Alcohol is Associated with a Lower Pneumonia Rate After Traumatic Brain Injury

Hadjibashi, Anoushiravan Amini; Berry, Cherisse; Ley, Eric J.; Bukur, Marko; Mirocha, James; Stolpner, Dennis; Salim, Ali

doi:10.1016/j.jss.2011.05.029

Cited by 24 publications

(19 citation statements)

References 27 publications

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“…Summarized, several experimental and clinical studies demonstrated beneficial effects of alcohol, which were associated with lower rates of pneumonia after TBI or even improved mortality rates after trauma or haemorrhagic shock [9, 11, 16]. Importantly, conflictive data have highlighted that alcohol use was not associated with the increased incidence of infectious post-injury complications or mortality, or even alcohol increased the risk for development of in-hospital complications [42, 43].…”

Section: Discussionmentioning

confidence: 99%

“…While chronic alcohol use was shown to correlate with negative outcomes, acute alcohol use has been demonstrated to positively influence the post-injury clinical course, or to have no effects on diverse outcome parameters in trauma patients [7, 8]. Notably in alcohol-intoxicated TBI patients lower incidence of early coagulopathy, pneumonia and mortality were reported [9, 10]. In an in vivo animal model of haemorrhagic shock, our group found significant anti-inflammatory influence of alcohol on trauma-induced inflammation, which was associated with improved survival [11].…”

Section: Introductionmentioning

confidence: 99%

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Ethanol Decreases Inflammatory Response in Human Lung Epithelial Cells by Inhibiting the Canonical NF-kB-Pathway

Mörs¹,

Hörauf²,

Kany³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Alcohol (ethanol, EtOH) as significant contributor to traumatic injury is linked to suppressed inflammatory response, thereby influencing clinical outcomes. Alcohol-induced immune-suppression during acute inflammation (trauma) was linked to nuclear factor-kappaB (NF-ĸB). Here, we analyzed alcohol`s effects and mechanisms underlying its influence on NF-ĸB-signaling during acute inflammation in human lung epithelial cells. Methods: A549-cells were stimulated with interleukin (IL)-1β, or sera from trauma patients (TP) or healthy volunteers, with positive/negative blood alcohol concentrations (BAC), and subsequently exposed to EtOH (170 Mm, 1h). IL-6-release and neutrophil adhesion to A549 were analyzed. Specific siRNA-NIK mediated downregulation of non-canonical, and IKK-NBD-inhibition of canonical NF-ĸB signaling were performed. Nuclear levels of activated p50 and p52 NF-ĸB-subunits were detected using TransAm ELISA. Results: Both stimuli significantly induced IL-6-release (39.79±4.70 vs. 0.58±0.8 pg/ml) and neutrophil adhesion (132.30±8.80 vs. 100% control, p<0.05) to A549-cells. EtOH significantly decreased IL-6-release (22.90±5.40, p<0.05) and neutrophil adherence vs. controls (105.40±14.5%, p<0.05). IL-1β-induced significant activation of canonical/p50 and non-canonical/p52 pathways. EtOH significantly reduced p50 (34.90±23.70 vs. 197.70±36.43, p<0.05) not p52 activation. Inhibition of canonical pathway was further increased by EtOH (less p50-activation), while p52 remained unaltered. Inhibition of non-canonical pathway was unchanged by EtOH. Conclusion: Here, alcohol`s anti-inflammatory effects are mediated via decreasing nuclear levels of activated p50-subunit and canonical NF-ĸB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ethanol Decreases Inflammatory Response in Human Lung Epithelial Cells by Inhibiting the Canonical NF-kB-Pathway

Mörs¹,

Hörauf²,

Kany³

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

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“…Furthermore, alcohol has been shown to lower cerebral blood flow (and consequently intracranial pressure), and reduce risk of post-admission pneumonia, which might partly explain the improved outcome. 23,29 However, it also has been shown that alcohol in high levels disturbs the body's ability to compensate for shock, causing significant hemodynamic and respiratory dysregulation. 16,30 Another aspect that should to be considered is the effect of alcohol on GCS score.…”

Section: Raj Et Almentioning

confidence: 99%

Acute Alcohol Intoxication and Long-Term Outcome in Patients with Traumatic Brain Injury

Raj

Skrifvars

Kivisaari

et al. 2015

Journal of Neurotrauma

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The effect of blood alcohol concentration (BAC) on outcome after traumatic brain injury (TBI) is controversial. We sought to assess the independent effect of positive BAC on long-term outcome in patients with TBI treated in the intensive care unit (ICU). We performed a retrospective analysis of 405 patients with TBI, admitted to the ICU of a large urban Level 1 trauma center between January 2009 and December 2012. Outcome was six-month mortality and unfavorable neurological outcome (defined as a Glasgow Outcome Scale score of 1 [death], 2, [vegetative state], or 3 [severe disability]). Patients were categorized by admission BAC into: no BAC (0.0&; n = 99), low BAC ( < 2.3&; n = 140) and high BAC ( ‡ 2.3&; n = 166). Logistic regression analysis, adjusting for baseline risk and severity of illness, was used to assess the independent effect of BAC on outcome (using the no BAC group as the reference). Overall six-month mortality was 25% and unfavorable outcome was 46%. Multivariate analysis showed low BAC to independently reduce risk of sixmonth mortality compared with no BAC (low BAC adjusted odds ratio [AOR] 0.41, 95% confidence interval [CI] 0.19-0.88, p = 0.021) and high BAC (AOR 0.58, 95% CI 0.29-1.15, p = 0.120). Furthermore, a trend towards reduced risk of six-month unfavorable neurological outcome for patients with positive BAC, compared to patients with negative BAC, was noted, although this did not reach statistical significance (low BAC AOR 0.65, 95% CI 0.34-1.22, p = 0.178, and high BAC AOR 0.59, 95% CI 0.32-1.09, p = 0.089). In conclusion, low admission BAC ( < 2.3&) was found to independently reduce risk of six-month mortality for patients with TBI, and a trend towards improved long-term neurological outcome was found for BAC-positive patients. The role of alcohol as a neuroprotective agent warrants further studies.

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“…In patients suffering a traumatic brain injury, positive blood alcohol levels have been associated with a survival advantage of up to 40% and a lower incidence of sepsis and pneumonia. These results have not been uniform, highlighting the limited available data [11][12][13][14][15][16][17]. These studies failed to include TEG measurements in a uniform fashion, leaving the true nature of the patient's coagulation status unknown.…”

Section: Introductionmentioning

confidence: 99%