The Impact of Interdisciplinary Care on Cost Reduction in a Geriatric Trauma Population.

The current growth of the geriatric population and increased burden on trauma services throughout the United States (US) has created a need for systems that can improve patient care and reduce hospital costs. We hypothesize that the multidisciplinary services provided through the Geriatric Injury Institute (GII) can reduce hospital costs, improve patient triage throughput, and decrease hospital length of stay (LOS). METHODS AND MATERIAL: We performed a single-center, retrospective chart review of our Level II trauma center registry and electronic medical records of patients ages 65 and older who satisfied trauma activation/code criteria between July 1, 2014, to June 30, 2016 (N = 663). Patients presenting from July 1, 2014, to June 30, 2015, were grouped as Pre-GII, while those presenting from July 1, 2015, to June 30, 2016, were grouped as Post-GII. Primary outcomes were emergency department (ED) triage time, overall LOS, and hospital costs. Secondary outcomes included patient disposition, mortality, and health assessments. Statistical comparisons were made using a one-way analysis of variance and Mann-Whitney U test. RESULTS: Pre-GII vs. Post-GII average ages and the Injury Severity Score (ISS) were not statistically different (p>0.05). The average LOS was similar between the Pre-GII and Post-GII groups (4.64 ± 4.42 days vs. 4.26 ± 5.58 days, p = 0.48). More patients were discharged earlier (≤ 4 days; 64% vs. 73%) as well as discharged to home (37% vs. 45%) in the Post-GII group. The total cost savings were $53,000 with a median savings of $1061 per patient ($8808 vs. $7747, p = 0.04). Savings were highest during the first two days of admission (p = 0.03). The reduction in ED triage time was not significant (310.7 minutes vs 219. 8 minutes, p > 0.05). CONCLUSION: With the increase in geriatric trauma, innovative models of care are needed. Our study suggests that the GII multidisciplinary approach to trauma services can lower overall hospital costs.

Effects of dietary flaxseed on atherosclerotic plaque regression.

Dietary flaxseed can retard the progression of atherosclerotic plaques. However, it remains unclear whether these antiatherogenic effects extend to plaque regression. In the present study, the therapeutic potential of dietary flaxseed on atherosclerotic plaque regression and vascular contractile function was evaluated using a novel rabbit model. Rabbits were randomly assigned to receive either a regular diet for 12 wk (group I) or a 1% cholesterol-supplemented diet for 4 wk followed by a regular diet for 8 wk (group II). The remaining experimental animals were treated as in group II but were fed for an additional 14 wk with either a regular diet (group III) or a 10% flaxseed-supplemented diet (group IV). Animals in group II showed clear evidence of plaque growth stabilization. Their vessels also exhibited significantly lower norepinephrine-induced contraction and an impaired relaxation response to acetylcholine compared with animals in group I. Dietary flaxseed supplementation resulted in a significant ≈40% reduction in plaque formation (P = 0.033). Animals in both groups II and III displayed improved contraction and endothelium-dependent vessel relaxation. Dietary flaxseed is a valuable strategy to accelerate the regression of atherosclerotic plaques; however, flaxseed intervention did not demonstrate a clear beneficial effect on the vessel contractile response and endothelium-dependent vasorelaxation.

An integrated approach for the mechanisms responsible for atherosclerotic plaque regression.

Atherosclerosis was originally considered to be an ongoing process that was inevitably associated with age. However, plaques are highly dynamic, and are able to progress, stabilize or regress depending on their surrounding milieu. A great deal of research attention has been focused on understanding the involvement of high-density lipoprotein in atherosclerotic plaque regression. However, atherosclerotic plaque regression encompasses a variety of processes that can be grouped into three main areas: removal of lipids and necrotic material; restoration of endothelial function and repair of denuded areas; and cessation of vascular smooth muscle cell proliferation and phenotype reversal. In addition to the role of high-density lipoproteins in lipid removal, resident macrophages and foam cells are able to regain motility and rapidly migrate on milieu improvement, moving both lipids and necrotic material to regional lymph nodes. Neighbouring endothelial cells can proliferate and replace dead and dysfunctional cells. Circulating endothelial progenitor cells can similarly restore vessel function. Finally, abrogation of smooth muscle cell proliferation occurs secondarily to these processes. This information is integrated in the current article to present a comprehensive and clear depiction of plaque regression. This integrated view of regression is essential to optimize the pharmaceutical targeting of the many processes and pathways involved in plaque regression.