Alcohol's Burden on Immunity Following Burn, Hemorrhagic Shock, or Traumatic Brain Injury

Abstract

Alcohol consumption contributes to increased incidence and severity of traumatic injury. Compared with patients who do not consume alcohol, alcohol-consuming patients have higher rates of long-term morbidity and mortality during recovery from injury. This can be attributed in part to an impaired immune response in individuals who consume alcohol. Acute and chronic alcohol use can affect both the innate and adaptive immune defense responses within multiple organ systems; the combination of alcohol use and injury results in increased susceptibility to bacterial and viral pathogens. This review examines the major deleterious effects of alcohol on immunity following tissue damage or traumatic injury, with a focus on alcohol's influence on the ability of the immune and major organ systems to fight disease and to repair damaged tissues following injury.

Figure 1

Salient gastrointestinal, pulmonary, and metabolic pathophysiological consequences of alcohol abuse prior to, or at the time of, burn injury. The decrease in gut barrier function leads to increased permeability and bacterial translocation that enhances the risk for bacterial infections and lung injury. Marked alterations in metabolic responses, characterized by altered adipokine profile consistent with increased insulin resistance, collectively contribute to greater morbidity and mortality post–burn injury.

Figure 2

Salient gastrointestinal, pulmonary, and neuroendocrine pathophysiological consequences of alcohol abuse prior to, or at the time of, hemorrhagic shock. The decreased hemodynamic counterregulatory response leads to decreased tissue perfusion, accentuated oxidative stress, and enhanced tissue injury. In addition, the alcohol/hemorrhaged host shows greater susceptibility to secondary infections leading to increased morbidity and mortality during the post-injury period.

Figure 3

Salient cardiovascular, pulmonary, and central nervous system pathophysiological consequences of alcohol abuse prior to, or at the time of, traumatic brain injury (TBI). The disruption in hemodynamic homeostasis resulting from TBI contributes to decreased cerebral perfusion pressure. The lung is affected through neurogenic mechanisms leading to neuropulmonary edema (NPE) and associated risk for acute lung injury (ALI) and adult respiratory distress syndrome (ARDS). In the brain (CNS), alcohol accentuates neuroinflammation, which is associated with neurobehavioral dysfunction that can potentially promote alcohol drinking. Together, these pathophysiological consequences increase morbidity and mortality from TBI.