Past Blood Alcohol Concentration and Injury in Trauma Center: Propensity Scoring

Beydoun, Hind A.; Teel, Alison; Crowder, Chris D.; Khànal, Suraj; Lo, Bruce M.

doi:10.1016/j.jemermed.2014.06.024

Cited by 7 publications

(6 citation statements)

References 20 publications

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“…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]. The authors correlate their findings to possible anti-inflammatory characteristic of alcohol, since in numerous studies, alcohol was reported to significantly impact the immune response by suppressing the pro-inflammatory response.…”

Section: Discussionmentioning

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

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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%

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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“…Current clinical studies have demonstrated that alcohol intoxication has been associated with decreased rates of pneumonia, or even improved mortality rates, after trauma or hemorrhagic shock in vivo (11, 12, 14). However, other findings highlight that alcohol did not increase the incidence of sepsis, other post-injury complications, or mortality (10, 56, 57). Interestingly, there is also evidence that alcohol intoxication elevated the risk for in-hospital complications (6).…”

Section: Discussionmentioning

confidence: 91%

Circulating Extracellular Vesicles and Their miR “Barcode” Differentiate Alcohol Drinkers With Liver Injury and Those Without Liver Injury in Severe Trauma Patients

et al. 2019

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Short Summary: Extracellular vesicles (EVs), released during tissue/cell injury, contain a “barcode” indicating specific microRNAs (miRs) that can uncover their origin. We examined whether systemic EVs possessing hepatic miR-signatures would indicate ongoing liver injury and clinical complications in trauma patients (TP). We grouped the patients of alcoholic drinkers into “alcohol-drinkers with liver injury (LI)” (EtOH with LI) or “alcohol-drinkers without LI” (EtOH w/o LI) and we compared these groups to “non-drinkers” (no EtOH). When we examined patient blood from the EtOH with LI group we found the total number of EVs to be increased, along with an increase in miR-122 and let7f—two EV-associated miRNAs—and several inflammation-associating cytokines, such as interleukin (IL)-6 and IL-33. In contrast, all of the aforementioned readouts were found to be decreased in the EtOH w/o LI group. These novel data demonstrate that hepatocyte damage in alcohol-intoxicated trauma patients presenting with liver injury can be reflected by an increase in circulating serum EVs, their specific miR-“barcode” and the concomitant increase of systemic inflammatory markers IL-6 and IL-33. Anti-inflammatory effect of alcohol-drinking in EtOH w/o LI can be presented by a reduced number of hepato-derived EVs, no upregulation of IL-6 and IL-33, and a miR “barcode” different from patients presenting with liver injury. Background: Alcohol abuse is associated with (neuro)protective effects related to (head) injuries, and with negative effects regarding infection rates and survival in severely injured trauma patients (TP). Extracellular vesicles (EVs), which are released during tissue and/or cell injury, can contain a “barcode” including specific microRNAs (miRs) that uncover their origin. We examined whether EVs with a hepatic miR signature can be systemically measured, and whether they can indicate ongoing liver injury in alcohol-intoxicated TP and foretell clinical complications. Patients/Methods: We enrolled 35 TP and measured blood EVs, IL-6, TNF-alpha, IL-1beta, IL-10 and IL-33, alcohol (ethanol, EtOH) concentration (BAC), GLDH, GGT, AST, ALT, leukocytes, platelets, and bilirubin. Within circulating EVs we measured the expression levels of miR-122, let7f, miR21, miR29a, miR-155, and miR-146a. Patients of alcohol-drinkers were grouped into “alcohol drinkers with liver injury (LI)” (EtOH with LI) or “alcohol drinkers without LI” (EtOH w/o LI) and compared to “non-drinkers” (no EtOH). We assessed systemic injury characteristics and the outcome of hospitalization with regard to sepsis, septic shock, pneumonia, or mortality. Results: EtOH with LI patients had significantly increased rates of pneumonia vs . the EtOH w/o LI group. EVs, IL-6, and IL-33 levels were significantly increased in EtOH with LI vs. EtOH w/o LI group ( p < 0.05). EV number correlated positively with ALT and IL-6 ( p ...

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“…One study found that a higher BAC was associated with more unintentional injury and increased head trauma; however, it was also associated with decreased extremity injury and no signi cant difference between ISS. 15 In contrast, Dultz et al found that intoxicated pedestrians struck by motor vehicles had higher ISS than non-intoxicated patients. 8 Yet another study found that patients with blunt head injuries from MVCs with a BAC from 8 to 100 mg/dL had increased mortality rates compared to those with higher BAC levels.…”

Section: Discussionmentioning

confidence: 93%

Higher Blood Alcohol Concentration is Related to Less Severe Injury Amongst Intoxicated Trauma Patients

Kumar

Prabhakaran

McIntyre

et al. 2020

Preprint

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Background Previous studies show varied results regarding the protective effects of alcohol intoxication upon injury and mortality in the setting of trauma. Our study aimed to determine the effects of blood alcohol content (BAC) amongst trauma patients with alcohol ingestion, upon injury type and severity, as well as outcomes. Methods This 4-year retrospective study (2013–2017) used an institutional trauma database to capture all Level 1 and 2 trauma patients (≥14 years old) with BAC > 10 mg/dL presenting to the emergency department at a Level 1 trauma center. Demographic variables including mechanism of injury (MOI) were collected. Patients’ BAC was compared to their calculated injury severity scores (ISS) and abbreviated injury scale (AIS) scores. Analysis included linear regression, T-tests and ANOVAs with Tukey’s post-hoc analysis for continuous variables and Fisher’s exact test for binary variables. Multivariate regression analysis was performed to determine independent predictors of injury severity. Results 332 intoxicated patients were identified (mean BAC: 210.2±87.14 mg/dL, range 12.7–460.0; 74.1% male; median age 35; range: 16–90). The median ISS was 6 (range: 1–48). Patients in motor vehicle collisions had lower BACs (186.0±5.59 mg/dL) than those who fell (233.8±10.42 mg/dL, p = 0.0002), were assaulted (230.4±14.04 mg/dL, p = 0.0261), or were pedestrians struck (259.4±14.17 mg/dL, p = 0.004). Overall, patients with higher BAC had lower GCS, lower ISS, and shorter intensive care unit (ICU) length of stay, but no differences in hospital stay, or ventilator days. Conclusions Trauma patients with higher BAC have lower ISS, less severe chest injury, and shorter ICU stays. These findings suggest that higher levels of alcohol ingestion may portend a protective effect in the setting of trauma with respect to severity of injury that does not mitigate the importance of education and injury prevention but warrants further study into the physiology of alcohol and trauma.

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Past Blood Alcohol Concentration and Injury in Trauma Center: Propensity Scoring

Cited by 7 publications

References 20 publications

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

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

Circulating Extracellular Vesicles and Their miR “Barcode” Differentiate Alcohol Drinkers With Liver Injury and Those Without Liver Injury in Severe Trauma Patients

Higher Blood Alcohol Concentration is Related to Less Severe Injury Amongst Intoxicated Trauma Patients

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