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Alcohol exposure, injury, and death in trauma patients.

ABSTRACT: The association of alcohol use with in-hospital trauma deaths remains unclear. This study identifies the association of blood alcohol content (BAC) with in-hospital death accounting for injury severity and mechanism.This study involves a historical cohort of 46,222 admissions to a statewide trauma center between January 1, 2002, and October 31, 2011. Blood alcohol was evaluated as an ordinal variable: 1 mg/dL to 100 mg/dL as moderate blood alcohol, 101 mg/dL to 230 mg/dL as high blood alcohol, and greater than 230 mg/dL as very high blood alcohol.Blood alcohol was recorded in 44,502 patients (96.3%). Moderate blood alcohol was associated with an increased odds for both penetrating mechanism (odds ratio [OR], 2.22; 95% confidence interval [CI], 2.04-2.42) and severe injury (OR, 1.25; 95% CI, 1.16-1.35). Very high blood alcohol had a decreased odds for penetrating mechanism (OR, 0.75; 95% CI, 0.67-0.85) compared with the undetectable blood alcohol group. An inverse U-shaped association was shown for severe injury and penetrating mechanism by alcohol group (p < 0.001). Moderate blood alcohol had an increased odds for in-hospital death (OR, 1.50; 95% CI, 1.25-1.79), and the odds decreased for very high blood alcohol (OR, 0.69; 95% CI, 0.54-0.87). An inverse U-shaped association was also shown for in-hospital death by alcohol group (p < 0.001). Model discrimination for in-hospital death had an area under the receiver operating characteristic curve of 0.64 (95% CI, 0.63-0.65).Injury severity and mechanism are strong intermediate outcomes between alcohol and death. Severe injury itself carried the greatest odds for death, and with the moderate BAC group at greatest odds for severe injury and the very high BAC group at the lowest odds for severe injury. The result was a similar inverse-U shaped curve for odds for in-hospital death. Clear associations between blood alcohol and in-hospital death cannot be analyzed without consideration for the different injuries by blood alcohol groups.Epidemiologic study, level III.

SUBMITTER: Afshar M

PROVIDER: S-EPMC4582442 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature

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Alcohol exposure, injury, and death in trauma patients.

Afshar Majid M Netzer Giora G Murthi Sarah S Smith Gordon S GS

The journal of trauma and acute care surgery 20151001 4

<h4>Background</h4>The association of alcohol use with in-hospital trauma deaths remains unclear. This study identifies the association of blood alcohol content (BAC) with in-hospital death accounting for injury severity and mechanism.<h4>Methods</h4>This study involves a historical cohort of 46,222 admissions to a statewide trauma center between January 1, 2002, and October 31, 2011. Blood alcohol was evaluated as an ordinal variable: 1 mg/dL to 100 mg/dL as moderate blood alcohol, 101 mg/dL to ...[more]

PMID: 26402540

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Project description:BackgroundAlcohol is a known modulator of the immune system and host-defense response. Alcohol abuse is common in trauma patients, although the influence of alcohol intoxication on the inflammatory response following major orthopaedic injury remains unknown. The aim of this investigation was to examine the influence of binge alcohol exposure on biomarkers of the systemic inflammatory response following bilateral traumatic femoral fracture in a rodent model.MethodsNinety-two Sprague-Dawley rats were administered intraperitoneal injections of either saline solution or alcohol for three days. These animals then underwent a sham procedure or bilateral femoral intramedullary pinning and mid-diaphyseal closed fracture via blunt guillotine. The animals were killed at specific time points after the injury. Serum and lung tissue were collected, and twenty-five inflammatory markers were analyzed by immunoassay. Histological sections of lung tissue were evaluated by a board-certified pathologist.ResultsBilateral femoral fracture significantly (p < 0.05) increased multiple serum biomarkers of inflammation. Binge alcohol treatment prior to injury significantly suppressed the increase in serum levels of interleukin (IL)-6, white blood cells, IL-2, IL-10, and C-reactive protein after the fracture. However, alcohol-treated animals were found to have increased pulmonary levels of IL-6, IL-1β, IL-2, and macrophage inflammatory protein-1α following bilateral femoral fracture. In addition, lung tissue harvested following alcohol treatment and injury demonstrated increased pathologic changes, including parenchymal, alveolar, and peribronchial leukocyte infiltration and significantly elevated pulmonary wet-to-dry ratio, indicative of pulmonary edema.ConclusionsOur results indicate that acute alcohol intake prior to bilateral femoral fracture with fixation in rats modulates the inflammatory response after injury in a tissue-dependent manner. Although serum biomarkers of inflammation were suppressed in alcohol-treated animals following injury, several measures of pulmonary inflammation including cytokine levels, histological changes, and findings of pulmonary edema were significantly increased following fracture with the presence of alcohol.

Dataset Information

Alcohol exposure, injury, and death in trauma patients.

Publications

Alcohol exposure, injury, and death in trauma patients.

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