Brain Injury
ISSN: 0269-9052 (Print) 1362-301X (Online) Journal homepage: http://www.tandfonline.com/loi/ibij20
Trends in alcohol use during moderate and severe
traumatic brain injury: 18 years of neurotrauma in
Pennsylvania
R. A. Bernier & F. G. Hillary
To cite this article: R. A. Bernier & F. G. Hillary (2016) Trends in alcohol use during moderate
and severe traumatic brain injury: 18 years of neurotrauma in Pennsylvania, Brain Injury, 30:4,
414-421, DOI: 10.3109/02699052.2015.1127998
To link to this article: http://dx.doi.org/10.3109/02699052.2015.1127998
Published online: 24 Feb 2016.
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Date: 18 July 2016, At: 06:13
http://tandfonline.com/ibij
ISSN: 0269-9052 (print), 1362-301X (electronic)
Brain Inj, 2016; 30(4): 414–421
© 2016 Taylor & Francis Group, LLC. DOI: 10.3109/02699052.2015.1127998
ORIGINAL ARTICLE
Trends in alcohol use during moderate and severe traumatic brain injury:
18 years of neurotrauma in Pennsylvania
R. A. Bernier1 & F. G. Hillary1,2
Department of Psychology, The Pennsylvania State University, University Park, PA, USA, and 2Hershey Medical Center, Hershey, PA, USA
Downloaded by [Lifespan Libraries], [Rachel Bernier] at 06:13 18 July 2016
1
Abstract
Keywords
Primary objective: Alcohol is a known risk factor for TBI, yet little is known about how rates of
alcohol use at time of injury differ across demographics and the stability of alcohol-related
injury over time. Further, findings examining the relationship between alcohol and outcome
are mixed. This study aimed to examine changes in alcohol-positive moderate-to-severe
traumatic brain injury (+aTBI) over two decades with focus on demographic factors, changes
in +aTBI frequency over time, mortality and acute outcome.
Methods: This retrospective study examined data collected from 1992–2009 by the
Pennsylvania Trauma Outcome Study (PTOS).
Results: Results reveal that the proportion of +aTBI has been generally stable across years.
However, there is an interaction of +aTBI incidence with mechanism of injury and age, with a
downward trend in +aTBI within MVA and fall and individuals 18–30 and 71+ years. Further,
consistent with several findings in the literature, alcohol was associated with higher rates of
survival and better FSD scores during acute recovery.
Conclusions: This study discusses findings in the context of a greater literature on TBI-related
alcohol and outcome. The injury-alcohol profiles highlighted could be used to inform future
allocation of resources toward prevention of, intervention for and care of individuals who
sustain TBI.
Adult brain injury, alcohol use, traumatic
brain injury
Introduction
Traumatic brain injury (TBI) is a debilitating neurological
insult that affects over 1 million people per year in the US
and leads to over 50 000 deaths per year [1]. Alcohol use is an
important risk factor for TBI [2,3], yet little is known about
how rates of alcohol differ by demographic variables, such as
age, gender and other variables, including hour of injury, in
individuals with moderate-to-severe injury; additionally, little
is known regarding how these specific relationships have changed over the past 20 years. Further, although there has been
much study of the relationship between alcohol use at time of
injury and outcome, the findings have been mixed and studies
infrequently examine the relationship between more nuanced
groups of individuals sustaining TBI and outcome. There is a
clear need to better understand the trends of alcohol-related
TBI. The goal of this study is to examine how alcohol-related
TBI is influenced by demographics and other factors, such as
time of day of admission to emergency department (ED).
Alcohol use is an important risk factor for TBI, with
prevalence of alcohol intoxication between 36–55% at the
time of injury [2,3]. However, there is little consensus surCorrespondence: F. G. Hillary, Department of Psychology, The
Pennsylvania State University, 313 Bruce V. Moore Building,
University Park, PA 16802-3106, USA. E-mail: [email protected]
Color versions of one or more of the figures in the article can be found
online at www.tandfonline.com/ibij.
