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At least 235 records · Page 13Linked to original sources
PubMed1999

Critical pathways: application to selected patient outcomes following coronary artery bypass graft.

As health care reform evolves in the United States, many hospitals are implementing strategies to contain the cost of coronary artery bypass graft (CABG) surgery. The purpose of this study was to examine the length of stay in the intensive care unit (ICU) after CABG surgery relative to the number of hours, postoperation, when ambulation occurred, and to examine the overall postoperative length of hospital stay. The study found a significant difference between ICU length of stay and the time when ambulation was initiated (t(150) = -2.68; p = .004). These results suggest that CABG patients with shorter ICU stays begin ambulation sooner, thus potentially reducing the risk of postoperative complications as well as cost. No other significant differences were demonstrated.

Adult↗
PubMed2001

Guidelines and critical pathways for severe hospital-acquired pneumonia.

Hospital-acquired pneumonia (HAP) is associated with high morbidity and mortality. Early, appropriate, and adequate empiric therapy can increase the chance of survival. In 1995, the American Thoracic Society provided guidelines for the initial treatment of immunocompetent HAP patients, which is one of the principal HAP management approaches available to physicians today. However, these guidelines have several important limitations, including a lack of recommendations for duration of therapy and no recognition of newer drugs such as cefepime, trovafloxacin, and meropenem. Furthermore, they fail to distinguish among similar compounds (ie, beta-lactam/beta-lactamase inhibitor combinations) or to recommend specific antibiotics. The clinician using these guidelines needs to address local patterns of antimicrobial resistance, especially in ICUs. Effective computerized antibiotic management programs that incorporate information on local patterns of antimicrobial resistance can assist physicians in empiric therapy decision making, improve patient quality of care, and reduce medical costs.

Algorithms↗
PubMed2002

The effect of a critical pathway on patients' outcomes after carotid endarterectomy.

BACKGROUND: In 1996, an integrated plan of care was implemented to improve quality of care for patients undergoing elective carotid endarterectomy. Goals were to reduce length of stay, costs, number of preoperative and intensive care unit admissions, and use of diagnostic procedures yet maintain good outcomes. OBJECTIVES: To determine whether use of the integrated plan of care met the goals. METHODS: Data on financial and process outcomes, use of angiographic diagnostic procedures, and demographics were retrieved from the hospital's database for all patients who had elective carotid endarterectomy without cerebral infarction. RESULTS: A total of 783 patients met inclusion criteria: 129 before implementation of the plan of care, 66 during the 6-month transition, and 588 after implementation. Preoperative angiography was done in 32% of patients before implementation, 11% during the transition, and 4% after implementation. Percentages of patients admitted to the intensive care unit were 77% before implementation, 24% during transition, and 9% after implementation. Mean lengths of stay were 2.93 days before implementation, 2.12 days during transition, and 1.68 days after implementation. Costs per case were $7798 before implementation, $5750 during transition, and $5387 after implementation. Analysis of variance revealed significant differences between groups in total length of stay (P = .001), preoperative length of stay (P<.001), and costs (P<.001). CONCLUSION: Use of the integrated plan of care reduced length of stay, costs, admissions to intensive care units, and use of cerebral angiography. Use of the plan improved resource utilization while maintaining quality of care.

Adult↗
PubMed2001

Ensuring quality cancer care by the use of clinical practice guidelines and critical pathways.

