Association of Alcohol With Mortality After Traumatic Brain Injury.
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ABSTRACT:
SUBMITTER: Albrecht JS
PROVIDER: S-EPMC5860552 | biostudies-literature | 2018 Feb
REPOSITORIES: biostudies-literature
Publications
Association of Alcohol With Mortality After Traumatic Brain Injury.
Albrecht Jennifer S JS Afshar Majid M Stein Deborah M DM Smith Gordon S GS
American journal of epidemiology 20180201 2
Although alcohol exposure results in reduced mortality after traumatic brain injury (TBI) in animal models, clinical trials based on proposed mechanisms have been disappointing and have reported conflicting results. Methodological issues common to many of these clinical studies may have contributed to the spurious results. Our objective was to evaluate the association between blood alcohol concentration (BAC) and in-hospital mortality after TBI, and overcome methodological problems of prior stud ...[more]
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Project description:BackgroundAcute alcohol intoxication is very common in patients with severe traumatic brain injury (TBI). Whether there is an independent association between alcohol intoxication and mortality is debated. This study hypothesized that alcohol intoxication is independently associated with less mortality after severe TBI (sTBI).MethodsThis retrospective observational cohort study included all patients with sTBI [head-Abbreviated Injury Score (AIS) ?3, corresponding to serious head injury or worse] admitted from 1 January 2011 to 31 December 2016 in an academic level I trauma center. Patients were classified as with alcohol intoxication or without intoxication based on blood alcohol concentration or description of alcohol intoxication on admission. The primary endpoint was in-hospital mortality. Multivariable logistic regression analysis, including patient and injury characteristics, was used to assess independent association with alcohol intoxication.ResultsOf the 2865 TBI patients, 715 (25%) suffered from alcohol intoxication. They were younger (mean age 46 vs. 68?years), more often male (80 vs. 57%) and had a lower median Glasgow Coma Scale upon arrival (14 vs. 15) compared to the no-intoxication group. There was no difference in injury severity by head AIS or Rotterdam CT. Alcohol intoxication had an unadjusted association with in-hospital mortality [unadjusted odds ratio (OR) 0.51; 95% confidence interval (CI), 0.38-0.68]; however, there was no independent association after adjusting for potentially confounding patient and injury characteristics (adjusted OR 0.72; 95% CI, 0.48-1.09).ConclusionIn this retrospective study, there was no independent association between alcohol intoxication and higher in-hospital mortality in emergency patients with sTBI.
| S-EPMC7919698 | biostudies-literature
Project description:OBJECTIVES:To examine the impact of early myocardial workload on in-hospital mortality following isolated severe traumatic brain injury. DESIGN:Retrospective cohort study. SETTING:Data from the National Trauma Databank, a multicenter trauma registry operated by the American College of Surgeons, from 2007 to 2014. PATIENTS:Adult patients with isolated severe traumatic brain injury (defined as admission Glasgow Coma Scale < 8 and head Abbreviated Injury Score ? 4). INTERVENTIONS:Admission rate-pressure product, categorized into five levels based on published low, normal, and submaximal human thresholds: less than 5,000; 5,000-9,999; 10,000-14,999; 15,000-19,999; and greater than 20,000. MEASUREMENTS AND MAIN RESULTS:Data from 26,412 patients were analyzed. Most patients had a normal rate-pressure product (43%), 35% had elevated rate-pressure product, and 22% had depressed rate-pressure product at hospital admission. Compared with the normal rate-pressure product group, in-hospital mortality was 22 percentage points higher in the lowest rate-pressure product group (cumulative mortality, 50.2%; 95% CI, 43.6-56.9%) and 11 percentage points higher in the highest rate-pressure product group (cumulative mortality, 39.2%; 95% CI, 37.4-40.9%). The lowest rate-pressure product group was associated with a 50% increased risk of mortality, compared with the normal rate-pressure product group (adjusted relative risk, 1.50; 95% CI, 1.31-1.76%; p < 0.0001), and the highest rate-pressure product group was associated with a 25% increased risk of mortality, compared with the normal rate-pressure product group (adjusted relative risk, 1.25; 95% CI, 1.18-1.92%; p < 0.0001). This relationship was blunted with increasing age. Among patients with normotension, those with depressed and elevated rate-pressure products experienced increased mortality. CONCLUSIONS:Adults with severe traumatic brain injury experience heterogeneous myocardial workload profiles that have a "U-shaped" relationship with mortality, even in the presence of a normal blood pressure. Our findings are novel and suggest that cardiac performance is important following severe traumatic brain injury.
