To determine whether ketamine use for tracheal intubation, compared to other sedative use, is associated with a lower risk of post-intubation hypotension in hemodynamically-unstable patients in the emergency department (ED), we analyzed the data of a prospective, multicenter, observational study—the second Japanese Emergency Airway Network (JEAN-2) Study—from February 2012 through November 2017. The current analysis included adult non-cardiac-arrest ED patients with a pre-intubation shock index of ≥0.9. The primary exposure was ketamine use as a sedative for intubation, with midazolam or propofol use as the reference. The primary outcome was post-intubation hypotension. A total of 977 patients was included in the current analysis. Overall, 24% of patients developed post-intubation hypotension. The ketamine group had a lower risk of post-intubation hypotension compared to the reference group (15% vs 29%, unadjusted odds ratio [OR] 0.45 [95% CI 0.31–0.66] p < 0.001). This association remained significant in the multivariable analysis (adjusted OR 0.43 [95% CI 0.28–0.64] p < 0.001). Likewise, in the propensity-score matching analysis, the patients with ketamine use also had a significantly lower risk of post-intubation hypotension (OR 0.47 [95% CI, 0.31–0.71] P < 0.001). Our observations support ketamine use as a safe sedative agent for intubation in hemodynamically-unstable patients in the ED.

ObjectiveTo prevent misjudgment of the severity of patients in the emergency department who initially seem non-severe but are in a critical state, methods that differ from the conventional viewpoint are needed. We aimed to determine whether vital sign changes between prehospital and in-hospital could predict in-hospital mortality among non-trauma patients.MethodsThis observational cohort study was conducted in two tertiary care hospitals. Patients were included if they were transported by ambulance for non-trauma-related conditions but were excluded if they experienced prehospital cardiopulmonary arrest, were pregnant, were aged <15 years, had undergone inter-hospital transfer, or had complete missing data regarding prehospital or in-hospital vital signs. The main outcome was in-hospital mortality, and the study variables were changes in vital signs, pulse pressure, and/or shock index between the prehospital and in-hospital assessments. Logistic regression analyses were performed to obtain adjusted odds ratios for each variable. Receiver operating characteristic curve analyses were performed to identify cut-off values that produced a positive likelihood ratio of ≥2.ResultsAmong the 2,586 eligible patients, 170 died in the two hospitals. Significantly elevated risks of in-hospital mortality were associated with changes in the Glasgow Coma Scale (cut-off ≤–3), respiratory rate (no clinically significant cut-off), systolic blood pressure (cut-off ≥47 mmHg), pulse pressure (cut-off ≥55 mmHg), and shock index (cut-off ≥0.3).ConclusionsNon-trauma patients who exhibit changes in some vital signs between prehospital and in-hospital have an increased risk of in-hospital mortality. Therefore, it is useful to incorporate these changes in vital signs to improve triaging and predict the occurrence of in-hospital mortality.

Background Although the shock index is known to predict mortality and other severe outcomes, deriving it requires complex calculations. Subtracting the systolic blood pressure from the heart rate may produce a simple shock index that would be a clinically useful substitute for the shock index. In this study, we investigated whether the simple shock index was equivalent to the shock index. Methods This observational cohort study was conducted at 2 tertiary care hospitals. Patients who were transported by ambulance were recruited for this study and were excluded if they were aged < 15 years, had experienced prehospital cardiopulmonary arrest, or had undergone inter-hospital transfer. Pearson’s product-moment correlation coefficient and regression equation were calculated, and two one-sided tests were performed to examine their equivalency. Results Among 5429 eligible patients, the correlation coefficient between the shock index and simple shock index was extremely high (0.917, 95% confidence interval 0.912 to 0.921, P < .001). The regression equation was estimated as sSI = 258.55 log SI. The two one-sided tests revealed a very strong equivalency between the shock index and the index estimated by the above equation using the simple shock index (mean difference was 0.004, 90% confidence interval 0.003 to 0.005). Conclusion The simple shock index strongly correlated with the shock index.

Background: Although the shock index is known to predict mortality and other severe outcomes, deriving it requires complex calculations. Subtracting the systolic blood pressure from the heart rate may produce a simple shock index that would be a clinically useful substitute for the shock index. In this study, we investigated whether the simple shock index was equivalent to the shock index.Methods: This observational cohort study was conducted at 2 tertiary care hospitals. Patients who were transported by ambulance were recruited for this study and were excluded if they were aged <15 years, had experienced prehospital cardiopulmonary arrest, or had undergone inter-hospital transfer. Pearson’s product-moment correlation coefficient and regression equation were calculated, and two one-sided tests were performed to examine their equivalency. Results: Among 5,429 eligible patients, the correlation coefficient between the shock index and simple shock index was extremely high (0.917, 95% confidence interval 0.912 to 0.921, P <.001). The regression equation was estimated as sSI = 258.55 log SI. The two one-sided tests revealed a very strong equivalency between the shock index and the index estimated by the above equation using the simple shock index (mean difference was 0.004, 90% confidence interval 0.003 to 0.005). Conclusion: The simple shock index strongly correlated with the shock index.

Myxoid liposarcoma (MLS) is thought to occur due to defective adipocytic differentiation in mesenchymal stem cells. A promising strategy for MLS treatment is the prevention of sarcomagenesis by promoting the terminal differentiation of MLS cells into adipocytes. Previous studies have reported that the suppression of megakaryoblastic leukemia 1 (MKL1) expression induces adipocytic differentiation in preadipocyte cell lines. The present study aimed to investigate the effects of MKL1 suppression on MLS cells. In the present study, MKL1 knockdown was demonstrated to promote the adipocytic differentiation of an MLS-derived cell line, designated 1955/91, under adipogenic conditions. This suggests that therapeutic targeting of the MKL1-associated molecular pathway has potential as a promising method of MLS treatment. However, the induction of adipogenesis by MKL knockdown was incomplete, and Oil Red O staining indicated that intracellular lipid droplets were only sporadically generated. Conversely, MKL1 knockdown reduced the growth of the MLS cells. As adipocytic differentiation in vitro requires cellular confluence, the decreased growth rate of the MLS cells following MKL1 knockdown could be attributed to the incomplete induction of adipogenesis. Translocated in liposarcoma-CCAAT/enhancer-binding protein homologous protein (TLS-CHOP) is an MLS-specific oncoprotein that is thought to play key roles in sarcomagenesis and the suppression of adipocytic differentiation. However, the results of western blotting analyses suggest that TLS-CHOP has limited effects on MKL1 expression in MLS cells and that MKL1 knockdown hardly affects TLS-CHOP expression. Thus, it is postulated that the inhibitory effect of TLS-CHOP on adipogenesis is not associated with MKL1 expression. However, MKL1 and the molecular pathway involving MKL1 appear to be attractive targets for the differentiation therapy of MLS.