PURPOSE: We describe the impact of clinical practice guidelines (CPGs) on improvement in oncology treatment processes or outcomes. METHODS: We performed a comprehensive search of the literature from 1966 to the present and a directed review of the literature. RESULTS: Improvements have been demonstrated in compliance with evidence-based guidelines or evidence-based medicine, and in short-term length of stay, complication rates, and financial outcomes. The data suggest that patient satisfaction can be maintained despite a shorter length of stay. There has been one example of province-wide improvement in disease-free and overall survival of breast cancer patients coincident with the adoption of CPGS: The components of successful guidelines can be summarized as follows: (1) development is based on evidence, with the guideline formulated by key physicians in the group; (2) the guidelines are disseminated to all affected health care professionals for critique; (3) implementation includes direct feedback on performance to physicians or general feedback on system performance; and (4) there is accountability for performance according to the guidelines. This accountability can consist of voluntary peer pressure to conform to evidence-based medicine, and it does not require a financial reward or penalty. CONCLUSION: Some attempts to improve practice have been moderately successful in achievement of reduced health care costs, reduced hospital length of stay, and possibly improved outcomes. Other methods that are still in use have been demonstrated to have little effect. Programs that have not succeeded have relied on voluntary change in practice behavior without incentives to change or have had no accountability component. Further research is needed to assess how guidelines are enacted in organizations other than those demonstrably committed to improvement, ways to improve compliance of health care providers who are not committed to change, and methods to improve accountability.

Critical Pathways↗
PubMed1999

Evidence-based guidelines and critical pathways for quality improvement.

Clinical practice guidelines have a long and distinguished tradition in pediatrics. Currently, the American Academy of Pediatrics has developed more than 15 practice guidelines and more than 250 clinical policy statements. In the past, practice guidelines have been used to improve care through the dissemination of evidence-based, clinically effective practices to pediatric practitioners. In the current environment this purpose has been broadened to include cost reduction, standardization of practice, and reduction of medical liability. This has led to both confusion and distrust on the part of the pediatrician. Practice guidelines are best understood as a tool to insure that children receive evidence-based care. They are best used in association with a set of outcome and performance measures that provide feedback to clinicians and allow for modification of the guidelines to meet the needs of the local patient population. The quality of practice guidelines is directly dependent on the quality of the medical evidence supporting the recommendation. Unfortunately only a small percentage of the evidence supporting practice guidelines comes from randomized clinical trials with the majority of the evidence coming from expert clinical panels. The success of practice guidelines in improving care for children has yet to be convincingly demonstrated. Currently, there is a dearth of well designed studies that document the effectiveness of practice guidelines. Their ultimate effectiveness will depend on both an improved evidence base and effective strategies for rapid dissemination of the recommendations. The development of evidence-based practice guidelines does not insure that it will have a major impact on physician practice. In the past, effective dissemination of new knowledge has been a long process, often taking years. This cycle time can be dramatically shortened through the development of networks of practice sites that share knowledge and experience in the implementation of practice guidelines and the use of strategies that take advantage of key groups in the dissemination process. When used appropriately, practice guidelines can provide an important adjunct to clinical research by facilitating the dissemination of new clinical findings and can provide an important platform for encouraging innovations in patient care.

Critical Pathways↗
PubMed2004

Vascular endothelial growth factor activation of intramembranous absorption: a critical pathway for amniotic fluid volume regulation.

OBJECTIVE: The purpose of this review is to propose a critical role for vascular endothelial growth factor (VEGF) in mediating the transfer of amniotic fluid from the amniotic compartment through the fetal membranes and fetal surface of the placenta into fetal blood. METHODS: Experimental findings in humans and animal models on the action of VEGF in mediating fluid transfer are reviewed and interpreted in order to postulate a proposed mechanism for VEGF regulation of amniotic fluid absorption through the fetal membranes and placenta. RESULTS: Recent scientific advances suggest that up-regulation of VEGF gene expression in the amnion and chorion is associated with increased transfer of amniotic fluid into fetal blood. The possible mechanisms of action for VEGF appear to involve regulation of intramembranous blood vessel proliferation and membrane transport via passive permeation as well as nonpassive transcytotic vesicular movement of fluid. CONCLUSION: Currently evolving concepts suggest that amniotic fluid volume is regulated through modulation of the rate of intramembranous absorption of amniotic fluid by both passive and nonpassive mechanisms. The permeability factor VEGF appears to be a critical regulator of amniotic fluid transport in the fetal membranes.

Absorption↗
PubMed2005

A protein secretion pathway critical for Mycobacterium tuberculosis virulence is conserved and functional in Mycobacterium smegmatis.

