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BACKGROUND: The objective of our study is to compare the predicted hospital admission disposition based on the level of risk as determined by the modified Trauma-Specific Frailty Index (mTSFI) score with those determined by arbitrary decisions made based on the Emergency Severity Index (ESI) severity level. METHODS: We surveyed 100 trauma patients ages 50 and older, admitted to a level 1 trauma center between April 2019 and July 2019. We retrospectively reviewed the hospital admission disposition of each patient under the ESI, which was then compared to the mTSFI-predicted hospital admission disposition. The mTSFI scores were calculated by surveying each patient. Statistical analysis was performed to identify any statistical significance of concordance and discordance when comparing the mTSFI and ESI. RESULTS: The average age was 57.6 ± 4.2 years old in the non-geriatric group vs 76.3 ± 7.3 years old in the geriatric group. There was a male predominance in both groups (61% vs 69.5%). The mTSFI identified a higher percentage of triage discordance in the non-geriatric group (73%) compared to the geriatric cohort (53%) (95% difference CI, [39.6-40], P = .05). DISCUSSION: Non-geriatric patients have higher recorded rate of frailty than previously recognized and screening should begin at age 50, not 65. The mTSFI may be an effective tool to appropriately triage adult trauma patients at increased risk due to frailty and may reduce in-hospital complications.

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Hemorrhagic shock-induced ischemia-reperfusion injury is characterized by an increase in microvascular permeability. This increase in permeability is thought to occur mainly via passive transport through interendothelial cell junctions. However, recent data have suggested that a transcellular (caveolae) transport mechanism(s) may also play a role after shock. The purpose of our study was to investigate the role of caveolae transport after hemorrhagic shock. After a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mmHg for 1 h in urethane-anesthetized Sprague-Dawley rats. Mesenteric postcapillary venules in a transilluminated segment of small intestine were examined to determine changes in permeability. Rats received an intravenous injection of fluorescein isothiocyanate-bovine albumin during the control period. The fluorescent light intensity emitted from the fluorescein isothiocyanate-bovine albumin was recorded with digital microscopy within the lumen of the microvasculature and was compared with the intensity of light in the extravascular space. The images were downloaded to a computerized image analysis program that quantitates changes in light intensity. This change in light intensity represents albumin extravasation. Our results demonstrated a marked increase in albumin leak after hemorrhagic shock that was significantly attenuated with two different inhibitors of transcellular transport, N-ethylmaleimide and methyl-beta-cyclodextrin. These data suggest that caveolae transport plays a significant role in microvascular permeability after hemorrhagic shock.

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BACKGROUND: Hypothermia is a frequent manifestation after trauma-induced hemorrhagic shock. Clinical studies have suggested that hypothermia is an independent risk variable predisposing patients to an increase in morbidity. Thus, most of the current goal-directed resuscitation protocols are aimed at the establishment of euthermia. However, recent data suggest that hypothermia may provide protection by attenuating the inflammatory response after hemorrhagic shock. The purpose of this study was twofold: to examine the effects of mild to moderate hypothermia on barrier function after hemorrhagic shock, and to determine the role of reactive oxygen species (ROS) in this process. METHODS: After a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mm Hg for 1 hour in urethane-anesthetized rats. Mesenteric postcapillary venules in a transilluminated segment of small intestine were examined to quantitate changes in permeability and ROS expression. Sprague-Dawley rats received an intravenous injection of fluorescein isothiocyanate (FITC)-albumin during the control period. The fluorescent light intensity emitted from the FITC-albumin was recorded with digital microscopy within the lumen of the microvasculature and compared with the intensity of light in the extravascular space. The images were downloaded to a computerized image analysis program that quantitates changes in light intensity. This change in light intensity represents albumin-FITC extravasation. RESULTS: Our results demonstrated a marked increase in albumin leakage after hemorrhagic shock that was significantly attenuated with mild (34 degrees C) and moderate (30 degrees C) hypothermia. In addition, hypothermia attenuated ROS expression after hemorrhagic shock. CONCLUSION: These data suggest that hypothermia may protect barrier integrity after hemorrhagic shock by inhibition of oxygen radical expression.

