The American Journal of Surgery (2015) 210, 87-92

Clinical Science

Alcohol intoxication may be associated with reduced truncal injuries after blunt trauma Douglas Z. Liou, M.D.a, Galinos Barmparas, M.D.a, Andrea Zaw, M.D.a, Marko Bukur, M.D., F.A.C.S.b, Ali Salim, M.D., F.A.C.S.c, Eric J. Ley, M.D., F.A.C.S.a,* a

Department of Surgery, Division of Trauma and Critical Care, Cedars-Sinai Medical Center, Los Angeles, CA, USA; bDepartment of Surgery, Division of Trauma and Critical Care, Broward Medical Center, Fort Lauderdale, FL, USA; cDepartment of Surgery, Division of Trauma and Critical Care, Brigham and Women’s Hospital, Boston, MA, USA

KEYWORDS: Alcohol intoxication; Blunt trauma; Motor vehicle collision

Abstract BACKGROUND: Prior studies suggest that positive blood alcohol concentration (BAC) is associated with lower mortality after motor vehicle collisions (MVCs). We investigated the relationship between increasing BAC and mortality after MVC. METHODS: A retrospective review of the Los Angeles County trauma database from January 2003 to December 2008 was performed. MVC patients greater than or equal to 16 years of age with admission BAC were considered. Patients were stratified by BAC as follows: BAC0 (,.01), BAC1 (.01 to .08), BAC2 (.09 to .16), BAC3 (.17 to .24), BAC4 (.25 to .32), and BAC5 (..32). Logistic regression was used to determine predictors of mortality. RESULTS: A total of 12,540 patients were included. Overall mortality rate was 2.2%. Mortality was lowest in BAC3 (1.6%) and BAC4 (1.3%), although the difference among all groups was not statistically significant (P 5 .07). Decreased rates of Injury Severity Score greater than or equal to 16 were noted with increasing BAC, which was largely because of reduced chest and abdomen/pelvis Abbreviated Injury Scale. Adjusted mortality was lower in BAC3 and BAC4 (both adjusted odds ratio .4, P , .001). CONCLUSION: A protective effect of alcohol after MVC may be related to decreased truncal injury burden rather than protection after head injury. Ó 2015 Elsevier Inc. All rights reserved.

Alcohol-related motor vehicle collisions (MVCs) are a major source of serious injury and death in the United States. In 2010, 10,228 people were killed in MVCs The authors declare no conflicts of interest. Presented at the 2013 Annual Meeting of the Western Surgical Association, November 2–5, 2013, Salt Lake City, Utah. * Corresponding author. Tel.: 11-310-423-5874; fax: 11-310-4230139. E-mail address: [email protected] Manuscript received September 27, 2014; revised manuscript October 31, 2014 0002-9610/$ - see front matter Ó 2015 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.amjsurg.2014.11.015

involving alcohol-impaired drivers, averaging one fatality every 51 minutes. This accounted for 31% of all vehiclerelated deaths during that year.1 The financial impact of alcohol-related crashes is significant, as the annual estimated cost of these crashes total more than $51 billion.2 Although alcohol-related traffic fatalities decreased over the past several years, alcohol-impaired driving remains a major health and economic burden in our society. In recent years, elevated serum alcohol levels and outcomes after trauma have received increased attention. Conclusions from clinical studies are discrepant, as some

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report increased injury severity and complications in patients with positive blood alcohol concentration (BAC),3,4 while others found no difference or even reduced mortality.5,6 Acute alcohol intoxication in the setting of traumatic brain injury (TBI) has been a major focus. Much of the literature supports a neuroprotective role of alcohol,7,8 particularly after severe TBI9–12 although the mechanism by which this occurs is unclear and a topic of ongoing study. The degree of intoxication may be an important factor, as higher BAC after TBI has been correlated with increasing survival benefit.13 Few studies explored the impact of alcohol intoxication on injury severity and mortality specifically after blunt trauma from MVCs. In the available literature, reduced injury severity14 and improved survival15 in MVC patients with high BAC was reported, although the reasons for this apparent protective effect are not entirely understood. Furthermore, there are little data on the specific injury patterns of intoxicated MVC patients in relation to varying BAC levels. The aim of this study was to compare injury severity and mortality after MVC stratified by increasing BAC. Our focus was to determine if a protective benefit was because of alterations in head injury or other regions of the body. We hypothesize that injury patterns in intoxicated drivers vary according to BAC, and the associated survival benefit is attributed to lower injury burden to specific body regions.

