Coding for Physical Restraint Status Among Hospitalized Patients: a 2019 National Inpatient Sample Analysis.

BACKGROUND: The reduction of physical restraint utilization in the hospital setting is a key goal of high-quality care, but little is known about the rate of restraint use in general hospitals in the USA. OBJECTIVE: This study reports the rate of physical restraint coding among acute care hospital discharges in the USA and explores associated demographic and diagnostic factors. DESIGN: The National Inpatient Sample, a de-identified all-payors database of acute care hospital discharges in the USA, was queried for patients aged 18 and older with a diagnosis code for physical restraint status in 2019. PARTICIPANTS: Hospitalized patients aged 18 and older. MAIN MEASURES: Demographics, discharge diagnoses, in-hospital mortality, length of stay, total hospital charges. KEY RESULTS: In total, 220,470 (95% CI: 208,114 to 232,826) hospitalizations, or 0.7% of overall hospitalizations, included a discharge code for physical restraint status. There was a 700-fold difference in coding for restraint utilization based on diagnosis, with 7.4% of patients with encephalitis receiving restraint diagnosis codes compared to < 0.01% of patients with uncomplicated diabetes. In an adjusted model, male sex was associated with an odds ratio of 1.4 (95% CI: 1.4 to 1.5) for restraint utilization coding, and Black race was associated with an odds ratio of 1.3 (95% CI: 1.2 to 1.4) relative to white race. CONCLUSIONS: In the general hospital setting, there is variability in physical restraint coding by sex, race, and clinical diagnosis. More research is needed into the appropriate utilization of restraints in the hospital setting and possible inequities in restraint utilization.

Nuclear localization of SMN and FUS is not altered in fibroblasts from patients with sporadic ALS.

Abstract Sporadic amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with no established biological marker. Recent observation of a reduced number of gems (survival motor neuron protein (SMN)-positive nuclear bodies) in cells from patients with familial ALS and the mouse models suggests an involvement of SMN in ALS pathology. At a molecular level, fused in sarcoma (FUS), one of the familial ALS-linked proteins, has been demonstrated to directly interact with SMN, while impaired nuclear localization of mutated FUS causes defective gem formation. Our objective was to determine whether gems and/or nuclear FUS levels in skin derived fibroblasts from sporadic ALS patients are consistently reduced and thus could constitute a novel and readily available biomarker of the disease. Fibroblasts from 20 patients and 17 age-matched healthy controls were cultured and co-immunostained for SMN and FUS. Results showed that no difference was detected between the two groups in the number of gems and in expression pattern of FUS. The number of gems negatively correlated with the age at biopsy in both ALS and control subjects. In conclusion, the expression pattern of SMN and FUS in fibroblasts cannot serve as a biomarker for sporadic ALS. Donor age-dependent gem reduction is a novel observation that links SMN with cellular senescence.