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The author acknowledges substantial use of material from this chapter in the previous edition.
Trauma is a major cause of pediatric morbidity and mortality, and a significant contributor to this disease burden is secondary infection. The etiologies of trauma-related infection tend to be bacterial, introduced into an injury either from sources already present in the host (e.g., the skin, or sinuses in a basilar skull fracture) or from the environment at the time of injury (e.g., Pseudomonas from a shoe introduced via a puncture injury). Trauma also can increase risk of a more remote infection, as occurs following traumatic splenectomy. Management and prevention of trauma-related infection requires knowledge of the types of injury for which prophylactic antimicrobial treatment is indicated, understanding of the likely pathogens to guide empiric antibiotic selection when infection occurs, and recognition of clinical scenarios in which vaccination or immunotherapy may be beneficial.
Unintentional injury is the leading cause of death among children <19 years, and accounts for approximately 9 million emergency department visits and 225,000 hospitalizations per year in the US. Infection that follows trauma may be due to the injury itself or usually a consequence of healthcare procedures and prolonged hospitalization that follow.
Among 523 pediatric patients admitted with trauma to an urban hospital in Florida, 78 (10.1%) incurred a secondary infection. The majority were nosocomially acquired bacterial infections that frequently were associated with indwelling medical devices and catheters, but 19% of infected patients had infection at the site of trauma including wound, intra-abdominal and intracranial infections. Infection was more common among patients with more severe or extensive injuries.
Severe injuries increase the susceptibility of a child to infection for several reasons. Breaks in the skin and mucosal barriers allow pathogens to gain entry, and accumulation of blood provides a favorable environment for bacterial growth. Devitalized or necrotic tissue at the injury site can harbor pathogens that can evade the defense mechanisms of the host. Foreign bodies introduced by the injury itself or as a consequence of hospitalization (e.g., catheters) allow entry and persistence of pathogens. Risk factors for infection in patients hospitalized for trauma include the severity of the injury, the presence of shock, the number of organs injured, and the amount of blood lost. , The physical environment in which the injury occurred may result in introduction of unusual or more virulent pathogens, such as those found in soil or bodies of water.
Trauma can adversely affect host defense mechanisms. Dysregulated cytokine-mediated immune activation occurring after severe injury can lead to the systemic inflammatory response syndrome. Impaired innate immune responses and decreased TNF production correlate with risk of infection in injured children. Complement is activated by injured tissue, thus decreasing complement levels, and antibody production also diminishes after blunt trauma.
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