by Welch’s analysis of variance on the ranks. Binary variables were compared across the 6 BAC groups by chi-square test. A P value of less than .05 was considered statistically significant. Multivariable logistic regression was used to assess variables associated with in-hospital mortality. The most frequently used covariates in trauma research for risk adjustment were included in the regression model,16 in particular age, sex, GCS (%8 vs .8), SBP (,90 vs R90 mm Hg), and ISS (R16 vs ,16). BAC levels were also included in the model, using BAC1 as the reference for comparison because of the highest mortality rate in that group. Adjusted odds ratios (AORs) and 95% confidence intervals were determined for each variable. All statistical analyses were conducted using SAS version 9.2 (SAS Institute, Cary, NC). This study was approved by the Institutional Review Board of Cedars-Sinai Medical Center.

Patients and Methods A retrospective review of Los Angeles County Trauma and Emergency Medicine Information System data from January 1, 2003 to December 31, 2008 was performed. The database was queried for all patients of driving age (16 years and older) with an injury mechanism of MVC and BAC drawn on arrival to the emergency department. Patients with complete data and admission BAC between 0 and .70 g/dL were included. Patients with BAC greater than .70 g/dL were excluded to minimize erroneous data in the analysis. The cohort was stratified into 6 groups according to admission BAC: BAC0 less than .01 g/dL, BAC1 .01 to .08 g/dL, BAC2 .09 to .16 g/dL, BAC3 .17 to .24 g/dL, BAC4 .25 to .32 g/dL, and BAC5 greater than .32 g/dL. An interval of .08 g/dL was selected, as this is the legal alcohol limit to operate a motor vehicle in the United States. Demographic and clinical data were compared among groups, including age, sex, admission Glasgow Coma Scale (GCS), admission systolic blood pressure (SBP), Injury Severity Score (ISS), regional Abbreviated Injury Scale (AIS), hospital length of stay (LOS), and mortality. Numerical variables were summarized by mean and standard deviation or median and interquartile range. Binary variables were summarized by frequency and percentage. Numerical variables were compared across the 6 BAC groups by analysis of variance and results were confirmed

Results A total of 12,540 patients met inclusion criteria and were analyzed. Mean age was 35.8 years and 71.8% of the patients were male. Overall morality was 2.2%. Mean admission GCS and SBP were 13.9 and 135 mm Hg, respectively. Mean ISS was 9.7% and 20.2% had ISS greater than or equal to 16. Mean injury severity by body region was low, with AIS less than 1 for each region. The regions with the highest frequency of serious injuries were chest (10.4%, AIS R3), extremities (9.6%, AIS R3), and head (8.6%, AIS R3). Mean hospital LOS was 5 days. Additional demographic and clinical data for the cohort are presented in Table 1. Comparison of patients stratified by admission BAC demonstrated differences in age, admission GCS, injury severity, and hospital LOS (Table 2). BAC2 had the youngest patients (31.8 years) and longest LOS (6.3 days), while BAC5 had the oldest patients (40.6 years) and shortest LOS (3.8 days) (both P , .001). A greater percentage of male sex was seen in the higher BAC groups (BAC0 63.6% vs BAC1 75.0% vs BAC2 77.8% vs BAC3 82.1% vs BAC4 84.7% vs BAC5 88.0%, P , .001) (Table 3). Admission GCS decreased with increasing BAC (BAC0 14.3 vs BAC1 14.1 vs BAC2 13.7 vs BAC3 13.5 vs BAC4 13.5 vs BAC5 12.9, P , .001); however, there were no differences in mean head AIS among the groups (P 5 .14). Admission SBP was relatively similar despite the noted statistical differences. Lowest mortality was seen in BAC3 (1.6%) and BAC4 (1.3%), although the mortality difference among groups was not significant (P 5 .07) (Table 3). There was an overall decrease in ISS with increasing admission BAC, with the lowest mean ISS observed in the highest BAC group (BAC0 9.8 vs BAC1 10.5 vs BAC2 11.1 vs BAC3 9.8 vs BAC4 8.1 vs BAC5 6.2, P , .001). The percentage of patients with serious injuries (ISS R16) in each group followed a similar decreasing trend (BAC0