History
Received 3 June 2015
Revised 7 November 2015
Accepted 1 December 2015
Published online 24 February 2016
rounding the effects of alcohol intoxication at time of injury
on TBI outcome and this point is reflected in a recent review
on alcohol exposure and TBI [4]. Some studies have shown
alcohol to be associated with decreased mortality [5,6]. In
contrast, other investigators found no relationship between
alcohol and mortality [7] and posited that factors other than
alcohol account for the positive correlation between alcohol
exposure at time of injury and outcome [8]. Others, still, have
found that alcohol is associated with higher rates of mortality
and complications [9], so the relationship between alcohol
and outcome after TBI remains uncertain.
While not definitive, the animal literature examining the
influence of acute alcohol intoxication on TBI is generally
more consistent. Alcohol use following TBI is associated with
attenuated short-term recovery in animal models [10]. Rats
exposed to alcohol vapour following mild TBI showed less
improvement on the neurological severity score (NSS) and
exhibited poorer cognitive outcome and higher expression of
markers of neuroinflammation compared with rats exposed to
room air [11]. Additionally, subjects who were administered
alcohol pre-injury experienced higher rates of mortality and
impaired ventilation [12], suggesting that individuals with
alcohol in their system at time of injury would have decreased
perfusion, resulting in greater tissue damage and worse
outcome. Further, alcohol intoxication in rats with TBI has
been associated with more severe apoptosis [13], suggesting
Alcohol and TBI
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DOI: 10.3109/02699052.2015.1127998
greater rates of neuronal loss and more extensive damage
compared to individuals who were not intoxicated at the
time of injury. Several questions about the relationship
between alcohol and outcome following TBI remain, even
in the animal literature. For example, alcohol exposure prior
to injury is associated with higher rates of survival and
decreased neuroinflammation, possibly due to the role of
alcohol as an immunomodulator [14–16]. Additionally, in a
sample of rats, alcohol consumption both pre-injury and postinjury was associated with better learning on the Morris
water maze task compared to rats exposed to ethanol preinjury only or not at all, potentially mediated by a lower
cerebral temperature [17]. These seemingly conflicting
findings highlight the complexity in this relationship and the
challenge in identifying the biological mechanisms
underlying this relationship.
In human studies, higher blood alcohol levels at time of
injury have been associated with poorer outcomes, such as
worse performance on cognitive measures [18] and increased
atrophy [19]. In contrast, a more recent study reported
that higher blood alcohol levels were associated with better
performance on several neuropsychological measures during
the acute recovery stage [20]. Taken together, outcome
research using both animal and human models demonstrates
the lack of consistency in findings, pointing to a complex
relationship between TBI outcome and alcohol likely
determined by a number of clinical, demographic and
injury-related factors.
Other less-studied alcohol-related factors are now receiving some attention, such as history of alcohol abuse prior to
injury [21] and the time of day at which the injury occurs.
In an Austrian sample, time of day was not found to be
predictive of outcome following TBI [22]. Interestingly,
these relationships seldom have been examined in the US.
In fact, despite the frequent study of alcohol and TBI, more
nuanced relations between alcohol use and TBI rates and
outcome, such as whether rates of alcohol use differ as a
function of age, gender and mechanisms of injury and how
these rates vary across time of day, rarely are considered. It
is anticipated that age and gender will be important determinants of alcohol use at the time of injury, with higher
incidence of alcohol-related TBI (+aTBI) observable in
young adults compared to elderly patients and men compared to women. What is less clear is whether there are
meaningful relationships between the mechanism of injury,
time of day and other demographic factors and rates of
alcohol use and outcome. Further, little is known about
changes in these relationships across years, even though
laws regarding alcohol, alcohol education and attitudes
toward driving under the influence of alcohol have changed.
For example, the state of Pennsylvania spent $1.22 million
in 2013–2014 and the 2015–2016 proposed budget is allotting $1.36 million on drug and alcohol abuse prevention
and treatment to modify behaviours around alcohol [23].
Knowing the relationships between these variables would
facilitate a more targeted prevention of TBI and additionally
would be useful in determining how resources should be
allocated toward TBI care in the future and may provide
additional insight into the nature of the relation between
alcohol and outcome.