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BACKGROUND: Hemorrhagic shock-related leukocyte adherence to endothelial cells is a key step in microvascular injury-related organ damage. Heme-oxygenase-1 (HO-1) metabolizes heme, a potent cytotoxic agent, to carbon monoxide and biliverdin. We hypothesized that changing HO-1 expression would change leukocyte adherence after hemorrhagic shock. METHODS: Rats were administered hemin, zinc protoporphyrin, or vehicle 6 hours before surgery. HO-1 expression was determined by reverse-transcriptase polymerase chain reaction in various tissues. Shock was induced in urethane-anesthetized animals by decreasing mean arterial blood pressure to 40 mm Hg for 60 minutes, followed by standard resuscitation measures. Leukocyte adherence was measured by intravital microscopy in rat mesenteric venules. RESULTS: Hemin, hemorrhagic shock, and the combination resulted in significantly increased HO-1 expression, whereas zinc-protoporphyrin (ZNPP) resulted in significantly decreased leukocyte adherence. After hemorrhagic shock and hemin administration, leukocyte adherence was significantly decreased 60 minutes into resuscitation (7.92 +/- 2.29 vs. 4.84 +/- 0.71 cells/100 microm, p < 0.05) and significantly increased after ZNPP plus shock (14.08 +/- 3.95, p

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Acute respiratory distress syndrome is a manifestation of acute injury to the lung, commonly resulting from sepsis, trauma, and severe pulmonary infections. Clinically, it is characterized by dyspnea, profound hypoxemia, decreased lung compliance, and diffuse bilateral infiltrates on chest radiography. Provision of supplemental oxygen, lung rest, and supportive care are the fundamentals of therapy. The management of acute respiratory distress syndrome frequently requires endotracheal intubation and mechanical ventilation. A low tidal volume and low plateau pressure ventilator strategy is recommended to avoid ventilator-induced injury. Timely correction of the inciting clinical condition is essential for preventing further injury. Various medications directed at key stages of the pathophysiology have not been as clinically efficacious as the preceding experimental trials indicated. Complications such as pneumothorax, effusions, and focal pneumonia should be identified and promptly treated. In refractory cases, advanced ventilator and novel techniques should be considered, preferably in the setting of clinical trials. During the past decade, mortality has declined from more than 50 percent to about 32 to 45 percent. Death usually results from multisystem organ failure rather than respiratory failure alone.

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The generation of oxygen radicals during leukocyte-endothelial cell interaction is considered to represent one of the fundamental steps of microvascular injury following ischemia and reperfusion. Indirect evidence also suggests that this relationship may be important following hemorrhagic shock. The purpose of this study was to characterize the temporal changes of reactive oxygen species (ROS) in the mesenteric microvascular endothelium, in vivo, as a consequence of hemorrhagic shock and reperfusion, and to correlate this ROS production to leukocyte adherence. Following a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mmHg for 1 h in urethane-anesthetized rats. Mesenteric venules in a transilluminated segment of small intestine were examined to quantitate changes in ROS generation and leukocyte adherence. Sprague-Dawley rats were injected with dihydrorhodamine 123, a hydroperoxide-sensitive fluorescent probe that is trapped within viable cells as a nonfluorescent form and then converted to the mitochondrion-selective form rhodamine 123 by hydroperoxides. The fluorescent light emission from rhodamine 123 was recorded with digital microscopy and downloaded to a computerized image analysis program. Our results demonstrated an 80% increase in ROS generation beginning within 5 min into resuscitation and a 10-fold increase in leukocyte adherence that occurred at 10 min after resuscitation. Both ROS generation and leukocyte adherence were attenuated with pre-shock administration of platelet activating factor (PAF) antagonist, WEB 2086, and the CD11/CD18a antibody, anti-LFA-1beta. Our findings suggest that ROS production in endothelial cells is increased during reperfusion following hemorrhagic shock and that the mechanism of expression is mediated in part by both PAF expression and subsequent leukocyte adherence.

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