D.Z. Liou et al. Table 1

Alcohol intoxication after blunt trauma

Demographics

Variable

n 5 12,540

Age, mean 6 SD Male, n (%) GCS Mean 6 SD Median (IQR) %8, n (%) SBP Mean 6 SD Median (IQR) ,90 mm Hg, n (%) ISS Mean 6 SD Median (IQR) R16, n (%) Head AIS Mean 6 SD Median (IQR) R3, n (%) Face AIS Mean 6 SD Median (IQR) R3, n (%) Chest AIS Mean 6 SD Median (IQR) R3, n (%) Abdomen/pelvis AIS Mean 6 SD Median (IQR) R3, n (%) Extremities AIS Mean 6 SD Median (IQR) R3, n (%) External AIS Mean 6 SD Median (IQR) R3, n (%) Hospital LOS Mean 6 SD Median (IQR) Mortality, n (%)

35.8 6 15.3 9,005 (71.8) 13.9 6 2.6 15 (14–15) 822 (6.6) 135.0 6 22.2 134 (121–148) 204 (1.6) 9.7 6 9.8 6 (3–13) 2,530 (20.2) .8 6 1.2 0 (0–2) 1,084 (8.6) .1 6 .5 0 (0–0) 104 (.8) .4 6 1.1 0 (0–0) 1,298 (10.4) .3 6 .8 0 (0–0) 430 (3.4) .5 6 1.0 0 (0–0) 1,199 (9.6) .5 6 .6 0 (0–1) 10 (.1) 5.0 6 15.4 2 (1–5) 271 (2.2)

AIS 5 Abbreviated Injury Scale; GCS 5 Glasgow Coma Scale; IQR 5 interquartile range; ISS 5 Injury Severity Score; LOS 5 length of stay; SBP 5 systolic blood pressure; SD 5 standard deviation.

20.6% vs BAC1 21.5% vs BAC2 24.3% vs BAC3 20.9% vs BAC4 15.7% vs BAC5 9.7%, P , .001) (Table 3). Mean AIS for all regions was statistically different among the groups (P , .001) except for head AIS (P 5 .14); however, all mean values were less than 1 and grossly similar in value. Of note, BAC5 had the lowest mean AIS for each region (Table 2). There were fewer severe injuries (AIS R3) for each region in the higher BAC groups. Marked decreases in severe injuries were seen in chest (BAC0 11.7% vs BAC1 11.2% vs BAC2 11.2% vs BAC3 9.0%

89 vs BAC4 6.7% vs BAC5 2.7%, P , .001), abdomen and pelvis (BAC0 3.6% vs BAC1 4.3% vs BAC2 4.5% vs BAC3 3.1% vs BAC4 2.0% vs BAC5 1.5%, P , .001), and extremities (BAC0 10.4% vs BAC1 11.4% vs BAC2 11.5% vs BAC3 9.1% vs BAC4 4.9% vs BAC5 2.5%, P , .001) (Table 3). Multivariable logistic regression identified predictors of increased mortality, which include age (40 to 59 years: AOR 1.7, P 5 .001; R60 years: AOR 5.2, P , .001), GCS less than or equal to 8 (AOR 13.8, P , .001), SBP less than 90 mm Hg (AOR 5.0, P , .001), and ISS greater than or equal to 16 (AOR 19.7, P , .001) (Table 4). Admission BAC of .17 to .24 g/dL (BAC3: AOR .4, P 5 .002) and .25 to .32 g/dL (BAC4: AOR .4, P 5 .01) were protective after adjusting for confounding variables.

