The Shieh Score as a Risk Assessment Instrument for Reducing Hospital-Acquired Pressure Injuries: A Prospective Cohort Study.

PURPOSE: The purpose of this study was to evaluate the Shieh Score's effectiveness in decreasing the rate of hospital-acquired pressure injuries when combined with an early warning notification system and standard order set of preventative measures. DESIGN: This was a prospective cohort study. SUBJECTS AND SETTING: This target population was nonpregnant, adult, hospitalized patients on inpatient and observation status at a tertiary hospital (Kaiser Permanente, Baldwin Park, California) during the 2020 year of the COVID-19 pandemic. METHODS: A new, risk assessment instrument, the Shieh Score, was developed in 2019 to predict hospitalized patients at high risk for pressure injuries. Data collection occurred between January 21, 2020, and December 31, 2020. When a hospital patient met the high-risk criteria for the Shieh Score, a provider-ordered pink-colored sheet of paper titled "Skin at Risk" was hung at the head of the bed and a standard order set of pressure injury preventative measures was implemented by nursing staff. RESULTS: Implementation of the program (Shieh Score, early warning system, and standard order set for preventive interventions) resulted in a 38% reduction in the annual hospital-acquired pressure injury rate from a mean incidence rate of 1.03 to 0.64 hospital-acquired pressure injuries per 1000 patient-days measured for the year 2020. CONCLUSION: The Shieh Score is a pressure injury risk assessment instrument, which effectively identifies patients at high risk for hospital-acquired pressure injuries and decreases the hospital-acquired pressure injury rate when combined with an early warning notification system and standard order set.

The Shieh Score as a Risk Assessment Tool for Hospital-Acquired Pressure Injuries: A Retrospective Cohort Study.

OBJECTIVE: To design a new risk assessment tool to identify patients at high risk for hospital-acquired pressure injuries. METHODS: The researchers developed the Shieh Score using retrospective data of 406,032 hospital admissions from January 2014 to December 2016 with 1,299 pressure injury cases from the pressure injury registry. A decision tree and best subset logistic regression were used to select predictors from demographic and clinical candidate variables, which were then used to construct the Shieh Score. RESULTS: The final Shieh Score included the following measures: sex, age, diabetes, glomerular filtration rate, albumin level, level of function, use of IV norepinephrine, mechanical ventilation, and level of consciousness. The Shieh Score had a higher Youden Index, specificity, and positive predictive value than the Braden Scale. However, the Braden Scale had a higher sensitivity compared with the Shieh Score. CONCLUSIONS: The Shieh Score is an alternative risk assessment tool that may effectively identify a smaller number of patients at high risk for hospital-acquired pressure injuries with a higher specificity and positive predictive value than the Braden Scale.

One-Month Postoperative Horizontal Strabismus Surgery Outcomes Using Adjustable and Nonadjustable Sutures.

INTRODUCTION: Previous series suggest adjustable sutures (AS) in adult strabismus surgery yield improved ocular alignment and better success rates compared to nonadjustable sutures (NAS). We questioned whether these differences are clinically significant and whether they justify the added time and discomfort required for AS. METHODS: We reviewed all available records of adults undergoing horizontal strabismus surgery by the last two authors between 2000 and 2014. Independently, the two surgeons developed a preference for NAS midway through the study period, permitting comparisons between two treatment groups. Results were assessed at one to two months postoperatively. The primary outcome was alignment in primary position at one to two months postoperatively. The secondary outcome was success rate, defined as <10PD residual or consecutive deviation. RESULTS: We included 184 patients, 68 with AS and 116 with NAS. No significant difference in primary position alignment at 1-2 months was noted between AS and NAS for esotropia (P = .26) or for exotropia (P = .10). Success rates were similar (P = .58 for esotropia and P = .34 for exotropia). DISCUSSION: Although we acknowledge limitations in this retrospective study, our results suggest that AS overall was not associated with improved alignment or success rates, compared to NAS, at 1- to 2- months postoperatively. CONCLUSIONS: Although adjustable sutures represent a valuable surgical option at the discretion of individual surgeons and their patients, we no longer routinely use AS in all adult cases. A prospective study to evaluate long-term outcomes would be helpful.

Cardiomyocyte orientation modulated by the Numb family proteins-N-cadherin axis is essential for ventricular wall morphogenesis.