415
Study goals and hypotheses
Using data from the Pennsylvania Trauma Outcome Study
(PTOS) containing clinical information for all individuals
who received Pennsylvania’s emergency services from
1992–2009 (n = 11 943), this study aims to: (1) characterize
the relationships between alcohol use and demographic and
situational factors influencing alcohol status, (2) examine how
alcohol influences outcome and (3) observe how these factors
have changed over time. It is hypothesized that time of day
will influence the incidence of +aTBI and that the rate of
+aTBI will decrease over the two decades of data collection
due to greater public efforts to raise awareness about the risks
associated with alcohol, in addition to laws reflecting this
shift in attitude (e.g. decreasing the legal limit of blood
alcohol level for individuals operating a vehicle). Finally, it
is hypothesized that alcohol at the time of injury will have
only a small effect on outcome, but will be associated with a
lower survival rate and decreased functional status at time
of discharge (FSD), based on the more recent literature
examining animal models of acute outcome.
Methods
This retrospective study examined clinical data collected from
January 1992–December 2009 by the Pennsylvania Trauma
Outcome Study (PTOS), a trauma registry formed by the
Pennsylvania Trauma Systems Foundation. The PTOS was
established in 1985 following the creation of the Emergency
Medical Service Act (Act 45) in July 1985 and contains information about every trauma case admitted to a PTSF-accredited
trauma centre. Hospitals in Pennsylvania that apply to the PTSF
are granted accreditation by a 20-member board of directors if
they follow the guidelines set forth by the American College of
Surgeons, Committee on Trauma. Trauma Centres who receive
accreditation are mandated to report data to the PTOS and
continued accreditation relies on their compliance with this
mandate. Although each trauma centre is responsible for the
quality of its data, all data are re-checked, assessed and corrected
and then integrated by the PTSF on a quarterly basis. As of 2009,
there were 31 trauma centres accredited by the PTSF, but the
present study only contains data from the 23 trauma centres that
have been accredited and present in the PTOS database each
year from 1992–2009.
Individuals from the PTOS who received a diagnosis
indicative of intracranial trauma (ICD-9-CM codes 850-854)
and whose total Glasgow Coma Scale (GCS) at time of
admission to the emergency department (ED) was greater
than or equal to 3 and less than or equal to 12 (moderate
and severe TBI) were included in these analyses. Only blunt
injuries were included in analyses.
Of the over 200 variables reported in the PTOS database,
the following variables were examined: age, gender, GCS,
mechanism of injury, blood alcohol level (BAL) at time of
admission to ED, time of admission the ED, year of admission
to the ED and functional status at discharge (FSD) (see Table I
for description of FSD). The only potentially identifying
information used in this study was date of birth and gender.
No other identifying information is included in the PTOS
database in order to ensure patient confidentiality.
N/A
N/A
N/A
N/A
N/A
Locomotion
Expression
Transfer mobility
Social interaction
Modified dependence
2
Independence with device
3
Complete independence
4
Requires total assistance to take
meals by mouth OR does not take
food by mouth but must rely on
other means of alimentations.
Requires maximal assistance to
walk 150 feet, OR does not walk
or operate a wheelchair
independently for 50 feet.
Requires supervision and minimal to moderate Requires assistance in preparation (e.g.
Eats and drinks independently (e.g.
physical assistance during drinking or eating.
opening carton) OR requires adaptive device opens cartons, pours liquids, eats and
Does not have any other means of alimentation. (e.g. spork), but is able to eat independently. drinks from dishes presented in
customary manner).
Requires supervision or minimum-to-moderate Walks minimum of 150 feet with brace, cane, Walks minimum of 150 feet without
assistive device and does not use a
crutches, etc. OR if not walking, operates
physical assistance to go 150 feet OR walks
independently only a short distance OR operates wheelchair independently for minimum of 50 wheelchair.
feet.
wheelchair independently for minimum of 50
feet.
Expresses complex ideas intelligibly
Does not express basic needs and Expresses thoughts in a telegraphic or confused Expresses complex ideas with mild
wants consistently, even with an pattern or requires prompts, cues or assistance difficulty, but communicates basic needs and and fluently, verbally or non-verbally,
from another person.
wants without difficulty.
including signing and writing.
augmentative communication
device or system, despite
prompting.