Comments In this study, we examined injury patterns, injury severity, and mortality in intoxicated patients after MVC. Through stratifying by BAC, we demonstrate an association between high admission BAC of .17 to .32 g/dL and reduced mortality. Lower BAC did not confer this survival benefit. The protective effect of high serum alcohol levels appears to be related to decreased truncal injuries, as we noted a decrease in serious chest, abdomen, and pelvis injuries when comparing along the same BAC spectrum. Decreased injuries to the extremities were also observed with increasing BAC, although death from isolated extremity injury in the civilian population is rare.17 Interestingly, there was no survival benefit in patients with the highest BAC (..32 g/dL), as these patients had higher mortality compared with patients with BAC between .17 and .32 g/dL. The reason for this finding is not entirely clear and contrasts the protective benefit of higher BAC in isolated TBI.13 We speculate that this may be because of the systemic detrimental or toxic effects of alcohol at extremely high concentrations. This is supported by the fact that injury severity was lowest in the highest BAC group despite the increase in mortality. Further research is necessary to explore this phenomenon more closely. No difference in head injury severity was detected in our series, which is contrary to prior studies evaluating alcohol intoxication in TBI.7,9–13 When examining the subset of patients with serious head injury (head AIS R3), however, a decreasing trend was noted with increasing BAC although this did not quite reach statistical significance (P 5 .05). The discrepancy between our findings and previously published data may be in part because of differing methodology, as existing literature focused on isolated severe TBI, whereas this study examined patients with all injuries. The neuroprotective effect of alcohol is potentially reduced in the setting of polytrauma.5 Prior studies investigating the relationship between alcohol intoxication and outcomes after MVC report similar but not entirely concordant findings.14,15,18,19 Plurad

90 Table 2

The American Journal of Surgery, Vol 210, No 1, July 2015 Continuous variables stratified by blood alcohol concentration

Variable Age, mean 6 SD GCS Mean 6 SD Median (IQR) SBP Mean 6 SD Median (IQR) ISS Mean 6 SD Median (IQR) Head AIS Mean 6 SD Median (IQR) Face AIS Mean 6 SD Median (IQR) Chest AIS Mean 6 SD Median (IQR) Abdomen/pelvis AIS Mean 6 SD Median (IQR) Extremities AIS Mean 6 SD Median (IQR) External AIS Mean 6 SD Median (IQR) Hospital LOS Mean 6 SD Median (IQR)

BAC0 (n 5 6,591) ,.01 g/dL

BAC1 (n 5 1,036) .01–.08 g/dL

BAC2 (n 5 1,353) .09–.16 g/dL

BAC3 (n 5 1,829) .17–.24 g/dL

BAC4 (n 5 1,207) .25–.32 g/dL

BAC5 (n 5 524) ..32 g/dL

37.7 6 17.2

32.9 6 13.6

31.8 6 12.0

32.3 6 11.3

35.2 6 12.2

40.6 6 12.0

14.3 6 2.3 15 (15–15)

14.1 6 2.6 15 (14–15)

13.7 6 3.0 15 (14–15)

13.5 6 3.0 15 (14–15)

13.5 6 2.8 14 (14–15)

12.9 6 3.1 14 (13–15)

138.0 6 22.9 134.7 6 22.5 131.0 6 21.7 130.8 6 20.4 131.5 6 19.6 132.4 6 20.9 137 (123–150) 135 (120–147) 130 (118–144) 131 (118–144) 131 (119–144) 132 (120–146) 9.8 6 9.9 6 (3–14)