The roles of cellular orientation during trabecular and ventricular wall morphogenesis are unknown, and so are the underlying mechanisms that regulate cellular orientation. Myocardial-specific Numb and Numblike double-knockout (MDKO) hearts display a variety of defects, including in cellular orientation, patterns of mitotic spindle orientation, trabeculation, and ventricular compaction. Furthermore, Numb- and Numblike-null cardiomyocytes exhibit cellular behaviors distinct from those of control cells during trabecular morphogenesis based on single-cell lineage tracing. We investigated how Numb regulates cellular orientation and behaviors and determined that N-cadherin levels and membrane localization are reduced in MDKO hearts. To determine how Numb regulates N-cadherin membrane localization, we generated an mCherry:Numb knockin line and found that Numb localized to diverse endocytic organelles but mainly to the recycling endosome. Consistent with this localization, cardiomyocytes in MDKO did not display defects in N-cadherin internalization but rather in postendocytic recycling to the plasma membrane. Furthermore, N-cadherin overexpression via a mosaic model partially rescued the defects in cellular orientation and trabeculation of MDKO hearts. Our study unravels a phenomenon that cardiomyocytes display spatiotemporal cellular orientation during ventricular wall morphogenesis, and its disruption leads to abnormal trabecular and ventricular wall morphogenesis. Furthermore, we established a mechanism by which Numb modulates cellular orientation and consequently trabecular and ventricular wall morphogenesis by regulating N-cadherin recycling to the plasma membrane.

Notch signaling regulates Hey2 expression in a spatiotemporal dependent manner during cardiac morphogenesis and trabecular specification.

Hey2 gene mutations in both humans and mice have been associated with multiple cardiac defects. However, the currently reported localization of Hey2 in the ventricular compact zone cannot explain the wide variety of cardiac defects. Furthermore, it was reported that, in contrast to other organs, Notch doesn't regulate Hey2 in the heart. To determine the expression pattern and the regulation of Hey2, we used novel methods including RNAscope and a Hey2 CreERT2 knockin line to precisely determine the spatiotemporal expression pattern and level of Hey2 during cardiac development. We found that Hey2 is expressed in the endocardial cells of the atrioventricular canal and the outflow tract, as well as at the base of trabeculae, in addition to the reported expression in the ventricular compact myocardium. By disrupting several signaling pathways that regulate trabeculation and/or compaction, we found that, in contrast to previous reports, Notch signaling and Nrg1/ErbB2 regulate Hey2 expression level in myocardium and/or endocardium, but not its expression pattern: weak expression in trabecular myocardium and strong expression in compact myocardium. Instead, we found that FGF signaling regulates the expression pattern of Hey2 in the early myocardium, and regulates the expression level of Hey2 in a Notch1 dependent manner.

Dramatic Reduction in Hospital-Acquired Pressure Injuries Using a Pink Paper Reminder System.

OBJECTIVE: The goal of this quality improvement project was to reduce the number of hospital-acquired pressure injuries (HAPIs) by flagging extremely high-risk patients with a pink paper reminder system and implementing a pressure injury prevention order set. METHODS: The pink paper reminder system is an innovative, cost-neutral, simple approach to identify patients at highest risk of pressure injury development who meet specific criteria. There are 2 steps to this intervention. First, study authors developed a new risk assessment tool, the pink paper criteria. When a patient met the specified criteria, a pink piece of paper titled "SKIN AT RISK" in a large font was hung at the head of his/her bed to reinforce preventive strategies. Next, a set of pressure injury preventive measures was ordered. PATIENTS: This quality improvement project included all adult hospitalized patients of all specialties based in 2 Kaiser Permanente hospitals. RESULTS: There was a 67% reduction in HAPI incidences following the initiation of the pink paper reminder system, from a mean rate of 1.2 to 0.4 incidence of HAPIs per 1000 patient-days measured over 4 years. CONCLUSIONS: Identifying and flagging patients who are at extremely high risk of pressure injuries and implementing an order set of pressure injury preventive measures dramatically reduced the rate of HAPIs per 1000 patient-days.

CDC42 is required for epicardial and pro-epicardial development by mediating FGF receptor trafficking to the plasma membrane.

The epicardium contributes to multiple cardiac lineages and is essential for cardiac development and regeneration. However, the mechanism of epicardium formation is unclear. This study aimed to establish the cellular and molecular mechanisms underlying the dissociation of pro-epicardial cells (PECs) from the pro-epicardium (PE) and their subsequent translocation to the heart to form the epicardium. We used lineage tracing, conditional deletion, mosaic analysis and ligand stimulation in mice to determine that both villous protrusions and floating cysts contribute to PEC translocation to myocardium in a CDC42-dependent manner. We resolved a controversy by demonstrating that physical contact of the PE with the myocardium constitutes a third mechanism for PEC translocation to myocardium, and observed a fourth mechanism in which PECs migrate along the surface of the inflow tract to reach the ventricles. Epicardial-specific Cdc42 deletion disrupted epicardium formation, and Cdc42 null PECs proliferated less, lost polarity and failed to form villous protrusions and floating cysts. FGF signaling promotes epicardium formation in vivo, and biochemical studies demonstrated that CDC42 is involved in the trafficking of FGF receptors to the cell membrane to regulate epicardium formation.

