The Journal of surgical research
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Missing life-threatening injuries is a persistent concern in any trauma program. Autopsy is a tool routinely utilized to determine an otherwise occult cause of death in many fields of medicine. It has been adopted as a required component of the trauma peer review (PR) process by both the American College of Surgeons and the Pennsylvania Trauma Foundation. We hypothesized that autopsy would not identify preventable deaths for augmentation of the PR process. ⋯ Autopsy does not identify causes of preventable in an otherwise highly functioning trauma program and may be a poor use of institutional resources. In fact, it adds few diagnoses when death occurs after a full trauma assessment has had time to take place. Autopsy may be of use to identify protocol failure in maturing trauma programs, to give answers to grieving families and in select situations where death was unanticipated even after a full evaluation took place.
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Functional outcomes after traumatic brain injury (TBI) can be significantly improved by discharge to posthospitalization care facilities. Many variables influence the discharge disposition of the TBI patient, including insurance status, patient condition, and patient prognosis. The literature has demonstrated an ethnic disparity in posthospitalization care referral, with Hispanics being discharged to rehabilitation and nursing facilities less often than non-Hispanics. However, this relationship has not been studied in a Hispanic-majority population, and thus, this study seeks to determine if differences in neurorehabilitation referrals exist among ethnic groups in a predominately Hispanic region. ⋯ This study suggests that patients of different ethnicities but comparable traumatic severity and insurance status receive different discharge dispositions post-TBI even in regions in which Hispanics are the demographic majority.
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Posttraumatic coagulopathy and inflammation can exacerbate secondary cerebral damage after traumatic brain injury (TBI). Tranexamic acid (TXA) has been shown clinically to reduce mortality in hemorrhaging and head-injured trauma patients and has the potential to mitigate secondary brain injury with its reported antifibrinolytic and antiinflammatory properties. We hypothesized that TXA would improve posttraumatic coagulation and inflammation in a murine model of TBI alone and in a combined injury model of TBI and hemorrhage (TBI/H). ⋯ Despite clinical data suggesting a mortality benefit, TXA did not modulate coagulation, inflammation, or biomarker generation in either the TBI or TBI/H murine models. Administration of TXA after TBI altered splenic leukocyte populations, which may contribute to a change in posttraumatic immune status. Future studies should be done to investigate the role of TXA in the development of posttraumatic immunosuppression and risk of nosocomial infections.
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Improvements in patient safety are critical to improving clinical outcomes. We present a resident-led interdisciplinary morbidity and mortality (M&M) conference utilizing postconference task forces to identify unique system issues, classify key contributors to interdisciplinary complications, and implement systems solutions. The conference also served to facilitate resident involvement in quality improvement projects. ⋯ House staff-led interdisciplinary M&M conference utilizing postconference task forces is an ideal setting to identify unique system issues and implement system-based improvement strategies.
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The regulation of erythropoiesis involves hematopoietic progenitor cells, bone marrow stroma, and the microenvironment. Following severe injury, a hypercatecholamine state develops that is associated with increased mobilization of hematopoietic progenitor cells to peripheral blood and decreased growth of bone marrow erythroid progenitor cells that manifests clinically as a persistent injury-associated anemia. Changes within the bone marrow microenvironment influence the development of erythroid progenitor cells. Therefore, we sought to determine the effects of lung contusion, hemorrhagic shock, and chronic stress on the hematopoietic cytokine response. ⋯ The bone marrow microenvironment was significantly altered following severe trauma in a rodent model. Prohematopoietic cytokines were downregulated, and the proinflammatory cytokine HMGB-1 had increased bone marrow expression. Modulation of the bone marrow microenvironment may represent a therapeutic strategy following severe trauma to alleviate persistent injury-associated anemia.