Incidence, prevalence, and occurrence rate of infection among adults hospitalized after traumatic brain injury: study protocol for a systematic review and meta-analysis

Scott, Brian; Roberts, Derek J.; Robertson, Helen Lee; Kramer, Andreas H.; Laupland, Kevin B.; Ousman, Shalina S.; Kubes, Paul; Zygun, David

doi:10.1186/2046-4053-2-68

Cited by 23 publications

(17 citation statements)

References 37 publications

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“…As is known, the most frequently seen extracranial complications following TBI is infection [5]. The incidence of infection following TBI is obviously higher than other noncranial insults such as polytrauma, burn injury, and major surgery [6]. This increased incidence of infection is attributed mainly to the systemic immune suppression arising directly from TBI [7], a view strengthened by recent studies that have provided evidence to clarify the alteration of the humoral or cellular immunity following TBI [8-11].…”

Section: Introductionmentioning

confidence: 99%

Acute Traumatic Brain Injury Induces CD4+ and CD8+ T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Yang

Chen

et al. 2019

Neuroimmunomodulation

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Objective: Traumatic brain injury (TBI) induces immunosuppression in the acute phase, and the activation of the sympathetic nervous system (SNS) might play a role in this process, but the mechanism involved is unknown. Herein, we explored the impact of acute (a)TBI on the peripheral immune system and its correlation with the SNS and the T cell exhaustion marker, PD-1 (programmed cell death-1). Methods: Flow cytometry (FCM) was performed to analyze the expression of T cell markers and intracellular cytokines, interferon-γ and tumor necrosis factor-α, and the T cell exhaustion marker, PD-1, in the peripheral blood mononuclear cells (PBMCs) of TBI rats. Enzyme-linked immunosorbent assay (ELISA) was performed to analyze the concentration of norepinephrine (NE) in the serum. Propranolol was administrated to block the SNS in vivo and NE stimulation was used to imitate the activation of the SNS in vitro. Results: We found that the concentration of NE was significantly elevated after TBI, and the dysfunction of CD4⁺ and CD8⁺ T cells was reversed by the SNS blocker propranolol in vivo and imitated by the SNS neurotransmitter NE in vitro. The expression of PD-1 on CD4⁺ and CD8⁺ T cells was upregulated after aTBI, which was reversed by propranolol administration in vivo and imitated by NE stimulation in vitro. Furthermore, the PD-1 blocker reversed the dysfunction of CD4⁺ and CD8⁺T cells in vitro. Conclusion: Our findings demonstrated that aTBI activated the SNS, and further upregulated the expression of PD-1 on CD4⁺ and CD8⁺ T cells, which, in turn, impaired their function and contributed to immunosuppression.

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Section: Introductionmentioning

confidence: 99%

Acute Traumatic Brain Injury Induces CD4+ and CD8+ T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Yang

Chen

et al. 2019

Neuroimmunomodulation

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“…These bacteria are common in adult and paediatric intensive care units (ICUs) [3,4] and have been associated with increased mortality rates and longer length of stay [5]. Such issues frequently involve patients with acquired brain injury (ABI) [6], who present several risk factors such as mechanical ventilation, longlasting impairment of consciousness and having undergone surgery [7,8]. While mechanical ventilation during short-term hospitalisation in ICUs is associated with higher risk of Marco Pozzi and Paolo Pellegrino authors contributed equally to this work.…”

Section: Introductionmentioning

confidence: 99%

Prevalence of respiratory colonisations and related antibiotic resistances among paediatric tracheostomised patients of a long-term rehabilitation centre in Italy

