The implementation of an early rehabilitation program is associated with reduced length of stay: A multi-ICU study.

INTRODUCTION: Survivors of critical illness face many potential long-term sequelae. Prior studies showed that early rehabilitation in the intensive care unit (ICU) reduces physical impairment and decreases ICU and hospital length of stay (LOS). However, these studies are based on a single ICU or were conducted with a small subset of all ICU patients. We examined the effect of an early rehabilitation program concurrently implemented in multiple ICUs on ICU and hospital LOS. METHODS: An early rehabilitation program was systematically implemented in five ICUs at the sites of two affiliated academic institutions. We retrospectively compared ICU and hospital LOS in the year before (1/2011-12/2011) and after (1/2012-12/2012) implementation. RESULTS: In the pre- and post-implementation periods, respectively, there were a total of 3945 and 4200 ICU admissions among the five ICUs. After implementation, there was a significant increase in the proportion of patients who received more rehabilitation treatments during their ICU stay (p < 0.001). The mean number of rehabilitation treatments per ICU patient-day increased from 0.16 to 0.72 (p < 0.001). In the post-implementation period, four of the five ICUs had a statistically significant decrease in mean ICU LOS among all patients. The overall decrease in mean ICU LOS across all five ICUs was 0.4 days (6.9%) (5.8 versus 5.4 days, p < 0.001). Across all five ICUs, there were 255 (6.5%) more admissions in the post-implementation period. The mean hospital LOS for patients from the five ICUs also decreased by 5.4% (14.7 vs. 13.9 days, p < 0.001). CONCLUSIONS: A multi-ICU, coordinated implementation of an early rehabilitation program markedly increased rehabilitation treatments in the ICU and was associated with reduced ICU and hospital LOS as well as increased ICU admissions.

Effects of weight loss and leptin on skeletal muscle in human subjects.

Maintenance of a 10% or greater reduced body weight results in decreases in the energy cost of low levels of physical activity beyond those attributable to the altered body weight. These changes in nonresting energy expenditure are due mainly to increased skeletal muscle work efficiency following weight loss and are reversed by the administration of the adipocyte-derived hormone leptin. We have also shown previously that the maintenance of a reduced weight is accompanied by a decrease in ratio of glycolytic (phosphofructokinase) to oxidative (cytochrome c oxidase) activity in vastus lateralis muscle that would suggest an increase in the relative expression of the myosin heavy chain I (MHC I) isoform. We performed analyses of vastus lateralis muscle needle biopsy samples to determine whether maintenance of an altered body weight was associated with changes in skeletal muscle metabolic properties as well as mRNA expression of different isoforms of the MHC and sarcoplasmic endoplasmic reticular Ca(2+)-dependent ATPase (SERCA) in subjects studied before weight loss and then again after losing 10% of their initial weight and receiving twice daily injections of either placebo or replacement leptin in a single blind crossover design. We found that the maintenance of a reduced body weight was associated with significant increases in the relative gene expression of MHC I mRNA that was reversed by the administration of leptin as well as an increase in the expression of SERCA2 that was not significantly affected by leptin. Leptin administration also resulted in a significant increase in the expression of the less MHC IIx isoform compared with subjects receiving placebo. These findings are consistent with the leptin-reversible increase in skeletal muscle chemomechanical work efficiency and decrease in the ratio of glycolytic/oxidative enzyme activities observed in subjects following dietary weight loss.

Leptin administration does not prevent the bone mineral metabolism changes induced by weight loss.

The objective was to examine the effects of weight loss and leptin administration following weight loss on calciotropic hormones and bone turnover. This was a prospective, single-blinded study of 12 subjects (8 women, 4 men; 2 nonobese, 10 obese; age range, 19-46 years) who were studied on an inpatient basis while maintaining their usual weight [Wt(initial)] and during maintenance of 10% weight loss while receiving twice-daily injections of either a placebo [Wt(-10%P)] or replacement doses of leptin [Wt(-10%L)]. The main outcome measures were markers of bone formation (bone alkaline phosphatase and procollagen type 1 amino terminal propeptide) and resorption (N-telopeptide) as well as parathyroid hormone, calcium, and 25-hydroxy vitamin D measured from fasting morning serum. As expected, serum leptin declined with weight loss. Bone alkaline phosphatase decreased by 12.3% ± 3.9% between Wt(initial) and Wt(-10%P) and remained suppressed after leptin administration (both P < .01 compared with baseline). N-telopeptides increased by 37.2% ± 11.3% from Wt(initial) to Wt(-10%L) (P < .01). Procollagen type 1 amino terminal propeptide, parathyroid hormone, calcium, and 25-hydroxy vitamin D did not change. These results suggest that both decreased bone formation and increased bone resorption underlie bone loss associated with weight loss. Leptin administration did not prevent the uncoupling of bone remodeling that accompanies weight loss.