Biomedical subjects

G S Smith

Publications and source records attributed to G S Smith.

At least 91 records · Page 5Linked to original sources

PubMed1998

Cyclooxygenase inhibition attenuates cholecystokinin-induced gastroprotection.

Cholecystokinin prevents gastric injury by an unknown mechanism. This study was conducted in conscious, fasted female rats in order to assess the role of endogenous prostaglandins as a potential protective mechanism for cholecystokinin-induced gastroprotection. Intravenous administration of cholecystokinin (0.05-5 nmol/kg) dose-dependently reduced macroscopic injury to the glandular portion of the stomach caused by 1 ml of orally administered acidified ethanol (150 mM hydrochloric acid-50% ethanol), an effect corroborated by histologic analysis. In time course studies, this protective action occurred as early as 10 min following cholecystokinin injection (5 nmol/kg intravenously), but was absent at 1 hr. Cyclooxygenase inhibition with either indomethacin (5 mg/kg intraperitoneally) or aspirin (100 mg/kg intraperitoneally) resulted in a partial reversal in cholecystokinin-induced gastroprotection, effects that were similar in magnitude. However, while indomethacin reduced gastric mucosal prostaglandin synthesis (enzyme-linked immunoassay) by 60%, aspirin almost totally abolished prostaglandin synthesis (95% reduction). Cholecystokinin (5 nmol/kg intravenously) did not significantly enhance gastric mucosal prostaglandin synthesis in the absence of cyclooxygenase inhibition. These data indicate that cholecystokinin requires the presence of endogenous prostaglandins in order to fully exert its gastroprotective actions. However, release of endogenous prostaglandins does not entirely explain the protective response, and additional factors likely participate in this action.

Animals↗

PubMed1998

The role of cyclooxygenase-1 and cyclooxygenase-2 in lipopolysaccharide and interleukin-1 stimulated enterocyte prostanoid formation.

Lipopolysaccharide is an inflammatory agent and interleukin-1 is a cytokine. Their pro-inflammatory effects may be mediated by prostanoids produced by inducible cyclooxygenase-2. The aim of this study was to determine the prostanoids produced by lipopolysaccharide and interleukin-1 stimulated enterocytes through the cyclooxygenase-1 and 2 pathways. Cultured enterocytes were stimulated with lipopolysaccharide or interleukin-1beta with and without cyclooxygenase inhibitors. Low concentrations of indomethacin and valerylsalicylic acid (VSA) were evaluated as cyclooxygenase-1 inhibitors and their effects compared with the effects of a specific cyclooxygenase-2 inhibitor, SC-58125. Prostaglandin E2, 6-keto prostaglandin F1alpha, prostaglandin D2 and leukotriene B4 levels were determined by radioimmunoassay. Immunoblot analysis using isoform-specific antibodies showed that the inducible cyclooxygenase enzyme (COX-2) was expressed by 4 h in LPS and IL-1beta treated cells while the constitutive COX-1 remained unaltered in its expression. Interleukin-1beta and lipopolysaccharide stimulated the formation of all prostanoids compared with untreated cells, but failed to stimulate leukotriene B4. Indomethacin at 20 microM concentration, and VSA inhibited lipopolysaccharide and interleukin 1beta stimulated prostaglandin E2, but not 6-keto prostaglandin F1alpha formation. SC-58125 inhibited lipopolysaccharide and interleukin-1beta stimulated 6-keto prostaglandin F1alpha but not prostaglandin E2 release. The specific cyclooxygenase-2 inhibitor also inhibited lipopolysaccharide produced prostaglandin D2 but not interleukin-1beta stimulated prostaglandin D2. While SC-58125 inhibited basal 6-keto prostaglandin-F1alpha formation it significantly increased basal prostaglandin E2 and prostaglandin D2 formation. As SC-58125 inhibited lipopolysaccharide and interleukin-1beta induced 6-keto prostaglandin F1alpha production but not prostaglandin E2 production, it suggests that these agents stimulate prostacyclin production through a cyclooxygenase-2 mediated mechanism and prostaglandin E2 production occurs through a cyclooxygenase-1 mediated mechanism. Prostaglandin D2 production appeared to be variably produced by cyclooxygenase-1 or cyclooxygenase-2, depending on the stimulus.

Animals↗

PubMed1998

Adaptive cytoprotection induced by ethanol in human intestinal cells: role of prostaglandins and calcium homeostasis.

