Pruitt, Basil A. Jr MD, FACS
From the Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Submitted for publication June 8, 2005.
Accepted for publication June 9, 2005.
This article was written for the proceedings from a conference entitled Alcohol Problems among Hospitalized Trauma Patients: Controlling Complications, Mortality, and Trauma Recidivism in Arlington, Virginia, May 28-30, 2003. It does not reflect the official policy or opinions of the Centers for Disease Control and Prevention (CDC) or the U.S. Department of Health and Human Services (HHS) and does not constitute an endorsement of the individuals or their programs—by CDC, HHS, or the federal government—and none should be inferred.
Reprint requests to: Basil A. Pruitt, Jr., MD, FACS, Department of Surgery, University of Texas Health Science Center at San Antonio, Mail Code 7740, 7703 Floyd Curl Drive, San Antonio, Texas 78229-3900; email: email@example.com
It is a privilege to be the moderator for this first session and I look forward to seeing the proceedings of this conference published as a supplement to the Journal of Trauma. I have briefly reviewed selected literature published since the first of the year. A study published in Addiction points out that worldwide, in the young adult group, 5% of all deaths are alcohol-related.1 The incidence of alcohol-related deaths shows great geographic variation nationally and globally. For example, in Europe, 25% of all deaths in young men are alcohol-related; in Eastern Europe alone, one-third of all young men die from alcohol-related causes.1 Not only do these figures raise significant epidemiologic concerns, but they also reflect the fact that alcohol induces perverse physiologic problems and exerts deleterious effects on literally every organ system in the body.
Broadly speaking, everyone knows ingesting alcohol causes acute depression of the central nervous system. But not everyone understands the long-term effects such as reduction of brain white matter and olfactory nerve dysfunction. In the cardiovascular system, vasodilation is the characteristic response to acute alcohol exposure, and cardiomyopathy is a common consequence of chronic ingestion. The endocrine response to alcohol ingestion includes release of catecholamines from the adrenal medulla and the inhibition of antidiuretic hormone which is produced by the pituitary gland. Those effects make alcohol ingestion the social test of renal function. Alcohol also acutely affects the metabolic system, causing alterations of thermoregulation and fat metabolism ranging from decreased serum leptin levels to an increase in high density lipoproteins. In the hematopoietic system, alcohol affects all cells ranging from the red cell to the Nκ cell. Alcohol further compromises the already impaired neutrophil function (the first line of immunologic defense) in AIDS patients and thereby complicates their treatment.2 In the musculoskeletal system, long-term excessive alcohol intake can induce a generalized myopathy analogous to the previously mentioned cardiomyopathy. In addition to the alcohol-induced diuresis just noted, alcohol may induce teratogenesis in the genitourinary system (exemplified by the fetal alcohol syndrome). These changes not only complicate the diagnosis and assessment of injury severity, but influence treatment of the trauma patient as well. Moreover, these effects combine to magnify the severity of injury. A study appearing in Alcoholism earlier this year found alcohol use to increase the observed injury above that predicted by vehicle crash, safety belt use, and age. Alcohol use increased the Injury Severity Score as revised in 1990 (ISS-90) by an average of 30%. If any concentration of alcohol was present in the blood, the adjusted odds ratio for serious injury was 1.59.3
As Dr. Hungerford mentioned, this conference follows an earlier one that addressed alcohol problems among emergency department patients. That conference identified several needs that should be kept in mind as we discuss the problems of alcohol and drug use in trauma patients. These needs include (1) development of a user- and patient-friendly minimum data set for reliable, accurate screening, (2) development of effective interventions acceptable to patients and staff, (3) reliable privacy and security of the data collected, (4) elimination of nonpayment for care, which serves as a disincentive for diagnosing alcohol as a contributing cause of injury, (5) changes in medical practice to increase screening and intervention activity, (6) development of new computer-based techniques for screening and intervention to use when the patient resides in the “therapeutic window” of an emergency room stay, and (7) increased funding for research.4
Several screening techniques show promising results for identifying patients at risk for repeated alcohol-related injury. In the April 2003 issue of the Journal of Trauma, Dr. Gentilello’s group published a study identifying both categorical and continuous variables readily assessed by brief patient contact. These variables predicted hazardous drinking in the succeeding year.5 Categorical variables were being male, unmarried, or assaulted. Continuous variables were age, blood alcohol concentration, drug use in the month before the injury, and number of days alcohol was used (days on which three or more drinks were consumed or nonprescription drugs were used). These variables were evaluated in 110 patients by face-to-face interviews during admission and phone interviews at 1, 4, and 12 months thereafter. Hazardous drinking was defined as consuming three or more drinks on one or more occasions in the preceding month. Among patients studied during the subsequent year, 39% were designated nonhazardous drinkers and remained such. Thirty-five percent were found to be hazardous drinkers, and they remained in that category. The remission rate for hazardous drinkers who changed their consumption patterns to nonhazardous was only 6%. Disappointingly, more than three times as many patients (20.1%) converted from non-hazardous to hazardous drinking in that year. The most significant clinical predictors of hazardous drinking were a blood alcohol concentration (BAC) of anything over zero at admission, any abuse of nonprescription drugs in the preceding month, and having been the victim of intentional injury. The study demonstrated that, on the basis of a brief and focused interview in the emergency room or surgical ICU, it is possible to identify target groups most apt to engage in hazardous drinking and most likely to benefit from intervention.
