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Death after traumatic injury has classically been described in terms of a trimodal distribution. Immediate and acute (<24 hours) deaths usually result from uncontrolled hemorrhage, but infections and multiple organ dysfunction syndrome, which often arise from infection, are responsible for a significant proportion of late deaths. Indeed, infection is responsible for most deaths in patients who survive longer than 48 hours after trauma.1 Trauma-related infections can be divided into those that result directly from the injury (eg, due to contamination that occurs in conjunction with the traumatic injury) and nosocomial infections that arise in the health care setting in conjunction with treatment of the injury. The pathogens involved can be exogenous or endogenous bacteria, depending on the mechanism of injury and/or the iatrogenic cause.

Most post-traumatic infections are polymicrobial, involving a mixture of aerobic and anaerobic organisms.2 In one series, 37–45% of all trauma patients experienced infectious complications during their initial hospitalization.3 In that same study, 80% of trauma patients who were in the intensive care unit (ICU) at least 7 days met the criteria for the systemic inflammatory response syndrome (SIRS). All caregivers need to understand the principles of surgical infections in the context of trauma patients. This chapter will review the following: factors that normally prevent infection, how trauma disrupts or overwhelms normal host defenses, recognition and treatment of the most common infectious complications after traumatic injury, principles of infection prevention, and how prophylaxis and prevention principles can be applied chronologically during the treatment of trauma patients.


Humans have evolved mechanisms to avoid infection despite the ubiquitous presence of bacteria in our environment and throughout our bodies. A recent review documented the magnitude and diversity of the human microbiota.4 Under normal circumstances there is a balance between our microbiota, intact environmental barriers, and host defenses (Fig. 18-1). Invasive surgical procedures or traumatic injury disrupts this balance and significantly increases the probability of developing an infection (Fig. 18-2). Microbes are abundant on the surface of the skin, within the oral cavity, and increase in numbers down the length of the gastrointestinal tract. Bacterial numbers differ at various locations, and the pathogenic species and their respective numbers at different anatomic sites are summarized in Table 18-1. Once inoculation of bacteria into normally sterile sites occurs, infection will ensue if bacteria proliferate faster than the host defense mechanisms eradicate them. Trauma generally results in a much greater disruption of normal barriers than occurs with elective surgery. Trauma may also have concomitant hypoperfusion (shock), devitalized tissue, and retained foreign bodies.


Under normal circumstances the determinants of infection, microbial factors, environmental factors, and host defenses interact such that there is no infection. (Adapted with permission from Meakins JL, et al. Host defenses. In: Howard RJ, Simmons RL, eds. Surgical Infectious Diseases. 2nd ed. Norwalk, CT: Appleton ...

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