OBJECTIVE: To determine whether adaptive cytoprotection exists in human intestinal cells under in vitro conditions and what role, if any, endogenous prostaglandins or calcium may play in mediating this protective response. SUMMARY BACKGROUND DATA: Adaptive cytoprotection can be defined as that process whereby the administration of a low concentration of a damaging agent, termed a "mild irritant," which by itself is not injurious, can attenuate gastrointestinal mucosal injury subsequently induced by the application of higher concentrations of the same or other necrotizing agents. Despite substantial investigation, the mediator or mediators of adaptive cytoprotection remain poorly understood. METHODS: Postconfluent Caco-2 cells were used in all experiments. Cellular death was quantitated using a dual-component fluorescent assay. Changes in intracellular calcium concentration were quantitated by measuring fluorescent signal changes of the single wavelength calcium indicator (Fluo-3). Finally, prostaglandin E2 release into the media was quantitated by radioimmunoassay. RESULTS: Pretreatment of Caco-2 cells with low concentrations of ethanol (mild irritant) significantly attenuated injury induced by higher damaging concentrations of ethanol. The protection conferred by the mild irritant was directly dependent on both the concentration of the irritant used and the duration of exposure and was abrogated when cells were pretreated with an endogenous prostaglandin inhibitor (indomethacin) or if the mild irritant was administered in calcium-free media. Cells exposed to ethanol had a significant and concentration-dependent increase in intracellular calcium concentration, an effect that was highly related to cellular injury. Pretreatment with a mild irritant significantly decreased intracellular calcium increases induced by not only ethanol but also by a calcium ionophore (A23187). Cells treated with low concentrations of ethanol demonstrated no significant elevation in prostaglandin E2 release. CONCLUSIONS: Adaptive cytoprotection induced by ethanol exists in human colonocytes under in vitro conditions independent of mucosal blood flow, neural innervation, or circulating humoral factors. The authors' data suggest that this response does not require endogenous prostaglandin synthesis but may involve processes whereby intracellular calcium accumulation is prevented.

Caco-2 Cells↗

PubMed1998

Creating injury episodes using medical claims data.

BACKGROUND: Health care episodes are traditionally created for a specific condition using defined relevant diagnosis and procedure codes and a start and end period. Our goal is to use 1987 to 1989 medical claims data to create distinct episodes of care as a result of injury. METHODS: Claims for 102,000 people younger than 65 years were obtained from Medstat Systems, Inc. Injury claims were identified by International Classification of Diseases, 9th Revision, Clinical Modification diagnosis codes and separated into 10 body regions. Using linked inpatient and outpatient claims data, we established clear zones--a maximum period for a return visit for medical treatment--for each of 10 body regions injured by hospitalization status. These clear zones were used to create episodes of injury. RESULTS: A total of 295,165 injury claims created 79,564 episodes of injury. Limb and trunk injuries typically have the most follow-ups in terms of number of claims and spacing between claims. Brain injuries, even for admitted patients, result in an average of fewer than two follow-up claims. On average, hospitalized patients require only one more follow-up than nonadmitted patients. CONCLUSIONS: This paper presents a method for identifying injury episodes using a medical claims database. The analysis suggests that follow-up to check for minor long-term sequelae of brain injury is rare.

Adult↗

PubMed1998

A prospective cohort study of blood donors: methodological issues in the investigation of injuries and chronic diseases.

Blood donors have made important contributions to research, most notably in cross-sectional seroprevalence studies. The proposed New Zealand Blood Donors Health Study is a prospective cohort study of 30,000 New Zealand donors designed to investigate the determinants of common injuries, cardiovascular disease and cancer. While robust from an analytic perspective, the execution of prospective cohort studies in many settings is impeded by methodological, economic and organisational barriers. We examined the operational considerations of implementing a large-scale cohort study at a transfusion centre and evaluated measures taken to optimise data collection procedures. A pilot study of 1,000 participants revealed donor motivation to participate in this research was high (91% response rate). Comprehensive exposure data on lifestyle, behavioural and psychosocial factors were obtained from 95% of participants. Substantial heterogeneity in levels of potential risk factors was noted among respondents. Detailed dietary habit information and a study blood sample were obtained from 67% and 100% of participants, respectively. Study recruitment and baseline data collection was feasible during routine donor visits with minimal interruption to donor centre staff and procedures. We conclude the study design and characteristics of the regional donor program enhance the efficiency and significance of the proposed research.