Pozzi¹,

Pellegrino²,

Galbiati³

et al. 2014

Eur J Clin Microbiol Infect Dis

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Patients with brain injury are prone to bacterial colonisations because of mechanical ventilation during intensive care and the long-term retention of tracheostomical tubes during rehabilitation. Reduced levels of isolation, typical of rehabilitation, could also contribute to propagate colonisations. We evaluated the presence of bacteria through different stages of healthcare, their antibiotic resistances and their clinical impact in a rehabilitation setting. This retrospective study included all tracheostomised patients referred to the paediatric brain injury unit of the Scientific Institute IRCCS E. Medea (Italy) over a six-year period. Data were collected from antibiograms regarding the presence of bacterial species and antibiotic resistances; clinical data were collected from medical records. Antibiograms revealed bacteria and antibiotic resistances typical of intensive care, while prevalence patterns were characteristic for each species (P. aeruginosa and S. aureus prevailing in the acute setting, K. pneumoniae, A. baumannii and others in rehabilitation). Despite very frequent antibiotic resistances, consistent with Italian averages, we observed a limited clinical impact for these colonisations. We analysed risk factors correlating to the development of respiratory symptoms and found a role for the acute clinical course after brain injury (having undergone neurosurgery; duration of intensive care stay) as well as for rehabilitation (duration of coma). Our data suggest that, in a long-term perspective, an appropriate balance is yet to be found between patient isolation and social interactions, to control respiratory colonisations and antibiotic resistances without compromising rehabilitation. They also suggest that regular containment measures should be complemented by thorough training to non-medic personnel and parents alike.

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“…The incidence of people with severe TBI is only 10%, but is associated with the highest mortality rate which ranges between 30% and 54% (11). About 50% od patients with severe TBI develops at least one infection as a complication of primary condition during hospitalization in ICU, resulting with fatal outcome in 28% of patients (9,12,13).…”

Section: Introductionmentioning

confidence: 99%

“…Patients with severe TBI present one of the most vulnerable group of patients for development of the second most common nosocomial infection called sepsis, whose incidence ranges between 10% and 41%. The leading cause is bacteremia, while something less frequent causes are fungemia, viremia, and parasitemia (9,16). Early diagnostic is essential for prompt prevention and treatment of this type of infection.…”

Section: Introductionmentioning

confidence: 99%

The incidence of nosocomial infections in patients with isolated severe traumatic brain injury

Valenčić¹,

Tokmadžić²,

Kuharić³

et al. 2015

SANAMED

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Introduction: Traumatic brain injury is the leading cause of death in children and adults in developed countries. Severe traumatic brain injury is classified with Glasgow Coma Scale score 8 and less. About 50% of patients with severe traumatic brain injury developes at least one infection as a complication of primary condition during hospitalization in the Intensive Care Unit, resulting with fatal outcome in 28% of patients. Ventilator-associated pneumonia is the leading infection that affects patients with severe traumatic brain injury, with an incidence between 41% and 74%. Following are sepsis and urinary tract infections. The aim: To analyze the number of patients with nosocomial infection and isolated severe traumatic brain injury hospitalized in the Intensive Care Unit of the Clinical Hospital Centre Rijeka, Croatia, from 31 st January 2013 to 31 st December 2014. Patients and methods: A two-year retrospective study included 46 patients with isolated severe traumatic brain injury and nosocomial infection hospitalized in the Intensive Care Unit of the Clinical Hospital Centre Rijeka,Croatia, in the period from 31 st January 2013 to 31 st December 2014. All medical data was collected from the Division of Intensive Care Unit, Clinical Hospital Centre Rijeka, Croatia. Results: From 67 patients with isolated severe traumatic brain injury, 46 (68,65%) of them developed nosocomial infection. There was statistically significant more male patients than female (p < 0.05). The average age of infected patients was 57,8 years. The leading were the infections of the respiratory system. Gram-negative bacteria Proteus mirabilis and Pseudomonas aerugnonsa were the leading pathogens. The average duration of the infection was 5,77 day. Duration of mechanical ventilation accounted for the majority of the patients more than 10 days. The average duration of treatment for all 46 patients was 10,475 days, and for 16 (34,78%) of them, the treatment outcome was lethal. Conclusion: Nosocomial infections are becoming a major public health problem. The emphasis must be set on the prevention which includes maintaining the hygiene and the antiseptic rules among the medical personnel of the Intensive Care Unit. Already developed infections must be adequately treated so the negative treatment outcomes can be reduced.

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Incidence, prevalence, and occurrence rate of infection among adults hospitalized after traumatic brain injury: study protocol for a systematic review and meta-analysis

Cited by 23 publications

References 37 publications

Acute Traumatic Brain Injury Induces CD4<sup>+</sup> and CD8<sup>+</sup> T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Acute Traumatic Brain Injury Induces CD4<sup>+</sup> and CD8<sup>+</sup> T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Prevalence of respiratory colonisations and related antibiotic resistances among paediatric tracheostomised patients of a long-term rehabilitation centre in Italy

The incidence of nosocomial infections in patients with isolated severe traumatic brain injury

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