Person:

Schmidt, Ulrich

Introduction: Immobilisation in the intensive care unit (ICU) leads to muscle weakness and is associated with increased costs and long-term functional disability. Previous studies showed early mobilisation of medical ICU patients improves clinical outcomes. The Surgical ICU Optimal Mobilisation Score (SOMS) trial aims to test whether a budget-neutral intervention to facilitate goal-directed early mobilisation in the surgical ICU improves participant mobilisation and associated clinical outcomes. Methods and analysis The SOMS trial is an international, multicentre, randomised clinical study being conducted in the USA and Europe. We are targeting 200 patients. The primary outcome is average daily SOMS level and key secondary outcomes are ICU length of stay until discharge readiness and ‘mini’ modified Functional Independence Measure (mmFIM) at hospital discharge. Additional secondary outcomes include quality of life assessed at 3 months after hospital discharge and global muscle strength at ICU discharge. Exploratory outcomes will include: ventilator-free days, ICU and hospital length of stay and 3-month mortality. We will explore genetic influences on the effectiveness of early mobilisation and centre-specific effects of early mobilisation on outcomes. Ethics and dissemination Following Institutional Review Board (IRB) approval in three institutions, we started study recruitment and plan to expand to additional centres in Germany and Italy. Safety monitoring will be the domain of the Data and Safety Monitoring Board (DSMB). The SOMS trial will also explore the feasibility of a transcontinental study on early mobilisation in the surgical ICU. Results: The results of this study, along with those of ancillary studies, will be made available in the form of manuscripts and presentations at national and international meetings. Registration This study has been registered at clinicaltrials.gov (NCT01363102).

Introduction: A paucity of literature exists regarding delays in transfer out of the intensive care unit. We sought to analyze the incidence, causes, and costs of delayed transfer from a surgical intensive care unit (SICU). Methods: An IRB-approved prospective observational study was conducted from January 24, 2010, to July 31, 2010, of all 731 patients transferred from a 20-bed SICU at a large tertiary-care academic medical center. Data were collected on patients who were medically ready for transfer to the floor who remained in the SICU for at least 1 extra day. Reasons for delay were examined, and extra costs associated were estimated. Results: Transfer to the floor was delayed in 22% (n = 160) of the 731 patients transferred from the SICU. Delays ranged from 1 to 6 days (mean, 1.5 days; median, 2 days). The extra costs associated with delays were estimated to be $581,790 during the study period, or $21,547 per week. The most common reasons for delay in transfer were lack of available surgical-floor bed (71% (114 of 160)), lack of room appropriate for infectious contact precautions (18% (28 of 160)), change of primary service (Surgery to Medicine) (7% (11 of 160)), and lack of available patient attendant ("sitter" for mildly delirious patients) (3% (five of 160)). A positive association was found between the daily hospital census and the daily number of SICU beds occupied by patients delayed in transfer (Spearman rho = 0.27; P < 0.0001). Conclusions: Delay in transfer from the SICU is common and costly. The most common reason for delay is insufficient availability of surgical-floor beds. Delay in transfer is associated with high hospital census. Further study of this problem is necessary.

MyD88 is an adaptor protein critical for innate immune response against microbial infection and in certain noninfectious tissue injury. The present study examined the role of MyD88 in myocardial inflammation and injury after ischemia-reperfusion (I/R). I/R was produced by coronary artery ligation for 30 min followed by reperfusion. The ratios of area at risk to left ventricle (LV) were similar between wild-type (WT) and MyD88-deficient (MyD88−/−) mice. However, 24 h after I/R, the ratios of myocardial infarction to area at risk were 58% less in MyD88−/− than in WT mice (14 ± 2% vs. 33 ± 6%, P = 0.01). Serial echocardiographic studies demonstrated that there was no difference in baseline LV contractile function between the two groups. Twenty-four hours after I/R, LV ejection fraction (EF) and fractional shortening (FS) in WT mice were reduced by 44% and 62% (EF, 51 ± 2%, and FS, 22 ± 1%, P < 0.001), respectively, and remained depressed on the seventh day after I/R. In comparison, EF and FS in MyD88−/− mice were 67 ± 3% and 33 ± 2%, respectively, after I/R (P < 0.001 vs. WT). Similarly, LV function, as demonstrated by invasive hemodynamic measurements, was better preserved in MyD88−/− compared with WT mice after I/R. Furthermore, when compared with WT mice, MyD88−/− mice subjected to I/R had a marked decrease in myocardial inflammation as demonstrated by attenuated neutrophil recruitment and decreased expression of the proinflammatory mediators keratinocyte chemoattractant, monocyte chemoattractant protein-1, and ICAM-1. Taken together, these data suggest that MyD88 modulates myocardial inflammatory injury and contributes to myocardial infarction and LV dysfunction during I/R.