Adolescent↗

PubMed1998

Drowning surveillance: how well do E codes identify submersion fatalities.

OBJECTIVES: The aim was to determine in New Zealand: (1) to what degree the International Classification of Diseases Supplementary Classification (ICD) external cause (E) codes for drowning identify all deaths involving drowning; (2) how the other drowning deaths are distributed across E codes; and (3) whether the proportion of drownings not identified by traditional ICD E codes has changed over time. METHODS: Mortality files for the period 1977-92, which were coded in the range E800-E999 (external causes of injury and poisoning), were searched electronically using the keyword "drown". RESULTS: 2718 cases that involved drowning were identified. This represents a 17.7% increase in the number of cases one would identify using ICD drowning E codes alone. The majority (65%) of the 408 drownings not coded as such were coded as motor vehicle traffic crashes. The number of drownings that were not identified by ICD E codes remained relatively constant over time, although the number of deaths E coded as drowning declined significantly in recent years. CONCLUSION: Standard ICD E codes for drowning do not identify all drowning related deaths, which may make comparisons of injury rates between countries difficult, especially for injuries such as drownings and burns that can be both nature of injury and external cause codes. Multiple cause coding and the inclusion of free text narratives are an important tool to improve the value of a country's vital statistics for injury prevention, and facilitate comparisons with other countries.

Cause of Death↗

PubMed1998

Harstad injury prevention study: prevention of burns in young children by community based intervention.

OBJECTIVE: To describe the long term effectiveness of a community based program targeting prevention of burns in young children. DESIGN: Quasiexperimental. SETTING: The Norwegian city of Harstad (main intervention), six surrounding municipalities (intervention diffusion), and Trondheim (reference). PARTICIPANTS: Children under age 5 years in the three study populations. METHODS: Outpatient and inpatient hospital data were coded according to the Nordic system, and collected as part of a national injury surveillance system. Burn data collection started in May 1985. The first 19.5 months of the study provided baseline data, while the last 10 years involved community based intervention, using a mix of passive and active interventions. RESULTS: The mean burn injury rate decreased by 51.5% after the implementation of the intervention in Harstad (p < 0.05) and by 40.1% in the six municipalities (not significant). Rates in the reference city, Trondheim, increased 18.1% (not significant). In Harstad and the six surrounding municipalities there was a considerable reduction in hospital admissions, operations, and bed days. Interventions with passive strategies were more effective, stove and tap water burns being eliminated in the last four years, while active strategies were less effective. CONCLUSIONS: A program targeting burns in children can be effective and sustainable. Local injury data provided the stimulus for community action.

Burns↗

PubMed1998

Hepatic infarction secondary to arterial insufficiency in native livers: CT findings in 10 patients.

PURPOSE: To describe the computed tomographic (CT) appearance of hepatic infarcts resulting from arterial insufficiency in native livers. MATERIALS AND METHODS: The authors retrospectively reviewed the clinical and imaging findings in 10 patients (five men, five women; age range, 28-70 years) with 14 hepatic infarcts seen over 3 years. CT scans were analyzed for infarct appearance, vessel patency, and evolution of infarct pattern over time. RESULTS: Hepatic infarction resulted from hepatobiliary surgery (n = 6), radiologic intervention (n = 3), and celiac occlusion secondary to antiphospholipid syndrome (n = 1). All 14 infarcts were of low attenuation, peripheral, and wedge-shaped. Occluded arterial vessels were identified in eight patients. Follow-up CT revealed infarct diminution with parenchymal atrophy and scarring (n = 5), progressive liquefaction (n = 2), or both parenchymal atrophy and progressive liquefaction (n = 1). CONCLUSION: Sudden interruption of hepatic arterial flow may cause acute native liver infarction. Patients at risk include those with underlying vascular disease who undergo complicated surgical procedures and those undergoing peripheral arterial embolization.

Adult↗

PubMed1998

Protection against ethanol injury by prostaglandin in a human intestinal cell line: role of microtubules.

