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Results for “Critical Pathways”

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At least 1,225 records · Page 68Linked to original sources
PubMed1998

Don't let data become too much of a good thing in clinical path, outcomes tracking efforts.

Too much of a good thing? Are you collecting too much data? At University of Iowa Hospitals and Clinics, caregivers were tracking every variance to every item on every clinical pathway. It was just too much work, and the reports weren't even useful. A new variance tracking system includes targeting three to 10 key events for each pathway and has resulted in greater tracking compliance and data accuracy.

Benchmarking↗
PubMedDate not supplied

Benefits of patient pathways in rheumatoid arthritis care.

Rheumatoid arthritis is a painful, inflammatory, chronic condition that often results in irreversible joint damage. This article uses the condition to highlight the benefits of patient pathways and illustrate how they can be developed.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Initiatives to build a competitive healthcare system: integrating service redesign and clinical pathways.

In this article, the authors describe how two separate initiatives (the redesign of hospital services and the development and implementation of clinical pathways) were integrated at an academic medical center. The lessons learned in integrating projects that were not conceived at the same time and in developing multidisciplinary teams to produce new case management tools may be used by clinicians and managers elsewhere. The service redesign project developed a role for senior, experienced nurses with clinical expertise and patient management skills to manage the care of groups of similar patients, focusing on patient outcomes. The clinical pathway project developed diagnostic related groups-based clinical pathways. The steps involved in clinical pathway development-stakeholder cooperation building, initiation of data collection tools, data analysis, implementation of the role of the expert nurse in "championing" the pathway, and evaluation of the effects of pathways-are discussed.

Critical Pathways↗
PubMedDate not supplied

Questions to ask: implementing a system for clinical pathway variance analysis.

Although it is agreed that there is a need for clinical pathway variance analysis, methods for creating a system are less well defined. To help others down this path, we have developed a list of questions around four core issues: data collection, data entry and analysis, data reporting, and organizational support. Our goal is to identify key questions related to variance management and provide a framework for clinical pathway variance analysis.

Analysis of Variance↗
PubMed2006

[Interdisciplinary clinical pathway for colorectal cancer].

Limited financial resources in public health care have led to the introduction of clinical pathways as a means to a better effectivity and efficacy. Colorectal cancer met the requirements for establishing such a pathway in a distinguished way: high patient volume, high costs, interdisciplinary multi-modal treatment concepts in a relevant frequency, and existing evidence based guidelines. This article gives an example of a clinical pathway for colorectal cancer as established in our hospital. The potential of such pathways to save costs as well as their implications on treatment results and patients' satisfaction will have to be critically analyzed in the future before their value can be definitely estimated.

Colorectal Neoplasms↗
PubMed1996

Multiple anterograde atrioventricular node pathways in patients with atrioventricular node reentrant tachycardia.

OBJECTIVES: This study sought to investigate electrophysiologic characteristics and possible anatomic sites of multiple anterograde slow atrioventricular (AV) node pathways and to compare these findings with those in dual anterograde AV node pathways. BACKGROUND: Although multiple anterograde AV node pathways have been demonstrated by the presence of multiple discontinuities in the AV node conduction curve, the role of these pathways in the initiation and maintenance of AV node reentrant tachycardia (AVNRT) is still unclear, and possible anatomic sites of these pathways have not been reported. METHODS: This study included 500 consecutive patients with AVNRT who underwent electrophysiologic study and radiofrequency ablation. Twenty-six patients (5.2%) with triple or more anterograde AV node pathways were designated as Group I (16 female, 10 male, mean age 48 +/- 14 years), and the other 474 patients (including 451 with and 23 without dual anterograde AV node pathways) were designated as Group II (257 female, 217 male; mean age 52 +/- 16 years). RESULTS: Of the 21 patients with triple anterograde AV node pathways, AVNRT was initiated through the first slow pathway only in 3, through the second slow pathway only in 8 and through the two slow pathways in 9. Of the five patients with quadruple anterograde AV node pathways, AVNRT was initiated through all three anterograde slow pathways in three and through the two slower pathways (the second and third slow pathways) in two. After radiofrequency catheter ablation, no patient had inducible AVNRT. Eleven patients (42.3%) in Group I had multiple anterograde slow pathways eliminated simultaneously at a single ablation site. Eight patients (30.7%) had these slow pathways eliminated at different ablation sites; the slow pathways with a longer conduction time were ablated more posteriorly in the Koch's triangle than those with a shorter conduction time. The remaining seven patients (27%) had a residual slow pathway after delivery of radiofrequency energy at a single or different ablation sites. The patients in Group I had a longer tachycardia cycle length, poorer retrograde conduction properties and a higher incidence of multiple types of AVNRT than those in Group II. CONCLUSIONS: Multiple anterograde AV node pathways are not rare in patients with AVNRT. However, not all of the anterograde slow pathways were involved in the initiation and maintenance of tachycardia. Radiofrequency catheter ablation was safe and effective in eliminating critical slow pathways to cure AVNRT.

