case occurred at
Intracranial infection is uncommon after TBI, but the outcome would be severe, both mortality and morbidity would increase.4,9,10 Of the 520 patients with TBI in this study, intracranial infection rate was 6.54%. Logistic regression indicated that cerebrospinal fluid leak and drainage were risk factors
TE D
for intracranial infection. There was no correlation between intracranial infection and admission GCS, prophylactic use of antibiotics, or multiple craniotomies. The low GCS indicates a severe head injury. Major TBI may result in immune paralysis and greater infection susceptibility. But in our study, severity of brain injury did not increase the rate of
EP
intracranial infection. The efficacy of antibiotic prophylaxis, especially during the perioperative period, in patients after TBI remains unclear.11 The risks of antibiotic use, including drug resistances
AC C
and economic burden, require clinical assessments to antibiotic administration.5,12-14 Although significant correlation between intracranial infection and multiple craniotomies, logistic regression analysis showed that the multiple craniotomies was not a risk factor for intracranial infection.
The drainage of lumbar and ventricular drainage was an independent risk factor for intracranial infection in our study. Ventricular drainage is associated with the meningitis in prospective and retrospective studies.5,15-17 The duration of the drainage seems to increase the risk of intracranial infection, especially if the drainage exceeds 3 days.9,18 Definite conclusions may not be drawn from our study, but it would be prudent to suggest the earlier removal of the drainage. The development
ACCEPTED MANUSCRIPT
of intracranial infection carried an independent association with CSF leak, in agreement with previous results.19, 20 Patients with CSF leak should be treated as soon as possible. There are some limitations in this study. First, this is a retrospective, nonrandomized trial, which may produce bias regarding to patient and data collection and analysis. However, we believe our data be
RI PT
useful, as we used strict inclusion criteria for TBI and standard infection definitions. Secondly, in modern intensive care units, intracranial pressure (ICP) monitor in the severe head injury patient is recommended by all guidelines based on available clinical evidence.21-23 ICP monitor may be one of risk factors in the development of intracranial infection.21,24,25 Due to the lack of relevant data, we did not analyze this factor. Finally, our regression analysis only revealed statistical associations, not
SC
cause and effect.
In conclusion, the results of this study indicate that intracranial infection is not common in patients
M AN U
with TBI. The communication of the CSF with the environment is an independent risk factor for intracranial infection after brain injury. Early and effective treatment of this targeted population is important to the prevention of intracranial infection. Further prospective studies using a comparative effectiveness approach may be employed to investigate whether varying infection prevention and
TE D
management strategies impacts the outcome.
References
1. Hyder AA, Wunderlich CA, Puvanachandra P, et al. The impact of traumatic brain injuries: a global perspective. Neuro Rehabilitation. 2007;22:341-353.
EP
2. Prasad K, Rai NK, Kumar A. Use of corticosteroids and other adjunct therapies for acute bacterial meningitis in adults. Curr Infect Dis Rep. 2012;14:445-453
AC C
3. Grimwood K, Anderson P, Anderson V, et al. Twelve year outcomes following bacterial meningitis: further evidence for persisting effects. Arch Dis Child. 2000;83:111-116. 4.Boque MC, Bodi M, Rello J. Trauma, head injury, and neurosurgery infections. Semin Respir Infect. 2000;15:280-286.
5.Kourbeti IS, Jacobs AV, Koslow M, et al. Risk factors associated with postcraniotomy meningitis. Neurosurgery 2007;60:317-25; discussion 325-326. 6.Park P, Garton HJ, Kocan MJ, et al. Risk of infection with prolonged ventricular catheterization. Neurosurgery. 2004;55:594-9; discussion 599-601.
ACCEPTED MANUSCRIPT
7.Harrison-Felix C, Whiteneck G, Devivo MJ, et al. Causes of death following 1 year postinjury among individuals with traumatic brain injury. J Head Trauma Rehabil. 2006;21:22-33. 8.Carney NA, Ghajar J. Guidelines for the management of severe traumatic brain injury. Introduction
RI PT
. J Neurotrauma. 2007;24 Suppl 1:S1-2. 9.Kourbeti IS, Vakis AF, Papadakis JA, et al. Infections in traumatic brain injury patient. Clin Microbiol Infect. 2012;18:359-364.
10.Briggs S, Ellis-Pegler R, Raymond N, et al. Gram-negative bacillary meningitis after cranial
SC
surgery or trauma in adults. Scand J Infect Dis. 2004;36:165-173.
11.Bellamy JL, Molendijk J, Reddy SK, et al. Severe infectious complications following frontal sinus fracture: the impact of operative delay and perioperative antibiotic use. Plast Reconstr Surg
M AN U
2013;132:154-162.
12.Park M, Markus P, Matesic D, et al. Safety and effectiveness of a preoperative allergy clinic in decreasing vancomycin use in patients with a history of penicillin allergy. Ann Allergy Asthma Immunol.2006;97:681-687.