Prostaglandins have been shown to protect the gastrointestinal (GI) epithelium from injury induced by various luminal insults independent of their known acid-inhibitory effects, a process termed "cytoprotection." The mechanism of this protective action remains unknown. The present investigation determined the role of microtubules (a major cytoskeletal component) in GI injury induced by ethanol (EtOH) and its prevention by 16,16-dimethylprostaglandin E2 (dmPGE2) using cells from a human colonic cell line known as Caco-2 cells. These cells were preincubated in Eagle's minimum essential medium with and without dmPGE2 (2.6 microM) for 15 min and subsequently incubated in media containing 1, 2.5, 5, 7.5, and 10% EtOH. The effects on cell viability and tubulin (the major protein backbone of microtubules) were then determined. EtOH concentrations > or = 2.5% extensively disrupted the microtubules as demonstrated by fragmentation, kinking, and perturbation of the microtubule organizer center. EtOH treatment also led to a significant decrease in the S2 (polymerized) fraction and an increase in the S1 (monomeric) pool of tubulin. Concomitant with these effects were marked decreases in cellular viability. DmPGE2 pretreatment abolished the disruption of microtubules, significantly increased the S2 fraction of tubulin, and increased cellular viability in cultures exposed to EtOH. Furthermore, pretreatment with colchicine, an inhibitor of microtubule assembly, prevented the cytoprotective action of dmPGE2. Taxol, a microtubule stabilizing agent, mimicked the effects of dmPGE2 by also enhancing microtubule integrity and increasing cellular viability in cells exposed to EtOH. Our data indicate that organization and stabilization of microtubules may play an essential role in the mechanism of prostaglandin-induced protection.

16,16-Dimethylprostaglandin E2↗

PubMed1998

Role of calcium in adaptive cytoprotection and cell injury induced by deoxycholate in human gastric cells.

We have developed an in vitro model of adaptive cytoprotection induced by deoxycholate (DC) in human gastric cells and have shown that pretreatment with a low concentration of DC (mild irritant, 50 microM) significantly attenuates injury induced by a damaging concentration of DC (250 microM). This study was undertaken to assess the effect of the mild irritant on changes in intracellular Ca2+ and to determine if these perturbations account for its protective action. Protection conferred by the mild irritant was lost when any of its effects on intracellular Ca2+ were prevented: internal Ca2+ store release via phospholipase C and inositol 1,4, 5-trisphosphate sustained Ca2+ influx through store-operated Ca2+ channels or eventual Ca2+ efflux. We also investigated the relationship between Ca2+ accumulation and cellular injury induced by damaging concentrations of DC. In cells exposed to high concentrations of DC, sustained Ca2+ accumulation as a result of extracellular Ca2+ influx, but not transient changes in intracellular Ca2+ content, appeared to precede and induce cellular injury. We propose that the mild irritant disrupts normal Ca2+ homeostasis and that this perturbation elicits a cellular response (involving active Ca2+ efflux) that subsequently provides a protective action by limiting the magnitude of intracellular Ca2+ accumulation.

Acclimatization↗

PubMed1998

Indomethacin increases susceptibility to injury in human gastric cells independent of PG synthesis inhibition.

Indomethacin and other nonsteroidal anti-inflammatory drugs are commonly used to indirectly deduce the possible role of PGs in a process being studied. The objective of this study was to determine if indomethacin, at concentrations comparable to plasma and tissue levels obtained in humans taking therapeutic doses, predisposes human gastric cells to injury through inhibition of PGs or acts through an alternate mechanism. The role of intracellular Ca2+ in this damaging process was also assessed. Indomethacin pretreatment, although by itself nondamaging, was associated with elevated intracellular Ca2+ concentrations and an increased cellular permeability, an effect that was dependent on extracellular Ca2+. Furthermore, indomethacin pretreatment significantly predisposed AGS cells to injury induced by two dissimilar agents (deoxycholate and A-23187), both of which are associated with intracellular Ca2+ accumulation. The addition of exogenous PGs did not reverse the predisposition to injury induced by indomethacin. The observed effects of indomethacin were dependent on concentration and not on ability to inhibit PG synthesis. Similar effects were not observed with equipotent concentrations of ibuprofen or aspirin. Finally, the exacerbation of deoxycholate-induced injury induced by indomethacin was not observed when extracellular Ca2+ was removed. Indomethacin, by disturbing intracellular Ca2+ homeostasis, predisposes human gastric cells to injury through mechanisms independent of PG synthesis. The current study suggests that data resulting from studies employing only indomethacin as a PG synthesis inhibitor should be interpreted with caution.

Calcimycin↗

PubMed1998

Comparison of sonograms and liver histologic findings in patients with chronic hepatitis C virus infection.