Adult↗
PubMed1999

Beta-adrenergic receptor-G protein-adenylyl cyclase signal transduction in the failing heart.

The beta-adrenergic receptor signal transduction pathway is critical for rapid adjustments to increased cardiovascular demand (e.g., during exercise). In the face of chronic stimulation of this pathway, as occurs in the pathogenesis of heart failure, beta-adrenergic receptor stimulation may become maladaptive. Under these conditions, elevation of circulating catecholamines and depletion of cardiac tissue stores of norepinephrine occur in the failing heart, resulting in desensitization. Whether or not stimulation or inhibition of the beta-adrenergic receptor signaling pathway is beneficial in heart failure is controversial. One approach to address this question is to specifically overexpress a component of the beta-adrenergic receptor signaling pathway in a transgenic mouse heart. We have characterized young and old adult mice with overexpressed cardiac G(s alpha) which couples the beta-adrenergic receptor to adenylyl cyclase. In younger animals, beta-adrenergic receptor stimulation results in an augmented heart rate and cardiac contractility. Over the life of the animal, however, a picture of cardiomyopathy develops. The result is a dilated heart with a large amount of fibrosis and myocyte hypertrophy, degeneration atrophy, and apoptosis. Conversely, chronic beta-adrenergic receptor blockade prevents the development of cardiomyopathy. These experiments support the point of view that chronic beta-adrenergic stimulation during the development of heart failure is deleterious and that protecting the heart with chronic beta-adrenergic receptor blockade is salutary, conceptually consistent with results of recent clinical trials examining the effects of beta-adrenergic receptor blockers in patients with heart failure.

Adenylyl Cyclases↗
PubMed1999

MAP kinase and cAMP filamentation signaling pathways converge on the unusually large promoter of the yeast FLO11 gene.

In Saccharomyces cerevisiae, two major signal transduction pathways, the Kss1 MAPK pathway and the cAMP-regulated pathway, are critical for the differentiation of round yeast form cells to multicellular, invasive pseudohyphae. Here we report that these parallel pathways converge on the promoter of a gene, FLO11, which encodes a cell surface protein required for pseudohyphal formation. The FLO11 promoter is unusually large, containing at least four upstream activation sequences (UASs) and nine repression elements which together span at least 2.8 kb. Several lines of evidence indicate that the MAPK and cAMP signals are received by distinct transcription factors and promoter elements. First, regulation via the MAPK pathway requires the transcription factors Ste12p/Tec1p, whereas cAMP-mediated activation requires a distinct factor, Flo8p. Secondly, mutations in either pathway block FLO11 transcription. Overexpression of STE12 can suppress the loss of FLO8, and overexpression of FLO8 can suppress the loss of STE12. Finally, multiple distinct promoter regions of the FLO11 promoter are required for its activation by either Flo8p or Ste12p/ Tec1p. Thus, like the promoters of the key developmental genes, HO and IME1, the FLO11 promoter is large and complex, endowing it with the ability to integrate multiple inputs.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed2003

Structural/functional aspects of ES-62--a secreted immunomodulatory phosphorylcholine-containing filarial nematode glycoprotein.

ES-62 is a major secreted glycoprotein of the rodent filarial nematode Acanthocheilonema viteae and homologue of molecules found in filarial nematodes which parasitise humans. The molecule consists of a tetramer of apparently identical monomers of ~62 kDa which we have shown by sedimentation equilibrium analytical ultracentrifugation to strongly associate. ES-62 is one of several filarial nematode proteins to contain the unusual post-translational modification of phosphorylcholine (PC) addition. Specifically, we have found that PC is attached to one of three distinct N-type glycans we have characterised on the molecule. The amino acid sequence of ES-62 shows 37-39% identity with a family of 6 other proteins, some of which have been predicted to be amino- or carboxy-peptidases. We have also found that ES-62 is able to interact with a number of cells of the immune system, specifically B- and T-lymphocytes, macrophages and dendritic cells. Lymphocytes exposed to ES-62 in vitro or in vivo are less able to proliferate in response to ligation via the antigen receptor. Peritoneal macrophages pre-exposed to the molecule are less able to produce the cytokines IL-12, IL-6 and TNF-alpha following subsequent incubation with the classical stimulators IFNgamma and LPS. Dendritic cells allowed to mature in the presence of ES-62 acquire a phenotype, which allows them to induce anti-inflammatory "TH2-type" responses. With respect to immunomodulation, the PC moiety of the parasite molecule appears to be predominantly responsible for the effects on lymphocyte proliferation at least and we have also found that its removal converts the murine IgG antibody response to ES-62 from solely IgG1 to mixed IgG1/IgG2a. ES-62 appears to interact with cells of the immune system in a PC-dependent manner and, at least in part, via a molecule of ~82 kDa. Studies of the interaction in lymphocytes show that it is associated with activation of certain signal transduction molecules including a number of protein tyrosine kinases and mitogen activated protein kinases (MAPkinases). Although such activation is insufficient to induce proliferation, it serves to almost completely desensitise the cells to antigen-receptor ligation-induced activation of the phosphoinositide 3-kinase (PI-3-kinase) and Ras/MAPkinase pathways, events critical for lymphocyte proliferation. Such desensitisation reflects ES-62-primed recruitment of a number of negative regulators of these pathways, such as the phosphatases SHP-1 and Pac-1.

