A systematic approach to developing a global surgery elective.

BACKGROUND: Interest in global health has been increasing for years among American residents and medical students. Many residency programs have developed global health tracks or electives in response to this need. OBJECTIVES: Our goal was to create a global surgery elective based on a synergistic partnership between our institution and a hospital in the developing world. DESIGN: We created a business plan and 1-year schedule for researching potential sites and completing a pilot rotation at our selected hospital. SETTING: We administered a survey to general surgery residents at the University of Cincinnati and visited medical facilities in Sierra Leone, Cameroon, and Malawi. PARTICIPANTS: The survey was given to all general surgery residents. A resident and a faculty member executed the fact-finding trip as well as the pilot rotation. RESULTS: Our general surgery residents view an international elective as integral to residency training and would participate in such an elective. After investigating 6 hospitals in sub-Saharan Africa, we conducted a pilot rotation at our selected hospital and gained the necessary information to organize a curriculum. We will begin sending senior residents for 8-week rotations in the coming academic year. CONCLUSIONS: By systematically approaching the process of creating a global surgery elective, we were able to gain considerable insight into choosing a location and organizing the elective.

Prior thermal injury accelerates endotoxin-induced inflammatory cytokine production and intestinal nuclear factor-κB activation in mice.

The objective of this study was to increase the understanding of the "second-hit" response in thermal injury. The authors hypothesized that prior thermal injury increases the endotoxin-induced inflammatory response of intestinal mucosa. Mice underwent sham or 25% TBSA scald injury. Seven days after injury, mice were injected with lipopolysaccharide. Blood, jejunum, and colon specimens were obtained at intervals. Serum, jejunal, and colon inflammatory cytokine levels were measured by enzyme-linked immunosorbent assay. Jejunal and colon nuclear factor (NF)-κB activation was measured by electrophoretic mobility shift assay. After remote thermal injury, lipopolysaccharide exposure led to an acute increase in serum interleukin (IL)-6, IL-10, and chemokine keratinocyte-derived chemokine (KC) levels. This correlated with lipopolysaccharide-induced increased IL-6 in colon and chemokine KC in the jejunum and colon in burned mice when compared with sham-injured mice. Lipopolysaccharide-induced NF-κB activation occurred more rapidly in jejunum and colon from burned mice compared with sham-injured mice. Prior thermal injury accelerates lipopolysaccharide-induced inflammatory cytokine production systemically in jejunum and colon. The "second hit" of lipopolysaccharide led to earlier intestinal NF-κB activation in burned mice compared with sham-injured mice. These results indicate that there is a heightened inflammatory response by jejunum and colon in response to a "second hit" of lipopolysaccharide after burn injury.

Hypobaric hypoxia exacerbates the neuroinflammatory response to traumatic brain injury.

OBJECTIVE: To determine the inflammatory effects of time-dependent exposure to the hypobaric environment of simulated aeromedical evacuation following traumatic brain injury (TBI). METHODS: Mice were subjected to a blunt TBI or sham injury. Righting reflex response (RRR) time was assessed as an indicator of neurologic recovery. Three or 24 h (Early and Delayed groups, respectively) after TBI, mice were exposed to hypobaric flight conditions (Fly) or ground-level control (No Fly) for 5 h. Arterial blood gas samples were obtained from all groups during simulated flight. Serum and cortical brain samples were analyzed for inflammatory cytokines after flight. Neuron specific enolase (NSE) was measured as a serum biomarker of TBI severity. RESULTS: TBI resulted in prolonged RRR time compared with sham injury. After TBI alone, serum levels of interleukin-6 (IL-6) and keratinocyte-derived chemokine (KC) were increased by 6 h post-injury. Simulated flight significantly reduced arterial oxygen saturation levels in the Fly group. Post-injury altitude exposure increased cerebral levels of IL-6 and macrophage inflammatory protein-1α (MIP-1α), as well as serum NSE in the Early but not Delayed Flight group compared to ground-level controls. CONCLUSIONS: The hypobaric environment of aeromedical evacuation results in significant hypoxia. Early, but not delayed, exposure to a hypobaric environment following TBI increases the neuroinflammatory response to injury and the severity of secondary brain injury. Optimization of the post-injury time to fly using serum cytokine and biomarker levels may reduce the potential secondary cerebral injury induced by aeromedical evacuation.

Omission of routine chest x-ray after chest tube removal is safe in selected trauma patients.

BACKGROUND: Definitive practice guidelines regarding the utility of chest x-ray (CXR) following chest tube removal in trauma patients have not been established. The authors hypothesized that the selective use of CXR following chest tube removal is safe and cost effective. METHODS: A retrospective review of chest tube insertions performed at a level I trauma center was conducted. RESULTS: Patients who underwent chest tube removal without subsequent CXR had a lower mean Injury Severity Score and were less likely to have suffered penetrating thoracic injuries. These patients received fewer total CXRs and had shorter durations of chest tube therapy and shorter lengths of stay following tube removal. Subsequent reinterventions were performed more frequently in the CXR group. The annual decrease in hospital charges by foregoing a CXR was $16,280. CONCLUSIONS: The selective omission of CXR following chest tube removal in less severely injured, nonventilated patients does not adversely affect outcomes or increase reintervention rates. Avoiding unnecessary routine CXR after chest tube removal could provide a significant reduction in total hospital charges.

Remote thermal injury increases LPS-induced intestinal IL-6 production.

BACKGROUND: Patients suffering from burn injury are at high risk for subsequent infection. Thermal injury followed by endotoxemia may result in a "second hit," causing an exaggerated inflammatory response with increased morbidity and mortality. The role of the intestine in this "second hit" response is unknown. We hypothesized that remote thermal injury increases the inflammatory response of intestinal mucosa to subsequent treatment with lipopolysaccharide (LPS). METHODS: Mice underwent sham or scald injury. Seven days after injury, mice were treated with LPS. Blood and bowel specimens were obtained. Serum and intestinal inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA). Changes in TLR-4 pathway components in intestine were measured by reverse transcription-polymerase chain reaction (RT-PCR), Western blot, and electrophoretic mobility shift assay (EMSA). Intestinal leukocyte infiltration was analyzed by myeloperoxidase assay. RESULTS: A "second hit" of injected LPS resulted in increased IL-6 in intestine of burned mice compared with sham. Similarly, jejunal IL-6 mRNA levels increased in mice with prior thermal injury, suggesting a transcriptional mechanism. Of transcription factors known to drive IL-6 expression, only AP-1 activation was significantly elevated by a "second hit" of LPS. CONCLUSION: Prior thermal injury potentiates LPS-induced IL-6 cytokine production in intestine. These results indicate a heightened inflammatory response to a second hit by intestine after burn injury.