| S-EPMC5953788 | biostudies-literature
Project description:STUDY OBJECTIVE:Out-of-hospital hypotension has been associated with increased mortality in traumatic brain injury. The association of traumatic brain injury mortality with the depth or duration of out-of-hospital hypotension is unknown. We evaluated the relationship between the depth and duration of out-of-hospital hypotension and mortality in major traumatic brain injury. METHODS:We evaluated adults and older children with moderate or severe traumatic brain injury in the preimplementation cohort of Arizona's statewide Excellence in Prehospital Injury Care study. We used logistic regression to determine the association between the depth-duration dose of hypotension (depth of systolic blood pressure <90 mm Hg integrated over duration [minutes] of hypotension) and odds of inhospital death, controlling for significant confounders. RESULTS:There were 7,521 traumatic brain injury cases included (70.6% male patients; median age 40 years [interquartile range 24 to 58]). Mortality was 7.8% (95% confidence interval [CI] 7.2% to 8.5%) among the 6,982 patients without hypotension (systolic blood pressure ?90 mm Hg) and 33.4% (95% CI 29.4% to 37.6%) among the 539 hypotensive patients (systolic blood pressure <90 mm Hg). Mortality was higher with increased hypotension dose: 0.01 to 14.99 mm Hg-minutes 16.3%; 15 to 49.99 mm Hg-minutes 28.1%; 50 to 141.99 mm Hg-minutes 38.8%; and greater than or equal to 142 mm Hg-minutes 50.4%. Log2 (the logarithm in base 2) of hypotension dose was associated with traumatic brain injury mortality (adjusted odds ratio 1.19 [95% CI 1.14 to 1.25] per 2-fold increase of dose). CONCLUSION:In this study, the depth and duration of out-of-hospital hypotension were associated with increased traumatic brain injury mortality. Assessments linking out-of-hospital blood pressure with traumatic brain injury outcomes should consider both depth and duration of hypotension.
| S-EPMC5614805 | biostudies-literature
Project description:ImportanceEmerging evidence suggests that harmful exposures during military service, such as traumatic brain injury (TBI), may contribute to mental health, chronic disease, and mortality risks.ObjectiveTo assess the mortality rates and estimate the number of all-cause and cause-specific excess deaths among veterans serving after the September 11, 2001, terrorist attacks (9/11) with and without exposure to TBI.Design, setting, and participantsThis cohort study analyzed administrative and mortality data from January 1, 2002, through December 31, 2018, for a cohort of US military veterans who served during the Global War on Terrorism after the 9/11 terrorist attacks. Veterans who served active duty after 9/11 with 3 or more years of care in the Military Health System or had 3 or more years of care in the Military Health System and 2 or more years of care in the Veterans Health Administration were included for analysis. The study used data from the Veterans Affairs/Department of Defense Identity Repository database, matching health records data from the Military Health Service Management Analysis and Reporting tool, the Veterans Health Administration Veterans Informatics and Computing Infrastructure, and the National Death Index. For comparison with the total US population, the study used the Centers for Disease Control and Prevention WONDER database. Data analysis was performed from June 16 to September 8, 2021.ExposureTraumatic brain injury.Main outcomes and measuresMultivariable, negative binomial regression models were used to estimate adjusted all-cause and cause-specific mortality rates for the post-9/11 military veteran cohort, stratified by TBI severity level, and the total US population. Differences in mortality rates between post-9/11 military veterans and the total US population were used to estimate excess deaths from each cause of death.ResultsAmong 2 516 189 post-9/11 military veterans (2 167 736 [86.2%] male; and 45 324 [1.8%] American Indian/Alaska Native, 160 178 [6.4%], Asian/Pacific Islander, 259 737 [10.3%] Hispanic, 387 926 [15.4%] non-Hispanic Black, 1 619 834 [64.4%] non-Hispanic White, and 43 190 [1.7%] unknown), 17.5% had mild TBI and 3.0% had moderate to severe TBI; there were 30 564 deaths. Adjusted, age-specific mortality rates were higher for post-9/11 military veterans than for the