Is Health Literacy Associated With Surgical Outcomes? A Systematic Review.

INTRODUCTION: Low levels of health literacy have been shown to increase healthcare utilization and negatively affect health outcomes within medical specialties. However, the relationship of health literacy with clinical, patient-centered, and process-oriented surgical outcomes is not as well understood. MATERIALS AND METHODS: We sought to systematically review the current evidence base regarding the relationship between health literacy and a range of outcomes in patients experiencing surgical care. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, we searched six databases and then identified and extracted data from 25 cross-sectional or cohort studies deemed eligible for a systematic review. RESULTS: Among included studies, strong evidence exists to support an association between low health literacy and worse patient-centered outcomes, as well as an association between low health literacy and poorer process-oriented surgical outcomes. However, the relationship between health literacy and clinical outcomes remains unclear. CONCLUSIONS: Substantial opportunities remain to improve our understanding of the impact of health literacy on surgical outcomes. Future work should expand the range of institutional and specialized surgical settings studied, implement a standardized set of validated health literacy assessment tools, include more diverse patient populations, and investigate a comprehensive range of patient-reported outcomes.

Utility of the LET-IN-OUT Clinical Decision Support Tool for Medical Risk Stratification Prior to Outpatient Total Hip or Knee Arthroplasty.

BACKGROUND: Musculoskeletal care teams can benefit from simple, standardized, and reliable preoperative tools for assessing discharge disposition after total joint arthroplasty. Our objective was to compare the predictive strength of the Ascension Seton Lower Extremity Inpatient-Outpatient (LET-IN-OUT) tool versus the American Society of Anesthesiologists Physical Status (ASA-PS) score for predicting early postoperative discharge. METHODS: We retrospectively extracted sociodemographic, surgical admission, postoperative day (POD) of discharge, 90-day readmissions, and predictions of the LET-IN-OUT and ASA-PS tools from the electronic records of 563 consecutive hip or knee arthroplasty patients (mean age 65 [SD 9.6], 54% women). Included patients who underwent a total hip arthroplasty (THA) or total knee arthroplasty (TKA) at a single health system between June 2020 and March 2021. We performed descriptive statistics and analyzed predictive values of each tool, defining "early discharge" primarily as discharge before the second postoperative day (POD 2), and secondarily as before 24 hours, and on the same calendar day (POD 0) as surgery. RESULTS: The LET-IN-OUT tool demonstrated superior predictive power among hip and knee arthroplasty patients compared to the ASA-PS tool for discharge prior to POD 2 (positive predictive value [PPV] 89 versus 83%, positive likelihood ratio [+LR] 2.0 versus 1.2), discharge before 24 hours (PPV 86 versus 70%, +LR 2.9 versus 1.2), and discharge on POD 0 (PPV 34% versus 30%, +LR 1.2 versus 1.1). CONCLUSIONS: The Ascension Seton Lower Extremity Inpatient-Outpatient tool predicted patients suitable for early discharge following THA or TKA and did so more effectively than the ASA-PS score.

AgRP Neurons Can Increase Food Intake during Conditions of Appetite Suppression and Inhibit Anorexigenic Parabrachial Neurons.

To maintain energy homeostasis, orexigenic (appetite-inducing) and anorexigenic (appetite suppressing) brain systems functionally interact to regulate food intake. Within the hypothalamus, neurons that express agouti-related protein (AgRP) sense orexigenic factors and orchestrate an increase in food-seeking behavior. In contrast, calcitonin gene-related peptide (CGRP)-expressing neurons in the parabrachial nucleus (PBN) suppress feeding. PBN CGRP neurons become active in response to anorexigenic hormones released following a meal, including amylin, secreted by the pancreas, and cholecystokinin (CCK), secreted by the small intestine. Additionally, exogenous compounds, such as lithium chloride (LiCl), a salt that creates gastric discomfort, and lipopolysaccharide (LPS), a bacterial cell wall component that induces inflammation, exert appetite-suppressing effects and activate PBN CGRP neurons. The effects of increasing the homeostatic drive to eat on feeding behavior during appetite suppressing conditions are unknown. Here, we show in mice that food deprivation or optogenetic activation of AgRP neurons induces feeding to overcome the appetite suppressing effects of amylin, CCK, and LiCl, but not LPS. AgRP neuron photostimulation can also increase feeding during chemogenetic-mediated stimulation of PBN CGRP neurons. AgRP neuron stimulation reduces Fos expression in PBN CGRP neurons across all conditions. Finally, stimulation of projections from AgRP neurons to the PBN increases feeding following administration of amylin, CCK, and LiCl, but not LPS. These results demonstrate that AgRP neurons are sufficient to increase feeding during noninflammatory-based appetite suppression and to decrease activity in anorexigenic PBN CGRP neurons, thereby increasing food intake during homeostatic need.SIGNIFICANCE STATEMENT The motivation to eat depends on the relative balance of activity in distinct brain regions that induce or suppress appetite. An abnormal amount of activity in neurons that induce appetite can cause obesity, whereas an abnormal amount of activity in neurons that suppress appetite can cause malnutrition and a severe reduction in body weight. The purpose of this study was to determine whether a population of neurons known to induce appetite ("AgRP neurons") could induce food intake to overcome appetite-suppression following administration of various appetite-suppressing compounds. We found that stimulating AgRP neurons could overcome various forms of appetite suppression and decrease neural activity in a separate population of appetite-suppressing neurons, providing new insights into how the brain regulates food intake.