The Snm protein secretion system is a critical determinant of Mycobacterium tuberculosis virulence. However, genes encoding components of this pathway are conserved among all mycobacteria, including the nonpathogenic saprophyte Mycobacterium smegmatis. We show that the Snm system is operational in M. smegmatis and that secretion of its homologous ESAT-6 and CFP-10 substrates is regulated by growth conditions. Importantly, we show that Snm secretion in M. smegmatis requires genes that are homologous to those required for secretion in M. tuberculosis. Using a gene knockout strategy in M. smegmatis, we have also discovered four new gene products that are essential for Snm secretion, including the serine protease mycosin 1. Despite the evolutionary distance between M. smegmatis and M. tuberculosis, the M. smegmatis Snm system can secrete the M. tuberculosis ESAT-6 and CFP-10 proteins, suggesting that substrate recognition is also conserved between the two species. M. smegmatis, therefore, represents a powerful system to study the multicomponent Snm secretory machine and to understand the role of this conserved system in mycobacterial biology.

Antigens, Bacterial↗
PubMed2001

The smad proteins and TGFbeta signalling: uncovering a pathway critical in cancer.

The critical role of TGFbeta in development and growth control is well established but the signalling pathway has only recently been elucidated. Identification of the Smads as TGFbeta's intracellular signalling mediators has led to an explosion of information on a novel signalling network that links the cell surface to the nucleus. Many cancers develop resistance to the growth-inhibitory effects of TGFbeta and mutations in signalling pathway components have been discovered that may underly tumour progression.

DNA-Binding Proteins↗
PubMed2000

Raf induces NF-kappaB by membrane shuttle kinase MEKK1, a signaling pathway critical for transformation.

NF-kappaB is regulated by inhibitor proteins (IkappaBs), which retain NF-kappaB in the cytoplasm. Signal-induced phosphorylation by the IkappaB-kinase complex containing the IkappaB-kinases 1 and 2 (IKK-1/2 or IKK-alpha/beta) and subsequent degradation of the IkappaB proteins are prerequisites for NF-kappaB activation. Many signals induce NF-kappaB, one of them being oncogenic Raf kinase. We investigated whether NF-kappaB induction is critical for Raf-mediated transformation. Here, we demonstrate that inhibition of NF-kappaB interferes with transformation by the Raf-oncogene, and we characterized the mechanism of NF-kappaB induction by activated Raf kinase and the tumor promoter phorbol 12-myristate 13-acetate (PMA). NF-kappaB activation by PMA and Raf critically depends on the IkappaB-kinase complex, most notably on IKK-2. A major signaling pathway induced by Raf is the mitogenic cytoplasmic kinase cascade. However, different inhibitors of this cascade do not affect PMA- and Raf-mediated NF-kappaB activation. Raf does not phosphorylate the IkappaB-kinase proteins directly. Raf rather synergizes with another membrane shuttle kinase MEKK1, and Raf-mediated activation of NF-kappaB is blocked by a dominant negative form of MEKK1. These results suggest that Raf induction of NF-kappaB is relayed by MEKK1, but not by the classical mitogenic cytoplasmic kinase cascade.

Animals↗
PubMedDate not supplied

[Opioid mechanisms for modulating pain: descending pathways. Critical review].

This paper presents an extensive review of contributions on opiate controlled descending projections modulating analgesia. While there is a quite definite agreement on the organisation and structure of these projections, their true physiological role remains quite dubious. The hypothesis so far formulated on the modalities of activation of these circuits apparently don't hold a critical re-examination.

Animals↗
PubMed2005

Metastin and its G protein-coupled receptor, GPR54: critical pathway modulating GnRH secretion.

