Source: Zink BJ, et al. Effects of ethanol in an experimental model of combined traumatic brain injury and hemorrhagic shock. Acad Emerg Med 1998;5:9-17.
Numerous studies have described the common link between substance abuse or intoxication and trauma.1,2While this association is strong, and causation is implied and accepted, the actual implications of the intoxication have only recently begun to be understood.

Specifically, if we accept that intoxicated patients are more likely to suffer traumatic events by virtue of their intoxication, what role does the actual intoxication have regarding assessment, management, and ultimate outcome? How often have we looked at an intoxicated patient in the ED who has suffered severe trauma but is alive, and said to ourselves, "If this happened to me, I would certainly have died"?

To many, there is the perception that the intoxication is protective. In the setting of blunt trauma, such as a motor vehicle crash, popular older theories stated that patients failed to tense-up at the moment of impact, thus, limiting their injuries. Others have concluded that intoxication not only predisposes to injury, but exacerbates the severity of the injury.

In a recent study, Zink and colleagues used an elegant design to evaluate the effects of acute ethanol intoxication on a model of simultaneous hemorrhagic shock and traumatic brain injury in pigs. Twenty-two animals were anesthetized, intubated, and cannulated for extensive invasive monitoring. Standard techniques were then used to incite reproducible head injuries and mimic hemorrhagic shock.

Prior to injury, the animals were divided into a control group and a treatment group. The treatment group was given oral ethanol at a dose that produced a mean ethanol level of 162 mg/dL at that time of injury. Before the injury, the ethanol-treated animals displayed lower mean arterial pressures, lower cerebral perfusion pressures, and higher hemoglobins, while all other physiologic parameters were similar. Following injury, ethanol-treated animals had shorter survival times associated with higher cerebral venous lactate levels and higher cerebral oxygen ratios. Zink et al conclude that the detrimental effects of ethanol probably resulted from impaired cardiovascular function.


This excellent study should reinforce the concept that substances that impair cardiovascular physiology and central nervous system function not only predispose to traumatic injury, but also can exacerbate the injury in experimental models. Yet, how do we rationalize the widely held belief that intoxicated trauma patients tend to have good outcomes in spite of surprisingly severe injuries? The answer, I think, comes from years of diligent attention to the slightest detail and conservatism in managing patients with altered mental status. This concept was best reinforced by Jurkovich and colleagues, who demonstrated that intoxicated patients tend to get intubated earlier, have more diagnostic peritoneal lavage, more head CT scanning, and more ICP monitoring than a group of non-intoxicated patients who were matched for injury severity score.3Thus, as always, the clinician is the great equalizer, and we can conclude that if intoxicated patients who make it to the hospital alive have good outcomes, it is because of our heightened awareness of potential injuries and the severity of those injuries. This study should only enhance that awareness.


1. Marx J. Alcohol and trauma.Emerg Med Clin North Am1990;8:929-938.

2. Edna TH. Alcohol influence and head injury. Acta Chir Scand 1982;48:209-212.

3. Jurkovich GJ, et al. Effects of alcohol intoxication on the initial assessment of trauma patients. Ann Emerg Med 1992;2:704-708.