Gray scale ultrasonographic images of the liver were correlated with histologic findings in patients with chronic hepatitis C virus infection. The gray scale patterns of 64 livers with chronic hepatitis C virus infection were categorized as normal, fatty, fibrofatty, fibrotic, or inflammatory and were graded as mild, moderate, or severe. Liver biopsy specimens also were analyzed for the presence of fat, inflammation, and fibrosis and graded similarly. No correlation was found between fatty and fibrofatty sonographic findings with any of the three histologic patterns. Correlations were found between fibrotic sonographic findings and both fibrotic and inflammatory histologic findings (r = 0.27; P = 0.03). Although some pathologic features of liver disease were detected by ultrasonography, no useful correlation was noted between results of sonography and histologic examination.

Adolescent↗

PubMed1998

Store-operated calcium influx in human gastric cells: role of endogenous prostaglandins.

BACKGROUND: Store-operated calcium influx (SOCI) appears to be a key component in regulating processes such as gene expression and cellular metabolism in nonexcitable cells. Our objective was to determine what effect, if any, prostaglandin inhibition had on SOCI in human gastric cells. METHODS: SOCI was induced in human gastric cells (AGS) with thapsigargin, a microsomal Ca++ adenosine triphosphatase inhibitor. Quantitation of SOCI was achieved by two different methods: sustained intracellular calcium elevation and manganese (Mn++) uptake. Endogenous prostaglandin E2 (PGE2) synthesis was measured by enzyme immunoassay. Three different nonsteroidal anti-inflammatory drugs (NSAIDs; indomethacin, ibuprofen, and aspirin) were used to minimize the nonspecific actions of any individual agent. RESULTS: SOCI in AGS cells was inhibited by the store-operated Ca+2 channel blocker lanthanum (La+3) but not the voltage-operated Ca+2 channel antagonists verapamil or nifedipine. Each of the three NSAIDs equally inhibited SOCI. The inhibition of SOCI induced by indomethacin was partially reversed by the addition of exogenous PGE2. Finally, AGS cells exposed to thapsigargin demonstrated significantly increased endogenous PGE2 release. CONCLUSIONS: These data suggest that NSAIDs inhibit (or endogenous prostaglandins modulate) SOCI in human gastric cells, at least in part. Because SOCI appears to be a critical mechanism involved in cell proliferation, this may provide one explanation of how NSAIDs inhibit (and endogenous prostaglandins enhance) gastric epithelial renewal and repair.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1998

Screening trauma patients for alcoholism according to NIAAA guidelines with alcohol use disorders identification test questions.

Drinking pattern criteria (drinking frequency and number of drinks per occasion) issued by the National Institute on Alcohol and Abuse and Alcoholism (NIAAA) to screen primary practice patients for alcohol problems were evaluated in 1216 injured patients treated in a regional trauma center. Vehicular crash victims predominated (50.2%, of whom 64.5% were drivers), followed by victims of violence (31.2%) and nonviolent-injury victims (18.5%). Alcohol Use Disorders Identification Test (AUDIT) questions #1 (drinking frequency) and #2 (drinks/day) were used to assess the patients for current alcohol dependence (CAD). AUDIT responses roughly approximating NIAAA guidelines (high threshold: drinks > or = 4 times/week, > or = 5 drinks/day) and those indicating less drinking (low threshold: drinks > or = 2-3 times/ week, > or = 3 drinks/day) were chosen. Comparisons were made relative to sensitivity and specificity of responses in detecting CAD. When low threshold responses were used for either question, sensitivity to detect CAD increased overall (#1 from 0.53 to 0.80, #2 from 0.62 to 0.88) as well as among the subgroups of patients, whereas specificity remained high or at acceptable levels overall (#1 from 0.95 to 0.82, #2 from 0.92 to 0.71) and among the subgroups of patients. Study findings suggest that, among injured drivers and other groups of trauma center patients, lesser amounts of drinking should be used as screening criteria for CAD than are used for the general population.

Accidents, Traffic↗

PubMed1997

Psychoactive substance use disorders among seriously injured trauma center patients.