Uses adaptive or assistive device such as a If walking or in wheelchair, performs
Requires maximal assistance to Requires assistance in set up or adaptive or
sliding board, a lift, grab bars, special seat, transfer safely.
total assistance to perform
assistive device, OR requires supervision of
brace or crutch. Performs transfer safely.
transfer.
minimal-to-moderate physical assistance to
perform transfer safely.
Interacts appropriately with staff,
Interacts appropriately < 25% of Requires some supervision under stressful or
Interacts appropriately with staff, other
other patients, and family members
the time or not at all, may need unfamiliar situations
patients and family members in structured
restraint.
situations and environments, may take more (e.g. controls temper and is aware that
than a reasonable time to adjust in a social words and actions have impact on
others.
situation.
Complete dependence
Paediatric
(< 2 years
old)
Feeding
1
0
Table I. Functional status at discharge (FSD).
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416
R. A. Bernier and F. G. Hillary
Brain Inj, 2016; 30(4): 414–421
Alcohol and TBI
DOI: 10.3109/02699052.2015.1127998
Variables and measures
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Mechanism of injury was classified as follows: ICD-9 e-codes
800–848 were classified as motor vehicle accidents (MVA),
880–888 were classified as falls and 910–997 were classified as
violence/assault. For the purposes of the study, MVA included
railroad collisions and other brain injuries that resulted from
vehicular collusions and assault included self-injurious behaviour,
in addition to any other assault-related brain injury, regardless of
role in assault (e.g. aggressor or victim). Age was examined in
four groups: individuals aged 18–30 years, individuals aged
31–50 years, individuals aged 51–70 years and individuals aged
71 years and older. Cases that did not meet age, ICD-9-CM code,
e-code or other criteria did not have results for a blood alcohol
level test in the ED or that were missing data were eliminated
from frequency and outcome analyses.
417
study included 11 943 patients who sustained moderate-tosevere TBI, as assessed by the Glasgow Coma Scale (GCS) at
time of admission to the ED, from 1992–2009 in the state of
Pennsylvania. Individuals with a GCS greater than or equal to
3 and less than or equal to 12 were included in the analyses.
Overall, 47.69% of TBI cases between 1992–2009 were
+aTBI at time of admission to the ED. Consistent with the
literature, men comprised 70.24% of all TBI between
1992–2009. Nearly three-quarters of the TBI cases occurred
in those aged 50 years and younger, with 34.87% of patients
aged 18–30 years, 32.51% aged 31–50 years, 15.88% aged
51–70 years and 16.75% aged 71 years and older. Consistent
with the broader TBI literature, 59.29% of the cases were the
result of motor vehicle accident (MVA), followed by 19.82%
resulting from fall and 12.20% resulting from assault (see
Table II for complete results).
Data analyses to address study goals
Examining +aTBI and demography and injury factors
Rates of +aTBI by gender, age and mechanism of injury
Frequency of TBI among individuals was calculated across
gender, mechanism of injury and age. To compare frequency
of alcohol use at time of injury, the number of +aTBI within
each demographic variable was divided by the total number
of TBI for a given variable, providing a percentage of +aTBI
moderate-to-severe TBI per demographic.
Perhaps somewhat counter-intuitively, +aTBI rates were
higher among individuals who survived for both men and
women (58.06% men, 36.32% women) compared to fatalities
(36.13% men, 20.00% women) (see Table II); 57.13% of
18–30 year-olds and 59.67% of 31–50 year-olds were
+aTBI at time of admission to the ED, but rates of +aTBI
diminished greatly in individuals aged 51 and older, with only
38.19% of patients aged 51–70 years and only 13.80% of
patients aged 71 years and older testing positive for alcohol
at time of admission. TBI resulting from assault were most
likely to be +aTBI at time of admission to the ED, with
60.47% of those patients testing positive for alcohol, followed
by TBI resulting from MVA (54.26%) and, lastly, TBI resulting from falls (39.63%) (see Table III).
Examining +aTBI effects over time
The second set of analyses sought to examine how the proportion of +aTBI cases varied across time of day; +aTBI
cases were examined by hour of admission to the emergency
department (ED) across gender, age and mechanism of injury.