total US population and increased with TBI severity. There were an estimated 3858 (95% CI, 1225-6490) excess deaths among all post-9/11 military veterans. Of these, an estimated 275 (95% CI, -1435 to 1985) were not exposed to TBI, 2285 (95% CI, 1637 to 2933) had mild TBI, and 1298 (95% CI, 1023 to 1572) had moderate to severe TBI. Estimated excess deaths were predominantly from suicides (4218; 95% CI, 3621 to 4816) and accidents (2631; 95% CI, 1929 to 3333). Veterans with moderate to severe TBI accounted for 33.6% of total excess deaths, 11-fold higher than would otherwise be expected.Conclusions and relevanceThis military veteran cohort experienced more excess mortality compared with the total US population than all combat deaths from 9/11/01 through 9/11/21, concentrated among individuals exposed to TBI. These results suggest that a focus on what puts veterans at risk for accelerated aging and increased mortality is warranted.
| S-EPMC8837911 | biostudies-literature
Project description:The aim of this study is to describe the traumatic brain injury (TBI) population and causes and identify factors associated with TBI hospitalizations and mortality in California.This is a cross-sectional study of 61,188 patients with TBI from the California Hospital Discharge Data 2001 to 2009. We used descriptive, bivariate, and multivariate analyses in SAS version 9.3.TBI-related hospitalizations decreased by 14% and mortality increased by 19% from 2001 to 2009. The highest percentages of TBI hospitalizations were due to other causes (38.4%), falls (31.2%), being of age ?75 years old (37.2%), being a males (58.9%), and being of Medicare patients (44%). TBIs due to falls were found in those age ?4 years old (53.5%), ?75 years old (44.0%), and females (37.2%). TBIs due to assaults were more frequent in Blacks (29.0%). TBIs due to motor vehicle accidents were more frequent in 15-19 and 20-24 age groups (48.7% and 48.6%, resp.) and among Hispanics (27.8%). Higher odds of mortality were found among motor vehicle accident category (adjusted odds ratio (AOR): 1.27, 95% CI: 1.14-1.41); males (AOR: 1.36, 95% CI: 1.27-1.46); and the ?75-year-old group (AOR: 6.4, 95% CI: 4.9-8.4).Our findings suggest a decrease in TBI-related hospitalizations but an increase in TBI-related mortality during the study period. The majority of TBI-related hospitalizations was due to other causes and falls and was more frequent in the older, male, and Medicare populations. The higher likelihood of TBI-related mortalities was found among elderly male ?75 years old who had motor vehicle accidents. Our data can inform practitioners, prevention planners, educators, service sectors, and policy makers who aim to reduce the burden of TBI in the community. Implications for interventions are discussed.
| S-EPMC3845866 | biostudies-literature
Project description:Our aim was to create simple and largely scalable machine learning-based algorithms that could predict mortality in a real-time fashion during intensive care after traumatic brain injury. We performed an observational multicenter study including adult TBI patients that were monitored for intracranial pressure (ICP) for at least 24?h in three ICUs. We used machine learning-based logistic regression modeling to create two algorithms (based on ICP, mean arterial pressure [MAP], cerebral perfusion pressure [CPP] and Glasgow Coma Scale [GCS]) to predict 30-day mortality. We used a stratified cross-validation technique for internal validation. Of 472 included patients, 92 patients (19%) died within 30 days. Following cross-validation, the ICP-MAP-CPP algorithm's area under the receiver operating characteristic curve (AUC) increased from 0.67 (95% confidence interval [CI] 0.60-0.74) on day 1 to 0.81 (95% CI 0.75-0.87) on day 5. The ICP-MAP-CPP-GCS algorithm's AUC increased from 0.72 (95% CI 0.64-0.78) on day 1 to 0.84 (95% CI 0.78-0.90) on day 5. Algorithm misclassification was seen among patients undergoing decompressive craniectomy. In conclusion, we present a new concept of dynamic prognostication for patients with TBI treated in the ICU. Our simple algorithms, based on only three and four main variables, discriminated between survivors and non-survivors with accuracies up to 81% and 84%. These open-sourced simple algorithms can likely be further developed, also in low and middle-income countries.
