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BACKGROUND: Recovery of walking independence in critically ill patients is required for safe discharge home. However, the pre-admission predictors affecting this outcome in this patient group are unknown. This study aimed to identify these predictors. METHODS: We included subjects who required mechanical ventilation for at least 48 h and could walk before admission. We investigated frailty, cognitive impairment, and malnutrition risk according to the pre-admission health status. Walking independence was defined as the ability to walk for at least 45 m on level ground. The primary outcome was the association between the time to event from an ICU discharge to walking independence, and pre-admission predictors were analyzed using a Fine-Gray proportional hazards regression. RESULTS: The rate of walking independence was 38.0 (100 cases/person-month; sample N = 144). In the proportional hazards regression model, adjusted for covariates, frailty (hazard ratio [HR] 0.08 [95% CI 0.01-0.67]), pre-frailty (HR 0.37 [95% CI 0.14-0.99]), cognitive impairment (HR 0.21 [95% CI 0.05-0.90]), and malnutrition risk (HR 0.20 [95% CI 0.07-0.58]) were associated with walking independence. CONCLUSIONS: Pre-admission frailty or pre-frailty, cognitive impairment, and malnutrition risk can help predict walking independence in critically ill patients who require mechanical ventilation.
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Aim: In-hospital cardiac arrest is an important issue in health care today. Data regarding in-hospital cardiac arrest in Japan is limited. In Australia and the USA, the Rapid Response System has been implemented in many institutions and data regarding in-hospital cardiac arrest are collected to evaluate the efficacy of the Rapid Response System. This is a multicenter retrospective survey of in-hospital cardiac arrest, providing data before implementing a Rapid Response System. Methods: Ten institutions planning to introduce a Rapid Response System were recruited to collect in-hospital cardiac arrest data. The Institutional Review Board at each participating institution approved this study. Data for patients admitted at each institution from April 1, 2011 until March 31, 2012 were extracted using the three keywords "closed-chest compression", "epinephrine", and "defibrillation". Patients under 18 years old, or who suffered cardiac arrest in the emergency room or the intensive care unit were excluded. Results: A total of 228 patients in 10 institutions were identified. The average age was 73 ± 13 years. Males represented 64% of the patients (82/146). Overall survival after in-hospital cardiac arrest was 7% (16/228). Possibly preventable cardiac arrests represented 15% (33/228) of patients, with medical safety issues identified in 8% (19/228). Vital sign abnormalities before cardiac arrest were observed in 63% (138/216) of patients. Conclusions: Approximately 60% of patients had abnormal vital signs before cardiac arrest. These patients may have an improved clinical outcome by implementing a Rapid Response System.
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The effects of hepatocyte growth factor (HGF) on barrier functions were investigated by a blood-brain barrier (BBB) in vitro model comprising a primary culture of rat brain capillary endothelial cells (RBEC). In order to examine the response of the peripheral endothelial cells to HGF, human umbilical vascular endothelial cells (HUVEC) and human dermal microvascular endothelial cells (HMVEC) were also treated with HGF. HGF decreased the permeability of RBEC to sodium fluorescein and Evans blue albumin, and dose-dependently increased transendothelial electrical resistance (TEER) in RBEC. HGF altered the immunochemical staining pattern of F-actin bands and made ZO-1 staining more distinct on the linear cell borders in RBEC. In contrast, HGF increased sodium fluorescein and Evans blue albumin permeability in HMVEC and HUVEC, and decreased TEER in HMVEC. In HMVEC, HGF reduced cortical actin bands and increased stress fiber density, and increased the zipper-like appearance of ZO-1 staining. Western blot analysis showed that HGF significantly increased the amount of ZO-1 and VE-cadherin. HGF seems to act on the BBB to strengthen BBB integrity. These findings indicated that cytoskeletal rearrangement and cell-cell adhesion, such as through VE-cadherin and ZO-1, are candidate mechanisms for the influence of HGF on the BBB. The possibility that HGF has therapeutic significance in protecting the BBB from damage needs to be considered.