10.5 6 10.2 8 (4–14)

11.1 6 10.8 9 (4–14)

9.8 6 9.8 6 (4–14)

8.1 6 8.4 5 (2–10)

6.2 6 7.3 4 (1–9)

.8 6 1.2 0 (0–2)

.7 6 1.2 0 (0–2)

.7 6 1.3 0 (0–2)

.8 6 1.3 0 (0–2)

.8 6 1.2 0 (0–2)

.6 6 1.0 0 (0–1)

.1 6 .5 0 (0–0)

.2 6 .5 0 (0–0)

.2 6 .6 0 (0–0)

.2 6 .6 0 (0–0)

.2 6 .5 0 (0–0)

.1 6 .4 0 (0–0)

.5 6 1.1 0 (0–0)

.5 6 1.1 0 (0–0)

.5 6 1.1 0 (0–0)

.4 6 1.0 0 (0–0)

.3 6 .9 0 (0–0)

.2 6 .7 0 (0–0)

.3 6 .8 0 (0–0)

.3 6 .8 0 (0–0)

.3 6 .9 0 (0–0)

.2 6 .7 0 (0–0)

.2 6 .6 0 (0–0)

.1 6 .6 0 (0–0)

.6 6 1.1 0 (0–1)

.6 6 1.1 0 (0–1)

.6 6 1.1 0 (0–1)

.5 6 1.0 0 (0–0)

.3 6 .8 0 (0–0)

.2 6 .6 0 (0–0)

.5 6 .6 0 (0–1)

.5 6 .6 0 (0–1)

.5 6 .6 0 (0–1)

.5 6 .6 0 (0–1)

.5 6 .6 0 (0–1)

.4 6 .6 0 (0–1)

4.8 6 13.8 2 (0–5)

5.9 6 18.6 2 (1–6)

6.3 6 24.4 2 (1–6)

4.9 6 11.1 2 (1–5)

4.0 6 10.1 1 (0–4)

3.8 6 20.2 1 (1–2)

ANOVA P value ,.001 ,.001 ,.001 ,.001

.14

,.001 ,.001 ,.001 ,.001 ,.001 ,.001

AIS 5 Abbreviated Injury Scale; ANOVA 5 analysis of variance; BAC 5 blood alcohol concentration; GCS 5 Glasgow Coma Scale; IQR 5 interquartile range; ISS 5 Injury Severity Score; LOS 5 length of stay; SBP 5 systolic blood pressure; SD 5 standard deviation.

et al15 performed a similar multicenter analysis of MVC patients who underwent blood alcohol screening on admission and correlated BAC to outcomes after dividing the cohort into negative (%.005 g/dL), low (..005 to ,.08 g/dL), and high (R.08 g/dL) alcohol groups. The authors noted no difference in injury severity among the groups but decreased mortality in severely injured patients with high BAC, whereas this study noted both decreased injury severity overall and decreased mortality in specific BAC groups. The reason for this discrepancy may be because of differences in BAC cutoffs used to define the groups. In our analysis, we stratified into 6 groups by increments of .08 g/dL and noted marked differences in ISS and mortality at higher BAC (R.17 g/dL) but less prominent differences with lower BAC. Stubig et al examined a series of over 37,000 patients and reported increased injury severity and mortality with alcohol intoxication.18 However, the authors categorized patients with BAC greater than or equal to .01 g% (or g/dL) as positive for intoxication.