| S-EPMC6881446 | biostudies-literature
Project description:ImportanceTraumatic brain injuries (TBIs) can have serious long-term consequences, including psychiatric disorders. However, few studies have assessed the association between TBI and risk of suicide.ObjectiveTo examine the association between TBI and subsequent suicide.Design, setting, and participantsRetrospective cohort study using nationwide registers covering 7 418 391 individuals (≥10 years) living in Denmark (1980-2014) with 164 265 624 person-years' follow-up; 567 823 (7.6%) had a medical contact for TBI. Data were analyzed using Poisson regression adjusted for relevant covariates, including fractures not involving the skull, psychiatric diagnoses, and deliberate self-harm.ExposureMedical contacts for TBI recorded in the National Patient Register (1977-2014) as mild TBI (concussion), skull fracture without documented TBI, and severe TBI (head injuries with evidence of structural brain injury).Main outcomes and measuresSuicide recorded in the Danish Cause of Death register until December 31, 2014.ResultsOf 34 529 individuals who died by suicide (mean age, 52 years [SD, 18 years]; 32.7% women; absolute rate 21 per 100 000 person-years [95% CI, 20.8-21.2]), 3536 (10.2%) had medical contact: 2701 with mild TBI, 174 with skull fracture without documented TBI, and 661 with severe TBI. The absolute suicide rate was 41 per 100 000 person-years (95% CI, 39.2-41.9) among those with TBI vs 20 per 100 000 person-years (95% CI, 19.7-20.1) among those with no diagnosis of TBI. The adjusted incidence rate ratio (IRR) was 1.90 (95% CI, 1.83-1.97). Compared with those without TBI, severe TBI (absolute rate, 50.8 per 100 000 person-years; 95% CI, 46.9-54.6) was associated with an IRR of 2.38 (95% CI, 2.20-2.58), whereas mild TBI (absolute rate, 38.6 per 100 000 person-years; 95% CI, 37.1-40.0), and skull fracture without documented TBI (absolute rate, 42.4 per 100 000 person-years; 95% CI, 36.1-48.7) had an IRR of 1.81 (95% CI, 1.74-1.88) and an IRR of 2.01 (95% CI, 1.73-2.34), respectively. Suicide risk was associated with number of medical contacts for TBI compared with those with no TBI contacts: 1 TBI contact, absolute rate, 34.3 per 100 000 person-years (95% CI, 33.0-35.7; IRR, 1.75; 95% CI, 1.68-1.83); 2 TBI contacts, absolute rate, 59.8 per 100 000 person-years (95% CI, 55.1-64.6; IRR, 2.31; 95% CI, 2.13-2.51); and 3 or more TBI contacts, absolute rate, 90.6 per 100 000 person-years (95% CI, 82.3-98.9; IRR, 2.59; 95% CI, 2.35-2.85; all P < .001 for the IRR's). Compared with the general population, temporal proximity since the last medical contact for TBI was associated with risk of suicide (P<.001), with an IRR of 3.67 (95% CI, 3.33-4.04) within the first 6 months and an incidence IRR of 1.76 (95% CI, 1.67-1.86) after 7 years.Conclusions and relevanceIn this nationwide registry-based retrospective cohort study individuals with medical contact for TBI, compared with the general population without TBI, had increased suicide risk.
