Implementation of a Frailty Assessment and Targeted Care Interventions and Its Association with Reduced Postoperative Complications in Elderly Surgical Patients.

BACKGROUND: Older patients with frailty syndrome have a greater risk of poor postoperative outcomes. In this study, we used a RE-AIM (reach, effectiveness, adoption, implementation, and maintenance) framework to implement an assessment tool to identify frail patients and targeted interventions to improve their outcomes. STUDY DESIGN: We implemented a 5-question frailty assessment tool for patients 65 years and older admitted to the general and vascular surgery services from January 1, 2018 to December 31, 2019. Identified frail patients received evidence-based clinical orders and nursing care plan interventions tailored to optimize recovery. A RE-AIM framework was used to assess implementation effectiveness through provider and nurse surveys, floor audits, and chart review. RESULTS: Of 1,158 patients included in this study, 696 (60.1%) were assessed for frailty. Among these, 611 patients (87.8%) scored as frail or intermediately frail. After implementation, there were significant increases in the completion rates of frailty-specific care orders for frail patients, including delirium precautions (52.1% vs 30.7%; p < 0.001), aspiration precautions (50.0% vs 26.9%; p < 0.001), and avoidance of overnight vitals (32.5% vs 0%). Floor audits, however, showed high variability in completion of care plan components by nursing staff. Multivariate analysis showed significant decreases in 30-day complication rates (odds ratio 0.532; p < 0.001) after implementation. CONCLUSIONS: A frailty assessment was able to identify elderly patients for provision of targeted, evidence-based frailty care. Despite limited uptake of the assessment by providers and completion of care plan components by nursing staff, implementation of the assessment and care interventions was associated with substantial decreases in complications among elderly surgical patients.

Loss of MINAR2 impairs motor function and causes Parkinson's disease-like symptoms in mice.

Parkinson's disease is the second most common human neurodegenerative disease. Motor control impairment represents a key clinical hallmark and primary clinical symptom of the disease, which is further characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta and the accumulation of α-synuclein aggregations. We have identified major intrinsically disordered NOTCH2-associated receptor 2 encoded by KIAA1024L, a previously uncharacterized protein that is highly conserved in humans and other species. In this study, we demonstrate that major intrinsically disordered NOTCH2-associated receptor 2 expression is significantly down-regulated in the frontal lobe brain of patients with Lewy body dementia. Major intrinsically disordered NOTCH2-associated receptor 2 is predominantly expressed in brain tissue and is particularly prominent in the midbrain. Major intrinsically disordered NOTCH2-associated receptor 2 interacts with neurogenic locus notch homologue protein 2 and is localized at the endoplasmic reticulum compartments. We generated major intrinsically disordered NOTCH2-associated receptor 2 knockout mouse and demonstrated that the loss of major intrinsically disordered NOTCH2-associated receptor 2 in mouse results in severe motor deficits such as rigidity and bradykinesia, gait abnormalities, reduced spontaneous locomotor and exploratory behaviour, symptoms that are highly similar to those observed in human Parkinson's spectrum disorders. Analysis of the major intrinsically disordered NOTCH2-associated receptor 2 knockout mice brain revealed significant anomalies in neuronal function and appearance including the loss of tyrosine hydroxylase-positive neurons in the pars compacta, which was accompanied by an up-regulation in α-synuclein protein expression. Taken together, these data demonstrate a previously unknown function for major intrinsically disordered NOTCH2-associated receptor 2 in the pathogenesis of Parkinson's spectrum disorders.

Extreme physiological plasticity in a hibernating basoendothermic mammal, Tenrec ecaudatus.

Physiological plasticity allows organisms to respond to diverse conditions. However, can being too plastic actually be detrimental? Malagasy common tenrecs, Tenrec ecaudatus, have many plesiomorphic traits and may represent a basal placental mammal. We established a laboratory population of T. ecaudatus and found extreme plasticity in thermoregulation and metabolism, a novel hibernation form, variable annual timing, and remarkable growth and reproductive biology. For instance, tenrec body temperature (Tb) may approximate ambient temperature to as low as 12°C even when tenrecs are fully active. Conversely, tenrecs can hibernate with Tb of 28°C. During the active season, oxygen consumption may vary 25-fold with little or no change in Tb During the austral winter, tenrecs are consistently torpid but the depth of torpor may vary. A righting assay revealed that Tb contributes to but does not dictate activity status. Homeostatic processes are not always linked, e.g. a hibernating tenrec experienced a ∼34% decrease in heart rate while maintaining constant body temperature and oxygen consumption rates. Tenrec growth rates vary but young may grow ∼40-fold in the 5 weeks until weaning and may possess indeterminate growth as adults. Despite all of this profound plasticity, tenrecs are surprisingly intolerant of extremes in ambient temperature (<8 or >34°C). We contend that while plasticity may confer numerous energetic advantages in consistently moderate environments, environmental extremes may have limited the success and distribution of plastic basal mammals.