13.Pitout JD, Sanders CC, Sanders WE Jr. Antimicrobial resistance with focus on beta-lactam
TE D
resistance in gram-negative bacilli. Am J Med.1997;103:51-59.
14.Antimicrobial prophylaxis in neurosurgery and after head injury. Infection in Neurosurgery Working Party of the British Society for Antimicrobial Chemotherapy. Lancet.1994;344:1547-1551. 15.Mayhall CG, Archer NH, Lamb VA, et al. Ventriculostomy-related infections. A prospective
EP
epidemiologic study. N Engl J Med. 1984;310:553-559. 16. Bota DP, Lefranc F, Vilallobos HR, et al. Ventriculostomy-related infections in critically ill
AC C
patients: a 6-year experience. J Neurosurg. 2005;103:468-472. 17.Lozier AP, Sciacca RR, Romagnoli MF, et al. Ventriculostomy-related infections: a critical review of the literature. Neurosurgery. 2002;51:170-181; discussion 181-182. 18.Lyke KE, Obasanjo OO, Williams MA, et al. Ventriculitis complicating use of intraventricular catheters in adult neurosurgical patients. Clin Infect Dis . 2001;33:2028-2033. 19.Mollman HD, Haines SJ. Risk factors for postoperative neurosurgical wound infection. A casecontrol study. J Neurosurg 1986;64:902-6.
ACCEPTED MANUSCRIPT
20.Alharfi IM, Stewart TC, Helali IA, et al. Infection Rates, Fevers, and Associated Factors in Pediatric Severe Traumatic Brain Injury. J Neurotrauma. 2014;31:452-458. 21. Morton R, Lucas TH 2nd, Ko A, et al. Intracerebral abscess associated with the Camino intracranial pressure monitor: case report and review of the literature. Neurosurgery. 2012;71:E193-
RI PT
198.
22.Gelabert-Gonzalez M, Ginesta-Galan V, Sernamito-Garcia R, et al. The Camino intracranial pressure device in clinical practice. Assessment in a 1000 cases. Acta Neurochir (Wien) .2006;148:435-441.
SC
23.Gambardella G, Zaccone C, Cardia E, et al. Intracranial pressure monitoring in children: comparison of external ventricular device with the fiberoptic system. Childs Nerv Syst. 1993;9:470-
M AN U
473.
24.Shapiro S, Bowman R, Callahan J, et al. The fiberoptic intraparenchymal cerebral pressure monitor in 244 patients. Surg Neurol. 1996;45:278-82.
25.Martinez-Manas RM, Santamarta D, de Campos JM, et al. Camino intracranial pressure monitor:
TE D
prospective study of accuracy and complications . J Neurol Neurosurg Psychiatry. 2000;69:82-86.
Characteristic
Male
AC C
Gender
EP
Table 1. Demographic information of patients with TBI.
Female
No. of patients
308 212
Injury Mechanism
Motor vehicle accident
370
Fall
78
ACCEPTED MANUSCRIPT
Assaultive
32
Others
40
127
6-8
225
9-12
112
13-15
56
SC
3-5
RI PT
GCS
Admission CT imaging Epidural hematoma
M AN U
78
Subdural hematoma
198
Intracerebral hematoma
298
Diffuse axonal injury
EP
TE D
65
AC C
Table 2. Risky factors for intracranial infection in the patients with TBI Factors
No. of patients
intracranial infection (%)
308
20 (6.49%)
212
12(5.66%)
168
6(3.57%)
P
Gender Male
Female Age (year)
0.853
ACCEPTED MANUSCRIPT
232
16(6.90%)
120
10(8.33%)
3-5
127
8(6.30%)
6-8
225
16(7.11%)
9-12
112
6(5.36%)
13-15
56
2(3.57%)
25 25-50
0.207
positive
137
negative
383
without Drainage with
AC C
without
0.770
20(14.60%) 12(3.13%)
228
15(6.58%)
292
17(5.82%)
EP
with
TE D
Prophylactic use of antibiotics
M AN U
Cerebrospinal fluid leak
SC
Admission GCS
RI PT
50
118
14(11.86%)
402
18(4.48%)
54
7(12.96%)
466
25(5.36%)
0.001
0.718
0.007
Multiple craniotomies ( 2) with
without
0.038
ACCEPTED MANUSCRIPT
Table 3. Multivariate logistic regression analysis of the association between risk factors and intracranial infection Factors
OR value
95% CI
Admission GCS scores
1.724.
0.725-3.326
Cerebrospinal fluid leak
2.071
1.636-4.378
Prophylactic use of antibiotics
0.988
0.133-2.135
Drainage
1.923
1.122-3.335
0.0165
Multiple craniotomies
1.542
0.763-3.375
0.3151
RI PT
P
0.0091
0.9169
SC
M AN U
Figure legends
0.8755
AC C
EP
TE D
Figure 1. The time of occurring intracranial infection in the patients with TBI.
AC C
EP
TE D
M AN U
SC
RI PT
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