| S-EPMC6142987 | biostudies-literature
Project description:More than 500,000 children sustain a traumatic brain injury (TBI) each year. Previous studies have described significant variation in inhospital mortality after pediatric TBI. The aim of this study was to identify facility-level characteristics independently associated with 30-day inhospital mortality after pediatric severe TBI. We hypothesized that, even after accounting for patient-level characteristics associated with mortality, the characteristics of facilities where patients received care would be associated with inhospital mortality. Using data from the National Trauma Data Bank from 2009-2012, we identified a cohort of 6707 pediatric patients hospitalized with severe TBI in 391 facilities and investigated their risk of 30-day inhospital mortality. Pre-specified facility-level characteristics (trauma certification level, teaching status, census region, facility size, nonprofit status, and responsibility for pediatric trauma care) were added to a Poisson regression model that accounted for patient-level characteristics associated with mortality. In multivariable analyses, patients treated in facilities located in the Midwest (risk ratio [RR]=1.42; 95% confidence interval [CI] 1.12-1.81) and South (RR=1.39; 95% CI: 1.12-1.72) regions had higher likelihoods of 30-day inhospital mortality compared with patients treated in the Northeast. Other facility-level characteristics were not found to be significant. To our knowledge, this is one of the largest investigations to identify regional variation in inhospital mortality after pediatric severe TBI in a national sample after accounting for individual and other facility-level characteristics. Further investigations to help explain this variation are needed to inform evidence-based decision-making for pediatric severe TBI care across different settings.
| S-EPMC4449626 | biostudies-literature
Project description:Background: A major contributor to unfavorable outcome after traumatic brain injury (TBI) is secondary brain injury. Low brain tissue oxygen tension (PbtO2) has shown to be an independent predictor of unfavorable outcome. Although PbtO2 provides clinicians with an understanding of the ischemic and non-ischemic derangements of brain physiology, its value does not take into consideration systemic oxygenation that can influence patients' outcomes. This study analyses brain and systemic oxygenation and a number of related indices in TBI patients: PbtO2, partial arterial oxygenation pressure (PaO2), PbtO2/PaO2, ratio of PbtO2 to fraction of inspired oxygen (FiO2), and PaO2/FiO2. The primary aim of this study was to identify independent risk factors for cerebral hypoxia. Secondary goal was to determine whether any of these indices are predictors of mortality outcome in TBI patients. Materials and Methods: A single-centre retrospective cohort study of 70 TBI patients admitted to the Neurocritical Care Unit (NCCU) at Cambridge University Hospital in 2014-2018 and undergoing advanced neuromonitoring including invasive PbtO2 was conducted. Three hundred and three simultaneous measurements of PbtO2, PaO2, PbtO2/PaO2, PbtO2/FiO2, PaO2/FiO2 were collected and mortality at discharge from NCCU was considered as outcome. Generalized estimating equations were used to analyse the longitudinal data. Results: Our results showed PbtO2 of 28 mmHg as threshold to define cerebral hypoxia. PaO2/FiO2 found to be a strong and independent risk factor for cerebral hypoxia when adjusting for confounding factor of intracranial pressure (ICP) with adjusted odds ratio of 1.78, 95% confidence interval of (1.10-2.87) and p-value = 0.019. With respect to TBI outcome, compromised values of PbtO2, PbtO2/PaO2, PbtO2/FiO2, and PaO2/FiO2 were all independent predictors of mortality while considered individually and adjusting for confounding factors of ICP, age, gender, and cerebral perfusion pressure (CPP). However, when considering all the compromised values together, only PaO2/FiO2 became an independent predictor of mortality with adjusted odds ratio of 3.47 (1.20-10.04) and p-value = 0.022. Conclusions: Brain and Lung interaction in TBI patients is a complex interrelationship. PaO2/FiO2 seems to be a major determinant of cerebral hypoxia and mortality. These results confirm the importance of employing ventilator strategies to prevent cerebral hypoxia and improve the outcome in TBI patients.
| S-EPMC7426476 | biostudies-literature
Project description: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 six-month 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.
| S-EPMC4291208 | biostudies-literature