Furthermore, patients who were not screened for alcohol were included in the negative BAC group. Only about 5% of patients (1,769 of 37,635) were screened at admission, and when examining this subgroup of intoxicated patients, a trend toward decreased ISS and mortality were noted. Phillips and Brewer19 reported an increase in both accident severity and serious injuries with higher BAC; however, this study included only accidents that involved fatalities. Data presented in this study suggest that the protective effect of alcohol after MVC is related to decreased truncal injuries based on reduced injury severity to the chest, abdomen, and pelvis in concordance with decreased mortality. This protection may contribute to reduced early mortality; however, other mechanisms may also be involved in providing delayed survival benefit. Alcohol intoxication in TBI has shown a lower incidence of coagulopathy20 and infectious complications such as pneumonia.21 TBI causes an immediate massive sympathetic response that leads to systemic inflammation, followed by progression to immune

D.Z. Liou et al. Table 3

Alcohol intoxication after blunt trauma

91

Categorical variables stratified by blood alcohol concentration

Variable, n (%)

BAC0 (n 5 6,591) ,.01 g/dL

BAC1 (n 5 1,036) .01–.08 g/dL

BAC2 (n 5 1,353) .09–.16 g/dL

BAC3 (n 5 1,829) .17–.24 g/dL

BAC4 (n 5 1,207) .25–.32 g/dL

BAC5 (n 5 524) ..32 g/dL

Chi-square P value

Male GCS %8 SBP ,90 mm Hg ISS R16 Head AIS R3 Face AIS R3 Chest AIS R3 Abdomen/pelvis AIS R3 Extremities AIS R3 External AIS R3 Mortality

4,191 311 82 1,355 572 48 772 236 687 6 149

777 64 17 223 91 6 116 45 118 1 29

1, 052 116 40 329 126 19 151 61 156 0 36

1,502 173 39 383 175 25 164 56 166 2 30

1,022 97 16 189 91 6 81 24 59 1 16

461 61 10 51 29 0 14 8 13 0 11

,.001 ,.001 ,.001 ,.001 .05 .002 ,.001 ,.001 ,.001 .91 .07

(63.6) (4.7) (1.2) (20.6) (8.7) (.7) (11.7) (3.6) (10.4) (.1) (2.3)

(75.0) (6.2) (1.6) (21.5) (8.8) (.6) (11.2) (4.3) (11.4) (.1) (2.8)

(77.8) (8.6) (3.0) (24.3) (9.3) (1.4) (11.2) (4.5) (11.5) (0) (2.7)

(82.1) (9.5) (2.1) (20.9) (9.6) (1.4) (9.0) (3.1) (9.1) (.1) (1.6)

(84.7) (8.0) (1.3) (15.7) (7.5) (.5) (6.7) (2.0) (4.9) (.1) (1.3)

(88.0) (11.6) (1.9) (9.7) (5.5) (0) (2.7) (1.5) (2.5) (0) (2.1)

AIS 5 Abbreviated Injury Scale; BAC 5 blood alcohol concentration; GCS 5 Glasgow Coma Scale; ISS 5 Injury Severity Score; SBP 5 systolic blood pressure.

dysfunction22 and delayed death from sepsis.23 Betablockers reduce sympathetic hyperactivity and the related immune dysfunction after TBI,24 which contributes to improved outcomes.25–27 Alcohol has a similar effect of blunting sympathetic discharge after trauma28,29 and may also reduce central nervous system-related immune depression. Reduced rates of infection in intoxicated patients after MVC has been previously reported.30 There are several limitations to this study. As with any retrospective analysis, conclusions are limited to associations between factors and causal relationships cannot be determined. Our data did not capture concurrent intoxicants, such as benzodiazepines or opioids, which can enhance respiratory depression and potentially impact outcomes. There were 38,208 patients involved in an MVC, of which 24,203 had documented admission BAC levels during the study period. Because of exclusions for missing data or data outside physiological ranges, 12,540 patients were included in the study. Therefore, only 63.3%

Table 4 Multivariable logistic regression for predictors of mortality Variable

AOR (95% CI)

P value

Age 40–59 years (vs ,40 years) Age R60 years (vs ,40 years) Male GCS %8 SBP ,90 mm Hg ISS R16 BAC0 (vs BAC1) BAC2 (vs BAC1) BAC3 (vs BAC1) BAC4 (vs BAC1) BAC5 (vs BAC1)