Additionally, +aTBI distributions were compared by year
across the demographic variables.
Rates of +aTBI across time of day by age and mechanism
of injury
Examining +aTBI as a predictor of outcome
To examine the relationship between +aTBI injuries at time of
admission to the ED and outcome, this study examined differences in survival rates between individuals who were +aTBI
and negative (–aTBI) and sought to explore whether mean FSD
differs between +aTBI and negative groups in patients who
survived by conducting independent sample t-tests.
Results
Demography of TBI
The original database contained 60 942 individuals who used
Pennsylvania’s trauma services. Analyses for the current
Patterns of +aTBI across time of day were similar between
age groups, with the exception of individuals aged 71 years
and older, who had lower rates of both –aTBI and +aTBI
compared to other age groups (see Figure 1). Distributions of
+aTBI showed similar patterns across mechanism of injury
(assault, fall, MVA), with rates of +aTBI dipping during the
late morning and early afternoon and sharply increasing in the
late evening and early morning. TBI resulting from assault
show the highest +aTBI rates, closely followed by MVA and
then fall. Although TBI resulting from assault have the highest rates of +aTBI, TBI resulting from MVA have the highest
number of +aTBI (see Figure 2).
Table II. Demographic information.
# TBI
% of total TBI
# +aTBI
% +aTBI
Overall
Male
Female
Assault
MVA
Fall
18–30
31–50
51–70
71+
11 943
100
5 696
47.69
8389
70.24
4552
54.26
3549
29.72
1143
32.21
1457
12.2
881
60.47
7081
59.29
3602
50.87
2367
19.82
938
39.63
4164
34.87
2379
57.13
3883
32.51
2317
59.67
1896
15.88
724
38.19
2000
16.75
276
13.80
418
R. A. Bernier and F. G. Hillary
Brain Inj, 2016; 30(4): 414–421
Table III. Comparison of survival of +/-aTBI.
Overall
Survivals
# +aTBI
# -aTBI
Total
% +aTBI
4992
4603
9595
52.03
(2309)
(2102)
(4411)
(52.35)
Male
Fatalities
704
1644
2348
29.98
(196)
(552)
(748)
(26.20)
Survivals
4027
2909
6936
58.06
(1827)
(1265)
(3092)
(59.09)
Female
Fatalities
525
928
1453
36.13
(147)
(316)
(463)
(31.75)
Survivals
964
1690
2654
36.32
(481)
(834)
(1315)
(36.58)
Fatalities
179
716
895
20
(49)
(236)
(285)
(17.19)
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* Values in parentheses exclude cases that required intubation.
Figure 4. Percentage +aTBI 1992–2009 by mechanism of injury.
Figure 1. Percentage +aTBI across day by age.
39%, with rates steadily decreasing across each mechanism of
injury, most notably in fall. However, rates over time differ by
age group and across mechanism of injury. For example, the
increasing number of TBI due to falls among the elderly, the
group least likely to have +aTBI, in part, could be accounting
for the observed decrease in rates of +aTBI overall.
Collapsing across mechanism of injury and examining
+aTBI within each of the age groupings individually shows
that between 1992–2009 rates have decreased among individuals 18–30 years old and among individuals 71 years and
older, but have remained relatively stable within individuals
31–50 years old and 51–70 years old (see Figures 3 and 4).
Figure 2. Percentage +aTBI across day by mechanism of injury.
Figure 3. Percentage +aTBI 1992–2009 by age.