Imaging Cleared Embryonic and Postnatal Hearts at Single-cell Resolution.

Single clonal tracing and analysis at the whole-heart level can determine cardiac progenitor cell behavior and differentiation during cardiac development, and allow for the study of the cellular and molecular basis of normal and abnormal cardiac morphogenesis. Recent emerging technologies of retrospective single clonal analyses make the study of cardiac morphogenesis at single cell resolution feasible. However, tissue opacity and light scattering of the heart as imaging depth is increased hinder whole-heart imaging at single cell resolution. To overcome these obstacles, a whole-embryo clearing system that can render the heart highly transparent for both illumination and detection must be developed. Fortunately, in the last several years, many methodologies for whole-organism clearing systems such as CLARITY, Scale, SeeDB, ClearT, 3DISCO, CUBIC, DBE, BABB and PACT have been reported. This lab is interested in the cellular and molecular mechanisms of cardiac morphogenesis. Recently, we established single cell lineage tracing via the ROSA26-CreERT2; ROSA26-Confetti system to sparsely label cells during cardiac development. We adapted several whole embryo-clearing methodologies including Scale and CUBIC (clear, unobstructed brain imaging cocktails and computational analysis) to clear the embryo in combination with whole mount staining to image single clones inside the heart. The heart was successfully imaged at single cell resolution. We found that Scale can clear the embryonic heart, but cannot effectively clear the postnatal heart, while CUBIC can clear the postnatal heart, but damages the embryonic heart by dissolving the tissue. The methods described here will permit the study of gene function at a single clone resolution during cardiac morphogenesis, which, in turn, can reveal the cellular and molecular basis of congenital heart defects.

Single-Cell Lineage Tracing Reveals that Oriented Cell Division Contributes to Trabecular Morphogenesis and Regional Specification.

The cardiac trabeculae are sheet-like structures extending from the myocardium that function to increase surface area. A lack of trabeculation causes embryonic lethality due to compromised cardiac function. To understand the cellular and molecular mechanisms of trabecular formation, we genetically labeled individual cardiomyocytes prior to trabeculation via the brainbow multicolor system and traced and analyzed the labeled cells during trabeculation by whole-embryo clearing and imaging. The clones derived from labeled single cells displayed four different geometric patterns that are derived from different patterns of oriented cell division (OCD) and migration. Of the four types of clones, the inner, transmural, and mixed clones contributed to trabecular cardiomyocytes. Further studies showed that perpendicular OCD is an extrinsic asymmetric cell division that putatively contributes to trabecular regional specification. Furthermore, N-Cadherin deletion in labeled clones disrupted the clonal patterns. In summary, our data demonstrate that OCD contributes to trabecular morphogenesis and specification.

Inhibition of cell-cell adhesion impairs directional epithelial migration on micropatterned surfaces.

The development of the vertebrate body plan with left-right (LR) asymmetry (also known as handedness and chirality) requires the emerging chiral morphogenesis of epithelial cells at specific embryonic stages. In this process, cell-cell adhesions coordinate cellular organization and collective cell migration, and are critical for the directional looping of developing embryonic organs. However, the underlying biophysical mechanism is not yet well understood. Here we modeled normal and delayed epithelial LR symmetry breaking with patterned epithelial chiral morphogenesis on microscale lines with various widths. The patterned cells exhibited biased migration wherein those on opposing boundaries migrated in different directions. Disrupting adherens junctions with ethylene glycol tetraacetic acid (EGTA) resulted in a decrease in velocity difference in opposing boundaries as well as the associated biased cell alignment, along with an increase in the overall random motion. Altering the distance between the opposing boundaries did not significantly alter alignment, but significantly disturbed the velocity profile of the cell migration field. Further examination of cell polarity indicated that disruption of adherens junctions did not affect cell polarization on the boundaries, but decreased the transmission of chiral bias into the interior region of the epithelial cell sheet. Overall, our results demonstrated the dependence of the scale of collective cell migration on the strength of cell-cell adhesion, and its effects on the chirality of a multicellular structure through mediating cell polarity in the vicinity of geometric boundaries. This study demonstrated that our 2D microscale system provides a simple yet effective tool for studying the influence of collective cell migration on LR symmetry breaking, and possibly for fetal drug screening to prevent birth defects related to alteration in cell-cell adhesion.