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BACKGROUND: Infection following severe injury is common and has a major impact on patient outcomes. The relationship between patient, injury, and physiologic characteristics with subsequent infections is not clearly defined. The objective of this study was to characterize the drivers and burden of all-cause infection in critical care trauma patients. METHODS: A prospective cohort study of severely injured adult patients admitted to critical care was conducted. Data were collected prospectively on patient and injury characteristics, baseline physiology, coagulation profiles, and blood product use. Patients were followed up daily for infectious episodes and other adverse outcomes while in the hospital. RESULTS: Three hundred patients (Injury Severity Score [ISS] >15) were recruited. In 48 hours or less, 29 patients (10%) died, leaving a cohort of 271. One hundred forty-one patients (52%) developed at least one infection. Three hundred four infections were diagnosed overall. Infection and noninfection groups were matched for age, sex, mechanism, and ISS. Infection rates were greater with any degree of admission shock and threefold higher in the most severely shocked cohort (p < 0.01). In multivariate analysis, base deficit (odds ratio [OR], 1.78, 95% confidence interval [CI], 1.48-1.94; p < 0.001) and lactate (OR, 1.36; 95% CI, 1.10-1.69; p = 0.05) were independently associated with the development of infection. Outcomes were significantly worse for the patients with infection. In multivariate logistic regression, infection was the only factor independently associated with multiple-organ failure (p < 0.001; OR, 15.4; 95% CI, 8.2-28.9; r = 0.402), ventilator-free days (p < 0.001; ß, -4.48; 95% CI, -6.7 to -2.1; r = 0.245), critical care length of stay (p < 0.001; ß, 13.2; 95% CI, 10.0-16.4; r = 0.466), and hospital length of stay (p < 0.001; ß, 31.1; 95% CI, 24.0-38.2; r = 0.492). CONCLUSION: Infectious complications are a burden for severely injured patients and occur early in the critical care stay. Severity of admission shock was predictive of infection and represents an opportunity for interventions to improve infectious outcomes. The incidence of infection may also have utility as an end point for clinical trials in trauma hemorrhage given the relationship with patient-experienced outcomes. LEVEL OF EVIDENCE: Prognostic/epidemiologic study, level II.

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UNLABELLED: Traumatic shock has been classified as a kind of hypovolemic shock similar to hemorrhagic shock. Since bacterial translocation has been observed in shock, this study investigated the difference in bacterial translocation during traumatic shock and hemorrhagic shock, and considered this effect on lung injury during sepsis. METHODS: Forty-eight male or female Sprague-Dawley rats were divided into 2 groups, hemorrhagic shock and traumatic shock. Bacterial translocation, endotoxin, and blood gas were evaluated. Alterations of the lungs morphologically and functionally were observed. RESULTS: Traumatic shock induced more bacterial translocation and endotoxemia from the gut. Blood gas analysis shows a more severe disorder in traumatic shock than in hemorrhagic shock. Pathological morphologic changes of lungs were more severe in traumatic shock than in hemorrhagic shock. CONCLUSIONS: Traumatic shock cause more bacterial translocation and endotoxemia which subsequently caused serial pathological alterations in lung morphologically and functionally than pure hemorrhagic shock does. These results suggest that this trauma activates more severe mechanism to damage lungs.

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Burn injury induces bacterial translocation (BT) from the gut in multiple animal models. Etiologic factors contributing to BT may be an ischemia-reperfusion injury to the gut, the release of inflammatory cytokines, oxygen metabolites and other mediators, and cytotoxic effects mediated by endotoxin (lipopolysaccharide). Bactericidal, permeability-increasing protein is a neutrophil granule protein with potent bactericidal and lipopolysaccharide-neutralizing activities. The use of this protein has not been previously reported in a burn-injury model. The purpose of this study was to determine whether recombinant bactericidal, permeability-increasing protein (rBPI23) affects the incidence of BT and myeloperoxidase content in lung tissue (a measure of leukocyte sequestration) in a burn-injury model. Mice received a 32% total body surface area, full-thickness, scald burn, and 10 mg/kg body weight rBPI23 in saline solution was given by intraperitoneal injection at 0, 3, and 6 hours after the burn. Control animals received intraperitoneal saline solution only. All animals received a total of 1 ml saline solution intraperitoneally immediately after burn injury for fluid resuscitation. At 24 hours after burn injury, mesenteric lymph nodes (MLN) were harvested, homogenized, and plated. Lung tissue was harvested and assayed for myeloperoxidase. Burned mice treated with rBPI23 had significantly (p = 0.005, Fisher's Exact Test, two-tailed) decreased incidence of BT, compared to burned mouse controls. Leukosequestration into lung tissues was not affected by rBPI23. Postburn administration of rBPI23 reduces but does not abolish the incidence of BT after burn injury in mice, perhaps by reducing intestinal injury during burn shock and the ischemia-reperfusion period by inhibiting the effects of lipopolysaccharide. An alternate explanation may be that rBPI23 could increase clearance and killing of bacteria by host defenses.

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Previous investigations of a treated model of hemorrhagic shock in the rat indicated the frequent occurrence of bacteremia that appeared to derive from the gut. This paper determines the incidence of bacteremia and endotoxemia during the acute shock period and compares this with similar observations in humans in varying degrees of shock. Studies in 26 rats indicated that bacteremia and endotoxemia was present in 50% and 87%, respectively, by the end of 2 hours at a mean arterial pressure of 30 mmHg. Observations in 50 patients admitted to the trauma unit showed that positive bacterial blood cultures were present in 56% when the admission systolic blood pressure was 80 mmHg or less (p less than 0.01 compared with either of the other groups). Endotoxemia was noticed in two such patients. Direct access of bacteria and endotoxin to the blood stream may occur during hemorrhagic or traumatic shock and is the probable cause of subsequent sepsis in traumatized patients when no other source is apparent.

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A mouse burn model was established to test the effect of nonlethal thermal injury on the translocation of indigenous bacteria from the gastrointestinal (GI) tract to other organs. Specific pathogen-free (SPF) mice were given 15% or 30% total body surface area burns, and the mesenteric lymph nodes (MLNs), spleens, livers, blood, and peritoneal cavities were cultured for translocated bacteria at various time intervals. No viable aerobic, facultatively anaerobic, or strictly anaerobic bacteria of the indigenous flora grew in cultures from the MLNs of these mice. Consequently, SPF mice were antibiotic decontaminated and then colonized with Escherichia coli to develop a model in which E coli maintains abnormally high cecal population levels and translocates continuously to the MLN. These mice received 15% or 30% thermal burns four days after colonization with E coli. The incidence of bacterial translocation and the numbers of E coli translocating to the MLN, spleen, liver, blood, and peritoneal cavity increased with increasing burn area compared with controls. Mice receiving 15% burns could not clear intravenously challenged E coli from their bloodstream, MLN, or liver. Thus, burn stress promotes the translocation of bacteria from the GI tract to other organs to cause bacteremia.

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