Rates of +aTBI over 1992–2009
Analyses of the rates of +aTBI from 1992–2009 show that
overall the percentage of +aTBI has decreased from 55% to
Outcome
Independent samples t-tests were conducted to test whether
mean FSD scores were significantly different between +aTBI
and –aTBI groups. Mean FSD scores were consistently
significantly higher in +aTBI groups, although effect sizes
varied by gender, age group and mechanism of injury (see
Table III). Mean GCS scores were not significantly different
between +aTBI and –aTBI groups, with the exception of TBI
due to fall; in this case, the –aTBI group GCS was higher than
the mean GCS score of the +aTBI group (see Table IV). This
comparison demonstrates that the association between +aTBI
and acute outcome is not due to injury severity as measured
by GCS. To eliminate intubation as a potential confound,
analyses were repeated excluding for individuals who were
intubated. Again, the +aTBI group had significantly higher
mean FSD scores across age groups and mechanisms of
injury, while GCS did not differ between +aTBI and –aTBI
groups, with the exception of the overall TBI, the TBI among
individuals 51–70 years old and TBI due to fall. In the three
latter cases in which GCS did differ significantly, GCS was
actually higher in the –aTBI groups, despite having
Alcohol and TBI
DOI: 10.3109/02699052.2015.1127998
419
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Table IV. Comparison of functional outcome of +/-aTBI by age and mechanism of injury.
Mean FSD
Overall
18–30
31–50
51–70
71+
Assault
MVA
Fall
Mean GCS
Overall
18–30
31–50
51–70
71+
Assault
MVA
Fall
Mean FSD*
Overall
18–30
31–50
51–70
71+
Assault
MVA
Fall
Mean GCS*
Overall
18–30
31–50
51–70
71+
Assault
MVA
Fall
–aTBI
+aTBI
Mean Dif.
Lower limit
Upper limit
t(6860.308) = –18.716, p < 0.001
t(2460.415) = –8.784, p < 0.001
t(1983.647 = –7.778, p < 0.001
t(950.767) = –5.542, p < 0.001
t(113.928) = –3.760, p < 0.001
t(564.816) = –6.716, p < 0.001
t(4516.683) = –12.335, p < 0.001
t(1119.354) = –10.312, p < 0.001
14.29
14.96
15.31
14.17
11.01
16.16
14.16
13.68
16.63
16.69
16.89
16.08
13.42
18.33
16.10
16.99
–2.34
–1.74
–1.57
–1.90
–2.41
–2.17
–1.94
–3.31
–2.58
–2.12
–1.98
–2.58
–3.68
–2.81
–2.25
–3.94
–2.09
–1.35
–1.17
–1.23
–1.14
–1.54
–1.63
–2.68
t(7141.613) = 1.791, p = 0.073
t(2715.271) = –1.623, p = 0.105
t(2185.784) = –0.373, p = 0.710
t(943.062) = –0.142, p = 0.887
t(124.188) = 0.339, p = 0.735
t(769.429) = –0.736, p = 0.462
t(4625.786) = 0.571, p = 0.568
t(1127.427) = 2.772, p = 0.006
6.07
5.43
6.04
6.28
7.33
6.63
5.59
7.14
5.93
5.62
6.09
6.31
7.20
6.79
5.54
6.57
0.14
–0.19
–0.05
–0.03
0.13
–0.16
0.05
0.57
–0.01
–0.41
–0.31
–0.45
–0.63
–0.60
–0.13
0.17
0.29
0.04
0.21
0.39
0.89
0.27
0.23
0.97
t(2905.280) = –15.143, p < 0.001
t(864.817) = –5.204, p < 0.001
t(826.294) = –5.524, p < 0.001
t(510.672) = –3.495, p < 0.001
t(55.826) = 0.224, p < 0.001
t(297.40) = –5.720, p < 0.001
t(1627.56) = –7.934, p < 0.001
t(626.875) = –9.239, p < 0.001
14.92
16.26
16.38
14.73
11.06
16.53
15.12
13.67
17.51
17.70
17.82
16.37
14.93
18.75
17.00
17.43
–2.59
–1.43
0.02
–1.64
–3.87
–2.21
–1.88
0.95
–2.93
–1.97
–0.33
–2.56
–5.52
–2.97
–2.34
0.50
–2.25
–0.89
0.37
–0.72
–2.21
–1.45
–1.41
1.39
8.49
7.86
8.30
8.82
9.37
9.19
8.27
9.11
8.07
7.76
8.28
8.16
9.16
8.05
8.04
8.17
0.42
0.10
0.02
0.66
0.21
0.15
0.23
0.95
0.21
–0.25
–0.33
0.14
–0.67
–0.36
–0.05
0.50
0.62
0.45
0.37
1.18
1.09
0.65
0.51
1.39
t(3272.520) = 4.013, p < 0.001
t(1009.406) = 0.559, p = 0.576
t(963.513) = 0.352, p = 0.900
t(490.565) = 2.512, p = 0.012
t(55.013) = 0.482, p = 0.632
t(455.892) = 0.571, p = 0.565
t(1729.551) = 1.602, p = 0.109
t(641.881) = 4.147, p < 0.001
* Values exclude cases that required intubation.