1.7 5.2 1.3 13.8 5.0 19.7 .7 .6 .4 .4 .8

.001 ,.001 .14 ,.001 ,.001 ,.001 .20 .11 .002 .01 .60

(1.2–2.4) (3.5–7.9) (.9–1.8) (10.2–18.7) (3.2–7.7) (12.5–31.0) (.5–1.2) (.3–1.1) (.2–.7) (.2–.8) (.3–1.9)

AOR 5 adjusted odds ratio; BAC 5 blood alcohol concentration; CI 5 confidence interval; GCS 5 Glasgow Coma Scale; ISS 5 Injury Severity Score; SBP 5 systolic blood pressure.

of patients had admission BAC and only 32.8% met study inclusion criteria, which may have altered our findings. The decision to obtain a BAC was based on the attending surgeon’s discretion. The indication in each case was not captured and is a limitation to the dataset. Complete data on comorbidities and chronic alcoholism were not available and therefore could not be included. The timing of death was not analyzed and may be important to delineate, as different mechanisms contribute to early deaths compared with late deaths. Finally, our series noted a relatively low mean ISS and regional AIS. Analysis of patients with serious injuries only may yield different findings. A regression model that captures the differences in AIS might find limited protective benefit related to BAC.

Conclusions Admission BAC between .17 and .32 g/dL predicts decreased mortality after MVCs. Increasing BAC correlates with lower overall injury severity, which was primarily because of decreased chest, abdomen, pelvis, and extremity injuries. There was no difference in head injury severity with varying BAC. Our findings suggest that the protective effect of alcohol after blunt trauma from MVCs may be related to decreased injury burden to the trunk rather than protection after head injury alone.

References 1. Department of Transportation (US), National Highway Traffic Safety Administration. Traffic Safety Facts 2010: Alcohol-impaired Driving. Washington, DC: National Highway Traffic Safety Administration; 2012. Available at: http://www-nrd.nhtsa.dot.gov/Pubs/811606.pdf. Accessed September 28, 2013. 2. Blincoe L, Seay A, Zaloshnja E, et al. The Economic Impact of Motor Vehicle Crashes, 2000. Washington, DC: Department of Transportation (US), National Highway Traffic Safety Administration; 2002.

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3. Melvan JN, Mooney J, Bagby GJ, et al. Drug and alcohol use complicate traumatic peripheral vascular injury. J Trauma Acute Care Surg 2013;75:258–65. 4. Swearingen A, Ghaemmaghami V, Loftus T, et al. Extreme blood alcohol level is associated with increased resource use in trauma patients. Am Surg 2010;76:20–4. 5. Zeckey C, Dannecker S, Hildebrand F, et al. Alcohol and multiple trauma: is there an influence on the outcome? Alcohol 2011;45: 245–51. 6. Yaghoubian A, Kaji A, Putnam B, et al. Elevated blood alcohol level may be protective of trauma patient mortality. Am Surg 2009;75: 950–3. 7. Scheyerer MJ, Du¨tschler J, Billeter A, et al. Effect of elevated serum alcohol level on the outcome of severely injured patients. Emerg Med J 2013;31:813–7. 8. Opreanu RC, Kuhn D, Basson MD. Influence of alcohol on mortality in traumatic brain injury. J Am Coll Surg 2010;210:997–1007. 9. Talving P, Plurad D, Barmparas G, et al. Isolated severe traumatic brain injuries: association of blood alcohol levels with the severity of injuries and outcomes. J Trauma 2010;68:357–62. 10. Berry C, Salim A, Alban R, et al. Serum ethanol levels in patients with moderate to severe traumatic brain injury influence outcomes: a surprising finding. Am Surg 2010;76:1067–70. 11. Salim A, Ley EJ, Cryer HG, et al. Positive serum ethanol level and mortality in moderate to severe traumatic brain injury. Arch Surg 2009;144:865–71. 12. Salim A, Teixeira P, Ley EJ, et al. Serum ethanol levels: predictor of survival after severe traumatic brain injury. J Trauma 2009;67:697–703. 13. Berry C, Ley EJ, Margulies DR, et al. Correlating the blood alcohol concentration with outcome after traumatic brain injury: too much is not a bad thing. Am Surg 2011;77:1416–9. 14. Mann B, Desapriya E, Fujiwara T, et al. Is blood alcohol level a good predictor for injury severity outcomes in motor vehicle crash victims? Emerg Med Int 2011;2011:616323. 15. Plurad D, Demetriades D, Gruzinski G, et al. Motor vehicle crashes: the association of alcohol consumption with the type and severity of injuries and outcomes. J Emerg Med 2010;38:12–7. 16. Haider AH, Saleem T, Leow JJ, et al. Influence of the National Trauma Data Bank on the study of trauma outcomes: is it time to set research best practices to further enhance its impact? J Am Coll Surg 2012;214: 756–68.

