Preinjury Functional Independence is not Associated with Discharge Location in Older Trauma Patients.

BACKGROUND: The purpose of this study was to evaluate the association between pre-injury Katz Index of Independence in Activities of Daily Living (Katz ADL) functional status and discharge to a facility in non-neurologically injured older trauma patients. METHODS: Data were obtained from 207 patients in the Trauma Medical Home study cohort. Multivariable logistic regression was performed to identify factors associated with non-home discharge. RESULTS: Average patient age was 67.9 (SD 11.1). Patients were predominantly white (89.4%) and female (52.2%) with a median ISS of 11 (IQR 9-14). The most common mechanism of injury was fall (48.3%), followed by motor vehicle crash (41.1%). Nearly all patients (94.7%) reported independence in activities of daily living prior to hospitalization for injury. Discharge disposition varied, 51.7% of patients were discharged home, 37.7% to subacute rehabilitation, 10.1% to acute rehabilitation and 0.5% to long-term acute care. There was no relationship between pre-injury independence and likelihood of discharge home (P = 0.1331). Age (P < 0.0001), BMI (P = 0.0002), Charlson comorbidity score of 3 or greater (P = 0.0187), being single (P = 0.0077), ISS ≥ 16 (P = 0.0075) and being female with self-reported symptoms of anxiety and/or depression over the past two weeks (P = 0.0092) were associated with significantly greater odds of non-home discharge. CONCLUSIONS: Pre-injury Katz ADL is not associated with discharge disposition, though other significantly associated factors were identified. It is imperative that discussions regarding discharge disposition are initiated early during acute hospitalization. Trauma programs could potentially benefit from implementing an inpatient intervention focused on building coping skills for older patients exhibiting symptoms of anxiety or depression.

Osteoblast/osteocyte-specific inactivation of Stat3 decreases load-driven bone formation and accumulates reactive oxygen species.

Signal transducers and activators of transcription 3 (Stat3) is a transcription factor expressed in many cell types including osteoblasts, osteocytes, and osteoclasts. STAT3 mutations cause a rare human immunodeficiency disease that presents reduced bone mineral density and recurrent pathological fractures. To investigate the role of Stat3 in load-driven bone metabolism, two strains of osteoblast/osteocyte-selective Stat3 knockout (KO) mice were generated. Compared to age-matched littermate controls, this selective inactivation of Stat3 significantly lowered bone mineral density (7-12%, p<0.05) as well as ultimate force (21-34%, p<0.01). In ulna loading (2.50-2.75N with 120 cycles/day at 2Hz for 3 consecutive days), Stat3 KO mice were less responsive than littermate controls as indicated by reduction in relative mineralizing surface (rMS/BS, 47-59%, p<0.05) and relative bone formation rate (rBFR/BS, 64-75%, p<0.001). Furthermore, inactivation of Stat3 suppressed load-driven mitochondrial activity, which led to an elevated level of reactive oxygen species (ROS) in cultured primary osteoblasts. Taken together, the results support the notion that the loss-of-function mutation of Stat3 in osteoblasts and osteocytes diminishes load-driven bone formation and impairs the regulation of oxidative stress in mitochondria.