Predictors of Discharge Destination From Acute Care in Patients With Traumatic Brain Injury: A Systematic Review.

OBJECTIVE: To systematically review studies on clinical and nonclinical predictors of discharge destination from acute care in patients with traumatic brain injury. METHODS: The search was conducted using 7 databases up to December 2016. A systematic review and in-depth quality synthesis were conducted on eligible articles that met the inclusion criteria. RESULTS: The search yielded 8503 articles of which 18 studies met the inclusion criteria. This study demonstrated that a larger proportion of patients with traumatic brain injury were discharged home. The main predictors of discharge to a setting with rehabilitation services versus home included increasing age, white and non-Hispanic race/ethnicity, having insurance coverage, greater severity of the injury, and longer acute care length of stay. Age was the only consistent factor that was negatively associated with discharge to inpatient rehabilitation facilities versus other institutions. CONCLUSION: Results of this study support healthcare providers in providing consultation to patients about the expected next level of cares while considering barriers that may helpful in effective discharge planning, decreasing length of stay and saving resources. These findings also suggest the need for further studies with a stronger methodology on the contribution of patients and families/caregivers to distinguish the predictors of discharge to dedicated rehabilitation facilities.

Predictors of discharge destination from acute care in patients with traumatic brain injury.

INTRODUCTION: Many studies have assessed the predictors of morbidity/mortality of patients with traumatic brain injury (TBI) in acute care. However, with the increasing rate of survival after TBI, more attention has been given to discharge destinations from acute care as an important measure of clinical priorities. This study describes the design of a systematic review compiling and synthesising studies on the prognostic factors of discharge settings from acute care in patients with TBI. METHODS AND ANALYSIS: This systematic review will be conducted on peer-reviewed studies using seven databases including Medline/Medline in-Process, Embase, Cochrane Database of Systematic Reviews, Cochrane CENTRAL, PsycINFO, CINAHL and Supplemental PubMed. The reference list of selected articles and Google Scholar will also be reviewed to determine other relevant articles. This study will include all English language observational studies that focus on adult patients with TBI in acute care settings. The quality of articles will be assessed by the Quality in Prognostic Studies tool. ETHICS AND DISSEMINATION: The results of this review will provide evidence that may guide healthcare providers in making more informed and timely discharge decisions to the next level of care for patient with TBI. Also, this study will provide valuable information to address the gaps in knowledge for future research. TRIAL REGISTRATION NUMBER: Trial registration number (PROSPERO) is CRD42016033046.

Lecithin cholesterol acyltransferase null mice are protected from diet-induced obesity and insulin resistance in a gender-specific manner through multiple pathways.

Complete lecithin cholesterol acyltransferase (LCAT) deficiency uniformly results in a profound HDL deficiency. We recently reported unexpected enhanced insulin sensitivity in LCAT knock-out mice in the LDL receptor knock-out background (Ldlr(-/-)×Lcat(-/-); double knock-out (DKO)), when compared with their Ldlr(-/-)×Lcat(+/+) (single knock-out (SKO)) controls. Here, we report that LCAT-deficient mice (DKO and Lcat(-/-)) are protected against high fat high sucrose (HFHS) diet-induced obesity without hypophagia in a gender-specific manner compared with their respective (SKO and WT) controls. The metabolic phenotypes are more pronounced in the females. Changes in endoplasmic reticulum stress were examined as a possible mechanism for the metabolic protection. The female DKO mice developed attenuated HFHS-induced endoplasmic reticulum stress as evidenced by a lack of increase in mRNA levels of the hepatic unfolded protein response (UPR) markers Grp78 and CHOP compared with SKO controls. The DKO female mice were also protected against diet-induced insulin resistance. In white adipose tissue of chow-fed DKO mice, we also observed a reduction in UPR, gene markers for adipogenesis, and markers for activation of Wnt signaling. In skeletal muscles of female DKO mice, we observed an unexpected increase in UCP1 in association with increase in phospho-AMPKα, PGC1α, and UCP3 expressions. This increase in UCP1 was associated with ectopic islands of brown adipocytes between skeletal muscle fibers. Our findings suggest that LCAT deficiency confers gender-specific protection against diet-induced obesity and insulin resistance at least in part through regulation in UPR, white adipose tissue adipogenesis, and brown adipocyte partitioning.