J Trauma
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Adult respiratory distress syndrome (ARDS) in trauma victims carries a mortality on the order of 50%. An early feature is an increased capillary permeability causing an extravasation of plasma proteins and water, leading to interstitial edema. In the kidney, the increase in microvascular permeability is manifested as increased albumin excretion detectable by sensitive immunoassay. ⋯ These data indicate that the capillary leak associated with the subsequent development of pulmonary dysfunction and ARDS can be detected within 8 hours of admission at the patient's bedside, thus providing a means of early identification of patients at greatest risk and allowing for early intervention.
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The development of trauma systems and trauma centers has had a major impact on the fate of the critically injured patient. However, some have suggested that care may be compromised if too many trauma centers are designated for a given area. As of 1987, the state of Missouri had designated six adult trauma centers, two Level I and four Level II, for the metropolitan Kansas City, Mo, area, serving a population of approximately 1 million people. To determine whether care was comparable between the Level I and II centers, we conducted a concurrent evaluation of the fate of patients with a sentinel injury, hepatic trauma, over a 6-year period (1987-1992) who were treated at these six trauma centers. ⋯ In a metropolitan trauma system, when Level I and II centers were compared for their ability to care for victims of hepatic trauma, there was no discernible difference in care rendered with respect to severity of injury, mortality, delays to the OR, or hospital length of stay. It was observed that more severe liver injuries were seen at Level I centers, but this did not seem to significantly affect care at Level II centers. There was a longer ICU stay observed at Level II centers owing to penetrating injuries, possibly because there were fewer penetrating injuries treated at these facilities. Although the bulk of patients were seen at Level I centers, care throughout the system was equivalent.
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Evaluating blunt abdominal trauma remains a resource intensive aspect of trauma care. Recently, emergency department ultrasound has been promulgated as a noninvasive diagnostic alternative. Consequently, we hypothesized that an ultrasound based key clinical pathway (KCP) would reduce the number of diagnostic peritoneal lavage (DPL) and computed tomographic (CT) scans required to evaluate blunt abdominal trauma without increased risk to the patient. ⋯ An ultrasound based KCP resulted in significant reductions in the use of invasive DPL and costly CT scanning in the evaluation of blunt abdominal trauma without risk to the patient.
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We have previously demonstrated a significant improvement in trauma patient outcome after the Advanced Trauma Life Support (ATLS) program in Trinidad and Tobago. In January of 1992, a Prehospital Trauma Life Support (PHTLS) program was also instituted. This study assessed trauma patient outcome after the PHTLS program. ⋯ Post-PHTLS mortality and morbidity were significantly decreased, suggesting a positive impact of the PHTLS program on trauma patient outcome.
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Intracerebral cytokine production is thought to be partially responsible for the brain edema and increased leukocyte adhesion seen after head injury by both a direct effect on vascular permeability and by causing leukocyte activation. Cerebrospinal fluid concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 are elevated after traumatic brain injury. The cerebral endothelium has not been investigated as a de novo source of cytokines after injury. ⋯ HCME subjected to percussion injury secreted significantly more TNF-alpha at 8 and 24 hours and significantly more IL-1beta at 4 and 24 hours compared with uninjured controls (p < 0.05, Student's t test). These data suggest that HCME production of inflammatory cytokines occurs after traumatic brain injury independent of systemic influences. In situ cytokine production by HCME after percussion trauma may mediate the increased cerebral leukocyte accumulation and cerebrovascular dysfunction observed after focal brain injury.