Assessing the Effectiveness of Engaging Patients and Their Families in the Three-Step Fall Prevention Process Across Modalities of an Evidence-Based Fall Prevention Toolkit: An Implementation Science Study.

BACKGROUND: Patient falls are a major problem in hospitals. The development of a Patient-Centered Fall Prevention Toolkit, Fall TIPS (Tailoring Interventions for Patient Safety), reduced falls by 25% in acute care hospitals by leveraging health information technology to complete the 3-step fall prevention process-(1) conduct fall risk assessments; (2) develop tailored fall prevention plans with the evidence-based interventions; and (3) consistently implement the plan. We learned that Fall TIPS was most effective when patients and family were engaged in all 3 steps of the fall prevention process. Over the past decade, our team developed 3 Fall TIPS modalities-the original electronic health record (EHR) version, a laminated paper version that uses color to provide clinical decision support linking patient-specific risk factors to the interventions, and a bedside display version that automatically populates the bedside monitor with the patients' fall prevention plan based on the clinical documentation in the EHR. However, the relative effectiveness of each Fall TIPS modality for engaging patients and family in the 3-step fall prevention process remains unknown. OBJECTIVE: This study aims to examine if the Fall TIPS modality impacts patient engagement in the 3-step fall prevention process and thus Fall TIPS efficacy. METHODS: To assess patient engagement in the 3-step fall prevention process, we conducted random audits with the question, "Does the patient/family member know their fall prevention plan?" In addition, audits were conducted to measure adherence, defined by the presence of the Fall TIPS poster at the bedside. Champions from 3 hospitals reported data from April to June 2017 on 6 neurology and 7 medical units. Peer-to-peer feedback to reiterate the best practice for patient engagement was central to data collection. RESULTS: Overall, 1209 audits were submitted for the patient engagement measure and 1401 for the presence of the Fall TIPS poster at the bedside. All units reached 80% adherence for both measures. While some units maintained high levels of patient engagement and adherence with the poster protocol, others showed improvement over time, reaching clinically significant adherence (>80%) by the final month of data collection. CONCLUSIONS: Each Fall TIPS modality effectively facilitates patient engagement in the 3-step fall prevention process, suggesting all 3 can be used to integrate evidence-based fall prevention practices into the clinical workflow. The 3 Fall TIPS modalities may prove an effective strategy for the spread, allowing diverse institutions to choose the modality that fits with the organizational culture and health information technology infrastructure.

The genetic basis of high-altitude pulmonary oedema.

High-altitude pulmonary oedema (HAPE) is a potentially fatal condition affecting fit and previously well individuals at altitudes in excess of 3000 m. This article discusses the mechanisms of HAPE, considers the contribution of hypoxic pulmonary vasoconstriction and alterations in sodium transport to the pathological process. It discusses the various biochemical mediators such as nitric oxide (NO), endothelin-1 (ET-1), and the renin-angiotensin-aldosterone system (RAS) that may be involved and considers possible oxygen-sensing mechanisms involved in hypoxic adaptation such as hypoxia-inducible factor-1 (HIF-1). Those who have had HAPE once run an unpredictable but significant risk of recurrence; therefore, there may be a constitutional or genetic component in its aetiology. This paper considers the possible involvement of genes that may be involved in physiological adaptation to hypoxia (e.g., angiotensin-1 [AT(1)]-converting enzyme [ACE], tyrosine hydroxylase, serotonin transporter [5-HTT], and endothelial NO synthase [eNOS] genes). As yet, no formal association has been identified between an identified genetic polymorphism and HAPE, but genetic variation provides a possible mechanism to explain interindividual variation in response to hypoxia and enhanced or reduced performance at altitude.

p38 MAP kinase: essential role in hypoxia-mediated human pulmonary artery fibroblast proliferation.

Pulmonary arterial hypertension (PAH) is a disease that results in thickening of the vascular wall. Some of the most prominent changes are seen in the adventitia as a result of fibroblast proliferation and increased extracellular matrix deposition. Previous work from this laboratory using animal models has shown that pulmonary but not systemic artery fibroblasts proliferate to hypoxic exposure and that this response is dependent on activation of p38 mitogen-activated protein kinase (p38MAPK). In this study, we wished to determine whether human pulmonary artery fibroblasts (HPAFs) behaved similarly under conditions of acute hypoxic exposure (35 mmHg for 24 h). Fibroblast proliferation was assessed by [(3)H]thymidine uptake and protein assays performed using Western blotting techniques. HPAFs proliferated in response to acute hypoxic exposure, human systemic artery fibroblasts did not. This hypoxia-mediated proliferation was p38 MAPK dependent and could be blocked using a specific p38 MAPK inhibitor. Hypoxia-inducible factor-1 (HIF-1) expression was increased in hypoxic pulmonary but not systemic cells and could be partially abrogated with the p38 inhibitor. This work in man confirmed our previous findings in animals that significant differences exist between the pulmonary and systemic circulations in response to hypoxic exposure. This study highlights the importance of p38 MAPK and HIF-1 in hypoxia-mediated proliferation of pulmonary artery adventitial fibroblasts.