Photoperiod, food availability, temperature, stress, and hormonal cues are some of the varied signals used by mammalian species to activate or suppress their timing of sexual maturation. All ultimately converge upon gonadotropin-releasing hormone (GnRH) secretion from the hypothalamus. Through its stimulation of LH and FSH from the pituitary, GnRH represents a critical step in the reproductive cascade. While few dispute this central role of GnRH, little is understood of the mechanisms influencing the developmental fate and physiologic controls of GnRH neurons. Identification of the signals which modulate pulsatile GnRH secretion is critical to advancing understanding of normal puberty and reproductive competency. The recent identification of loss-of-function mutations in GPR54, a receptor for kisspeptin-1, has highlighted a new pathway for the timing of puberty and reproductive control.

Animals↗
PubMed2002

[Important meanings of the critical path in risk management].

The wave of change that roared through other industries has now reached healthcare. New care management and process improvement tools are emerging. Foremost among those tools will be critical pathways. Critical pathway documents describe care processes for a specific patient population. They explicitly show what will occur during the course of treatment; which care providers will perform the activities; and what outcomes are expected from the activities. Critical pathway system includes the tools to accomplish risk management, stuff communication, quality control, stuff education, and discharge management. And furthermore, critical pathway documents give healthcare providers tools to deal with the most important changes in health care; disclosure, standardization, specification outcome, making care algorithm, and continuous quality improvement. These risk management systems in a critical pathway program are critical to the success of the overall medical care process. And vital to the success of a critical pathway system is the standardization of healthcare and the variance management system.

Algorithms↗
PubMed1998

Cell type-specific angiotensin II-evoked signal transduction pathways: critical roles of Gbetagamma subunit, Src family, and Ras in cardiac fibroblasts.

Angiotensin II (Ang II) induces hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts. To determine the molecular mechanism by which Ang II displayed different effects on cardiac myocytes and fibroblasts, we examined signal transduction pathways leading to activation of extracellular signal-regulated kinases (ERKs). Ang II-induced ERK activation was abolished by pretreatment with pertussis toxin and by overexpression of the Gbetagamma subunit-binding domain of the beta-adrenergic receptor kinase 1 in cardiac fibroblasts but not in cardiac myocytes. Inhibition of protein kinase C strongly inhibited activation of ERKs by Ang II in cardiac myocytes, whereas inhibitors of tyrosine kinases but not of protein kinase C abolished Ang II-induced ERK activation in cardiac fibroblasts. Overexpression of C-terminal Src kinase (Csk), which inactivates Src family tyrosine kinases, suppressed the activation of transfected ERK in cardiac fibroblasts. Ang II rapidly induced phosphorylation of Shc and association of Shc with Grb2. Cotransfection of the dominant-negative mutant of Ras or Raf-1 kinase abolished Ang II-induced ERK activation in cardiac fibroblasts. Overexpression of Csk or the dominant-negative mutant of Ras had no effects on Ang II-induced ERK activation in cardiac myocytes. These findings suggest that Ang II-evoked signal transduction pathways differ among cell types. In cardiac fibroblasts, Ang II activates ERKs through a pathway including the Gbetagamma subunit of Gi protein, tyrosine kinases including Src family tyrosine kinases, Shc, Grb2, Ras, and Raf-1 kinase, whereas Gq and protein kinase C are important in cardiac myocytes.

Angiotensin II↗
PubMed2005

Critical pathways in microbial virulence.

The virulence of a microbe represents a combination of complex factors including the agent's transmissibility and the severity of the disease associated with infection and is also significantly influenced by the susceptibility of the colonized host. Virulence factors may be defined as those products of the organism which are required to complete the various stages of the life cycle leading to pathology in the host. In this review, we examine some of the approaches which have been adopted in other fields of infectious disease in order to categorically identify virulence factors using a classical genetics approach with relevant models or human subjects. The absence of an accurate experimental model for periodontal disease means that our understanding of the microbial virulence determinants and pathways in this disease remains hypothetical and based largely on observations in vitro. However, factors which enable the organism to persist in spite of the elevated immune and inflammatory pressure at sites of disease are liable to be critical. Periodontal bacterial genomics is liable to make a significant impact on the field through an increased appreciation of the role of gene acquisition and gene loss in the evolution of periodontal bacteria and of the consequences of strain variation in gene content on virulence potential.

Animals↗