Amino Acid Sequence↗
PubMed2005

BRCA1 and BRCA2 pathways and the risk of cancers other than breast or ovarian.

OBJECTIVE: Germline mutations in the tumor suppressor genes BRCA1 and BRCA2 predispose women to breast and ovarian cancer. Female carriers of BRCA1 or BRCA2 gene mutations have very high lifetime risks for breast and ovarian cancers. Genetic abnormalities occur in all cancers, so BRCA-related pathways are critical because they serve to safeguard genetic content. Although protecting genetic information is a general function, BRCA-related pathways seem largely specific to preventing breast and ovarian cancer. The objective of this study was to resolve this difference between the theoretical functions of BRCA genes and their specific clinical effects. DATA SOURCES, DATA EXTRACTION, DATA SYNTHESIS: The author collected data published in > 30 epidemiologic studies on the incidence of cancers other than breast or ovarian in mutation carriers and in large populations eligible for mutation testing. Data were extracted and used directly as published whenever possible with a minimum of statistical manipulation. CONCLUSIONS: Although mutations target breast and ovary, a broader spectrum of cancers also occur with statistically significant elevated frequencies. Risks for "all cancers except breast or ovary" are elevated, with some population subgroups differing with regard to how frequently elevated risks were found at individual sites. Additional sites at risk included stomach, pancreas, prostate, and colon. The increased risk ranged from about 20% to 60%, with the greatest increases in risk in stomach and pancreas. The collected data show BRCA-pathway functions are probably required at multiple sites, not just in breast or ovary. Known interactions and relationships among BRCA-related pathways strongly support the idea that their inactivation provides growth or survival advantages for a variety of cancers. The data suggest applying an increased level of clinical alertness to those with defects in BRCA-related pathways. Identifying molecules that confer growth or survival advantages to BRCA-related cancers may provide broadly useful targets for chemotherapy or chemoprevention.

BRCA1 Protein↗
PubMed2000

A three-tier clinical information systems design model.

Modern health care institutions are often multi-site organisations that implement heterogeneous information management systems interacting with distributed databases. Advances in treatment modality/technology and rapidly changing information technology create increasing demand for changes/redevelopment of many health information applications. These features spawn the need for solutions to (a) guarantee data exchange across different types of applications and database management systems, and (b) reduce the costs of systems development and modification. This paper explores the concept of 'middleware services' as a solution to achieve these goals. It reports on the successful application of a component-based 3-tier system architecture to develop a computerised clinical pathways management system. The implementation experience confirms a number of significant benefits of the 3-tier structure including, reusability, flexibility, significant reduction in costs and efforts of systems development, and provision of easy, open migration pathway for future change of technology and system redevelopment.

Critical Pathways↗
PubMed2002

The construction and implementation of a psychosocial interventions care pathway within a low secure environment: a pilot study.

This paper builds on previous articles that explore the use of psychosocial interventions within inpatient settings. There are obvious difficulties in the implementation of psychosocial interventions in practice. The authors suggest that one method of developing psychosocial interventions within services is to provide organizational support to clinicians. This paper explores the development and initial implementation of a psychosocial care pathway within an inpatient setting to provide such support. It concludes with a summary of the immediate effect of the pathway on care.

Critical Pathways↗
PubMedDate not supplied

A clinical pathway for deep vein thrombosis.

The use of low molecular weight heparin to treat deep vein thrombosis at home represents a relatively new patient population for home care agencies. Use of a clinical pathway provides a framework for defining expected outcomes of care and direction for patient assessment, care, monitoring, and documentation. Implementation and evaluation of a clinical pathway are described.

Adult↗