OBJECTIVE: To assess the prevalence of psychoactive substance use disorders (PSUDs) among a large, unselected group of seriously injured trauma center patients, using a standardized diagnostic interview and criteria. DESIGN: Prevalence study. SETTING: A level I regional trauma center. PATIENTS: Trauma center patients fulfilling the following criteria were eligible subjects: aged 18 years or older, admission from injury scene, length of stay of 2 days or longer, and intact cognition. OUTCOME MEASURES: The PSUDs were diagnosed using the Structured Clinical Interview (SCID) for the Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition (DSM-III-R) and were categorized as abuse or dependence and past or current (within past 6 months). The SCID results were analyzed with respect to demographic factors, injury type, and blood alcohol concentration and urine toxicology results, using chi2 and logistic regression techniques. RESULTS: Of the 1220 patients approached for study, 1118 (91.6%) consented. More than half (54.2%) had a diagnosis of a PSUD in their lifetime. Approximately 90% of alcohol and other drug use diagnoses were for dependence and more than 62% were current. Overall, 24.1% of patients were currently alcohol dependent (men, 27.7%; women, 14.7%; P<.001), and 17.7% were currently dependent on other drugs (men, 20.2%; women, 11.2%; P<.001). Current alcohol dependence rates were not associated with race; rates of dependence on other drugs were higher among nonwhites and victims classified with intentional injuries. While 54.3% of blood alcohol-positive patients were currently alcohol dependent and 38.7% of patients with positive urine screening test results for drugs other than alcohol and nicotine were currently drug dependent, 11.7% of blood alcohol-negative and 3.9% of drug-negative patients, respectively, had current diagnoses of dependence on psychoactive substances. CONCLUSIONS: A high percentage of seriously injured trauma center patients are at risk of having current PSUDs. Patients with positive toxicology screening test results and/or positive screening questionnaire responses should be referred for formal evaluation and treatment.

Adult↗

PubMed1997

Three perspectives on work-related injury surveillance systems.

This paper reviews surveillance approaches for occupational injuries and evaluates three emerging methodologies for the enhancement of work-related injury surveillance: (1) narrative data analysis, (2) data set linkage, and (3) comprehensive company-wide surveillance systems. All three methods are the result of new applications of computer hardware and software that have apparent strengths and limitations. A major strength is the improved description of work exposures and related injuries leading to better understanding of injury etiology. This understanding, however, is limited by the data quality and completeness entered on records at the time of the injury. We recommend (1) more widespread inclusion of narrative text in databases, analyses of which can be a valuable supplement to injury coded data; (2) the increased use of data set linkage studies to combine injury and work-history data; and (3) the development of comprehensive company-wide surveillance systems to expedite the use of epidemiologic data for occupational injury prevention activities. Further development of these methods and others is encouraged, especially in light of technological advancements in data capture, analysis and presentation. Only through such efforts can we best apply epidemiologic principles to preventing injuries in the workplace.

Accidents, Occupational↗

PubMed1997

Alternative approaches to analytical designs in occupational injury epidemiology.

In this paper, we discuss the theoretical framework upon which observational studies of occupational injuries are based. Following a general description of how causal effects are estimated, the challenges faced by researchers working in this area are outlined, with an emphasis on case-control studies. These challenges include defining the at-risk period for workers whose tasks change over time and whose hazard period may be very brief, evaluating the underreporting of both exposures and injuries, and considering the effects of multiple injuries per individual on study design and data analysis. We review both the theoretical and practical considerations in the design and conduct of traditional case-control studies, based on the collection of individual level data, as well as other approaches, such as using information culled from administrative and descriptive databases, and case-control studies in which the plant or work site is the unit of analysis. The case-crossover design is also reviewed and its utility for reducing confounding due to differences between individuals by self-matching is highlighted. While this design has not yet been applied to the work setting, its potential for increasing our understanding of the causes of acute-onset occupational injuries seems promising. Finally, a variety of hybrid designs are discussed, including combinations of case-control, case-crossover, and cohort designs.

Accidents, Occupational↗

PubMed1997

Alcoholism at the time of injury among trauma center patients: vehicular crash victims compared with other patients.

A structured in-depth interview employing standardized criteria was used to determine the prevalence of lifetime and current alcohol dependence (alcoholism) in unselected consecutive patients admitted to a regional Level I trauma center. Of 629 patients, 157 (25.0%) were current alcoholics at the time of injury. An additional 87 (13.8%) were diagnosed as lifetime non-current alcoholics. There was no significant difference in the rates of current alcohol dependence among patients injured in vehicular crashes (23.5%), other unintentional trauma victims (29.3%), and those injured as a result of violence (24.6%). Of BAC+ (blood alcohol concentration positive) patients, 54.5% were current alcoholics. However, 14.4% of alcohol-negative patients were also diagnosed as alcohol dependent.

Accidents, Traffic↗