Several studies indicate that intervention programs can minimize and prevent alcohol-related recidivism. A review published earlier this year in Addiction presented results of the Cochran Collaboration Systematic Review of alcohol prevention programs. These results can only be classified as disappointing.1 Fifty-six studies were reviewed with ineffectiveness observed in 20 (36%) of them. Regarding short- and medium-term prevention, the review determined that no firm effectiveness conclusions could be made. On the basis of these data, it was impossible for the authors to determine whether such brief interventions did any good or not. The authors interpreted data on the effect of long-term prevention programs (more than three years in duration) as showing promise. In contrast, recent reports show that pharmacologic intervention may be useful in patients who are identified to be at risk. After a month of treatment, Topiramate appears to be effective in reducing alcohol consumption in patients. It blocked excessive dopamine transmission by increasing the activity of gamma amino butyric acid and inhibited the ability of glutamate to release dopamine.6
There are very important differences between primary prevention programs and brief interventions. Primary prevention programs are usually broad educational programs aimed at the general public and generally focus on preventing excessive drinking or, with youth, drinking at all. In contrast, brief interventions are often conducted during the immediate post-injury window of opportunity and focus only on patients whose high risk drinking behavior has been identified by screening. Moreover, for high-risk patients, the amount of treatment required to reduce alcohol consumption varies, based on the severity of the drinking problem. Patients who have severe problems, such as true alcohol dependence, probably need some type of long-term care, in addition to a brief intervention. Reported earlier this year in Addiction, a study by R. H. Moos and B. S. Moos showed that rapid entry into treatment and the duration of treatment for alcohol-use disorders were more important than the intensity of treatment. Consequently, the authors concluded that treatment programs should be structured to begin promptly and emphasize continuity.7 However, patients who receive a brief intervention before showing signs of true addiction appear to be amenable to interventions that require only one treatment session. In another study of intervention effectiveness, A. J. Smith et al. randomized males 16 to 35 years of age who were treated for an alcohol-related facial injury to either usual treatment or usual treatment plus a single brief motivational intervention session. At one year follow up, the proportion drinking at hazardous levels had not decreased significantly in the usual treatment group, but had in the group receiving the brief intervention with the greatest effect in those patients considered to be hazardous drinkers.8 These reports suggest that while brief interventions appear to have efficacy, further research should be done on primary prevention strategies.
Our job in this conference is to determine how recommendations from the earlier conference, which were focused on emergency departments, can be refocused on trauma patients to improve screening techniques and develop effective intervention programs to reduce death and disability caused by alcohol- and drug-related injury. To identify and quantify the impact alcohol and other drugs have on trauma care, we have three A-Team speakers to conduct the first workshop: Dr. Eugene Moore will speak on “Alcohol and Trauma—The Perfect Storm”; Dr. Donald D. Trunkey will present “A Rational Approach to Formulating Public Policy on Substance Abuse”; and finally, Dr. Charles E. Lucas will discuss “The Impact of Street Drugs on Trauma Care.”
1.Foxcroft DR, Ireland D, Lister-Sharp DJ et al. Longer-term primary prevention for alcohol misuse in young people: a systematic review. Addiction. 2003;98:397–411.
2.Chen Y, Mendoza S, Davis-Gorman G et al. Neutrophil activation by murine retroviral infection during chronic ethanol consumption. Alcohol and Alcohol. 2003;38:109–114.
3.Waller PF, Hill EM, Maio RF et al. Alcohol effects on motor vehicle crash injury. Alcohol Clin Exp Res. 2003;27:695–703.
4.Hungerford DW, Pollock DA, eds. Alcohol Problems Among Emergency Department Patients: Proceedings of a Research Conference on Identification and Intervention. Arlington, Virginia, 19–21 March 2001. Atlanta, GA: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention; 2002.
5.Dunn C, Latzick D, Russo J et al. Hazardous drinking by trauma patients during the year after injury. J Trauma. 2003;54:707–712.
6.Pisano M. Alcoholism breakthrough seen. San Antonio Express-News. May 16, 2003:B1.
7.Moos RH, Moos BS. Long-term influence of duration and intensity of treatment on previously untreated individuals with alcohol use disorders. Addiction. 2003;98:325–337.
8.Smith AJ, Hodgson RJ, Bridgeman K et al. A randomized controlled trial of a brief intervention after alcohol-related facial injury. Addiction. 2003;98:43–52.
© 2005 Lippincott Williams & Wilkins, Inc.