significantly lower FSD scores. However, it is important to
consider that, because FSD scores are assigned at time of
discharge, this analysis was limited to individuals who survived and were assessed at time of discharge from the trauma
centre.
across time of day is fairly consistent across mechanism of
injury and age group. Lastly, even after considering injury
severity and other demographic factors, alcohol is consistently associated with higher rates of survival and better
acute outcome scores in these data. Each of these findings
is considered in turn below.
Discussion
The primary goal of this study was to examine how alcoholrelated TBI has changed over the past two decades, including
the influence of alcohol on TBI outcome. A broad overview
of the data reveal that the rate of +aTBI has been generally
stable across time (1992–2009); however, when examining
age sub-groups, a downward trend among individuals of
18–31 years and 71 years and older was evident. Similar
downward trends in +aTBI were apparent based upon the
mechanism of injury; declines in TBI were evident among
cases of TBI due to fall and MVA for all ages. With regard to
the downward trend in +aTBI during MVA, it is possible that
interventions to increase public awareness about the danger of
operating a vehicle while intoxicated, in conjunction with
more stringent laws regarding driving under the influence of
alcohol, have had a positive result. This study also observed
that the pattern of the proportion of individuals with +aTBI
Trends in alcohol-related TBI
Over the past several decades public service announcements
and anti-drinking and driving campaigns have been launched
to promote responsible alcohol consumption and increase
awareness of the risks of alcohol-related injury [24]. In
Pennsylvania, laws have been passed reflecting the goal to
reduce use of intoxicating substances while driving; in 2003,
the legal limit of concentration of alcohol in an individual’s
blood or breath was lowered from 0.10 to 0.08% [25]. Both
the percentage and raw number of +aTBI resulting from
MVA have decreased among individuals aged 18–30.
Although this age group still represents the group with the
highest likelihood and raw number of +aTBI due to MVA,
the decrease in both raw number and percentage of +aTBI is
encouraging and suggests that perhaps efforts geared toward
420
R. A. Bernier and F. G. Hillary
Brain Inj, 2016; 30(4): 414–421
this age group have been successful, providing support for the
efficacy of such targeted interventions.
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Predictors of alcohol-related TBI
There are a number of injury-alcohol profiles highlighted
here that could be used to inform future allocation of
resources toward prevention of, intervention for and care of
TBI. Consistent with prior epidemiological research, demographic factors were an important indicator of +aTBI, with
men between the ages of 18–30 having the highest incidence
of TBI overall (65%) and women between the ages of 51–70
having the lowest (24.9%). For all age groups, men were more
likely to be using alcohol at the time of injury; these data are
consistent with other studies demonstrating that men are more
likely to use intoxicating substances at the time of sustaining
a TBI [26].
There also appears to be a maximum risk cycle over the
course of the 24-hour cycle for +aTBI that is influenced by
age. With the exception of individuals 71 years and older,
individuals are most likely to have +aTBI during the evening,
night and early morning, with +aTBI peaking between the
hours of 12 am and 4 am. Individuals 71 years and older
demonstrated a similar, but attenuated pattern, exhibiting
much lower rates of +aTBI over the course of the 24-hour
cycle. These patterns were nearly identical across mechanism
of injury, although the rate of +aTBI due to fall was somewhat lower in the late evening and early morning. Parsing
apart these patterns further, it is interesting to note that the
risk for +aTBI due to MVA increases earlier in the day for
individuals 31–50 years old. It is possible that this observed
pattern reflects the context in which these individuals are
more likely to consume alcohol; that is, members of this age
group are likely to be working full-time and perhaps are more
likely to be engaging in work-related social events, shifting
alcohol consumption to post-work or early evening. By examining distinct windows of time during the day, the current data
reveal an interesting pattern of +aTBI incidence that might be
obscured when relying on aggregated, collapsed data
regarding and alcohol use at time of injury. More specific
examinations of this relationship could be useful in terms of
informing understanding of how efforts to prevent +aTBI
should be aimed in the future.