17. Dorlac WC, DeBakey ME, Holcomb JB, et al. Mortality from isolated civilian penetrating extremity injury. J Trauma 2005;59:217–22. 18. Stu¨big T, Petri M, Zeckey C, et al. Alcohol intoxication in road traffic accidents leads to higher impact speed difference, higher ISS and MAIS, and higher preclinical mortality. Alcohol 2012;46:681–6. 19. Phillips DP, Brewer KM. The relationship between serious injury and blood alcohol concentration (BAC) in fatal motor vehicle accidents: BAC 5 0.01% is associated with significantly more dangerous accidents than BAC 5 0.00%. Addiction 2011;106:1614–22. 20. Lustenberger T, Inaba K, Barmparas G, et al. Ethanol intoxication is associated with a lower incidence of admission coagulopathy in severe traumatic brain injury patients. J Neurotrauma 2011;28:1699–706. 21. Hadjibashi AA, Berry C, Ley EJ, et al. Alcohol is associated with a lower pneumonia rate after traumatic brain injury. J Surg Res 2012; 173:212–5. 22. Meisel C, Schwab JM, Prass K, et al. Central nervous system injuryinduced immune deficiency syndrome. Nat Rev Neurosci 2005;6: 775–86. 23. Pfeifer R, Tarkin IS, Rocos B, et al. Patterns of mortality and causes of death in polytrauma patientsdhas anything changed? Injury 2009;40: 907–11. 24. Heffernan DS, Inaba K, Arbabi S, et al. Sympathetic hyperactivity after traumatic brain injury and the role of beta-blocker therapy. J Trauma 2010;69:1602–9. 25. Inaba K, Teixeira PG, David JS, et al. Beta-blockers in isolated blunt head injury. J Am Coll Surg 2008;206:432–8. 26. Salim A, Hadjizacharia P, Brown C, et al. Significance of troponin elevation after severe traumatic brain injury. J Trauma 2008;64:46–52. 27. Cotton BA, Snodgrass KB, Fleming SB, et al. Beta-blocker exposure is associated with improved survival after severe traumatic brain injury. J Trauma 2007;62:26–33; discussion 33–5. 28. Woolf PD, Cox C, McDonald JV, et al. Effects of intoxication on the catecholamine response to multisystem injury. J Trauma 1991;31: 1271–5; discussion 1275–6. 29. Woolf PD, Cox C, Kelly M, et al. Alcohol intoxication blunts sympatho-adrenal activation following brain injury. Alcohol Clin Exp Res 1990;14:205–9. 30. Kapur JH, Rajamanickam V, Fleming MF. Can the blood alcohol concentration be a predictor for increased hospital complications in trauma patients involved in motor vehicle crashes? Int J Environ Res Public Health 2010;7:1174–85.

©2015 Elsevier

Alcohol intoxication may be associated with reduced truncal injuries after blunt trauma.

Prior studies suggest that positive blood alcohol concentration (BAC) is associated with lower mortality after motor vehicle collisions (MVCs). We inv...
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