Alcohol-related TBI and outcome
The current study revealed that +aTBI was associated with
higher FSD scores acutely. This finding, although represented
in the literature, was somewhat surprising in its consistency in
these data. This pattern held true when mean GCS scores at
time of admission were not significantly different between
patients who tested negative and positive for alcohol as well
as when GCS was significantly lower in the group of patients
who tested +aTBI (although it is possible that GCS was
artificially lower due to the effects of intoxication). Further,
patients admitted to the ED for TBI who tested positive for
alcohol had higher rates of survival. Still, this robust pattern
suggests that alcohol may hold subtle protective effects.
However, there are caveats to these findings. Alcohol is a
known risk factor for TBI and it is highly probable that, in the
absence of intoxication, the number of overall injuries would
be reduced (e.g. less likely to make poor driving decisions or
engage in a physical altercation). Second, individuals who
tested negative for alcohol had higher rates of complications
(e.g. in the overall sample, 29.6% and 43.1% in +aTBI and –
aTBI, respectively) during their hospital stay compared to
those who tested positive for alcohol. However, even when
considering complications as a covariate in an ANCOVA,
BAL accounted for a similar amount of variance and BAL
remained significantly associated with higher outcome (see
Table V).
Study limitations and future directions
There are several study limitations requiring discussion. The
PTOS contains comprehensive clinical information regarding
the initial injury, but lacks measures of pre-morbid functioning, which likely accounts for appreciable variance in patient
outcome. For example, cognitive reserve has been found to be
a protective factor in neurological disorders [27,28] and could
play a protective role in acute recovery following TBI.
Additionally, there is no information regarding pre-morbid
alcohol use or other health factors which may also contribute
to outcome. Further, only cases with reported results of alcohol testing from the ED could be included and it is possible
that cases in which alcohol played a more harmful role were
not included if the patient did not survive long enough to be
tested. Thus, there is the potential that data regarding alcohol
that is missing has skewed the data in such a way that testing
positive for alcohol was associated with higher rates of survival and with better acute functional outcome scores. Finally,
this study was limited to acute outcomes and does not take
into account the relationship between alcohol and long-term
outcome. More long-term measures of outcome could hold
very different results and having a more specific measure of
outcome could illuminate more subtle differences in the
recovery processes of individuals who sustained a TBI with
and without the presence of alcohol.
Table V. Coefficients.*
Unstandardized coefficients
Model
1
a
(Constant)
Complications
BAL
Standardized Coefficients
Correlations
B
Std. Error
Beta
t
Sig.
Zero-order
Partial
Part
13.976
–2.657
0.007
0.072
0.057
0.000
–0.468
0.171
193.867
–46.298
16.954
0.000
0.000
0.000
–0.497
0.251
–0.477
0.195
–0.461
0.169
Dependent Variable: FSD.
Alcohol and TBI
DOI: 10.3109/02699052.2015.1127998
Conclusions
Taken together, the findings of this study reveal a positive
relationship between alcohol and acute outcome following
TBI, although this likely remains a complex relationship
with multiple factors contributing to outcome. Despite these
limitations, this study yielded consistent findings that warrant
further exploration. These results add to the equivocal literature that exists and bolster the idea that there is a complex
relationship between alcohol and outcome. The exact nature
of the relationship must be parsed apart using animal models
in order to test specific hypotheses experimentally and
through the use of human studies that consider pre-morbid
variables and in addition use long-term outcome measures to
document outcome more comprehensively.
10.
11.
12.
13.
14.
15.
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Acknowledgements
The authors would like to thank the Pennsylvania Trauma
Outcome Study, Nathan McWilliams, and Brandon Merritt
for their contributions to this manuscript.
16.
17.
Declaration of interest
The authors report no conflicts of interest. The authors alone
are responsible for the content and writing of the paper.
18.
19.
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