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Even the little guys can make use of protocols. A clinical pathway program at 80-bed Valley View Hospital in Glenwood Springs, CO, has saved the facility millions of dollars and hundreds of bed days.
AIM: The aim of this research was to draw a pathway diagram for people with mental disorders in Psie Pole epidemiological catchment area, which significantly differs from Zabkowice epidemiological catchment area because of urbanisation and social status of citizens. Then to compare data characterising both pathways diagrams. METHOD: In the period of two months between 1st February 2001 and 31st March 2001 all patients age 15 and over who applied to the Psychiatric Service in the "Psie Pole" epidemiological catchment area, were assessed by psychiatrists for their eligibility to enter the study. Those who had fulfilled the entry criteria were interviewed using a Polish version of WHO's encounter form (EF) by the mental health professionals during their initial interview. Data from both catchment areas were compared. RESULTS: In the "Psie Pole" and "Zabkowice" catchments areas the main pattern of pathways to psychiatric care was similar. There were significant differences in the symptoms presented, diagnoses and intervals between both epidemiological catchment areas. CONCLUSIONS: The urban/semi urban and social status differences didn't influence the pathways to psychiatric care in "Psie Pole" and "Zabkowice" catchment areas.
A study at one medical center showed that nurses were spending 2.5 hours per shift documenting patient care. After charting by exception was integrated with a clinical pathway, charting time dropped to 0.82 hours per shift. Results of a pilot project on an orthopedic/neurologic patient care unit are discussed.
Mitogen-activated protein kinase (MAPK) signaling pathways are critical for the sensing and response of eukaryotic cells to extracellular changes. In Schizosaccharomyces pombe, MAPK Pmk1/Spm1 has been involved in cell wall construction, morphogenesis, cytokinesis, and ion homeostasis, as part of the so-called cell integrity pathway together with MAPK kinase kinase Mkh1 and MAPK kinase Pek1. We show that Pmk1 is activated in multiple stress situations, including hyper- or hypotonic stress, glucose deprivation, presence of cell wall-damaging compounds, and oxidative stress induced by hydrogen peroxide or pro-oxidants. The stress-induced activation of Pmk1 was completely dependent on Mkh1 and Pek1 function, supporting a nonbranched pathway in the regulation of MAPK activation. Fluorescence microscopy revealed that Mkh1, Pek1, and Pmp1 (a protein phosphatase that inactivates Pmk1) are cytoplasmic proteins. Mkh1 and Pek1 were also found at the septum, whereas Pmk1 localized in both cytoplasm and nucleus as well as in the mitotic spindle and septum during cytokinesis. Interestingly, Pmk1 subcellular localization was unaffected by stress or the absence of Mkh1 and Pek1, suggesting that its activation by the Mkh1-Pek1 cascade takes place at the cytoplasm and/or septum and that the active and inactive forms of this kinase cross the nuclear membrane. Cdc42 GTPase and its effectors, p21-activated kinases Pak2 and Pak1, are not upstream elements controlling the basal level or the stress-induced activation of Pmk1. However, Sty1 MAPK was essential for proper Pmk1 deactivation after hypertonic stress in a process regulated by Atf1 transcription factor. These results provide the first evidence for the existence of cross-talk between two MAPK cascades during the stress response in fission yeast.
Using a novel flow chamber assay system and whole blood, we show that leukocytes from septic individuals have a four-fold elevation of adhesion, but not rolling, on a P-selectin/beta2-integrin substrate. Most leukocytes from septic patients (but not healthy controls) that bound vascular cell adhesion molecule 1 (VCAM-1) were neutrophils. All adhesion was inhibited with an antibody specific for the VCAM-1 ligand alpha4-integrin. The alpha4-integrin was present on neutrophils from septic patients but not on neutrophils from patients with localized bacterial infections. The plasma milieu of septic patients was sufficient to induce neutrophils from healthy subjects to bind VCAM-1 under flow conditions. This is the first description of alpha4-integrin/VCAM-1 pathway of neutrophil recruitment in human disease. This pathway may provide a new therapeutic target to reduce inappropriate neutrophil adhesion without altering the normal yet critical beta2-integrin-mediated adhesive function of neutrophils.
OBJECTIVE: To study the effects of an inpatient asthma clinical pathway on the processes and outcomes for children who were admitted to a hospital for the treatment of asthma. DESIGN: Before-and-after study. SETTING: A private nonprofit academic children's hospital in Seattle, Wash. PATIENTS AND METHODS: Three hundred forty-two admissions of 297 patients in the first year of the asthma clinical pathway were compared with 353 admissions of 292 similar patients in the previous year. Patients who required intensive care, were younger than 2 years, or had a major chronic disease were excluded. INTERVENTION: Asthma was chosen for the development of a clinical pathway because of its large number of admissions, involvement of multiple health care providers (nurses, physicians, and respiratory therapists), predictable hospital course, and variable lengths of hospital stay. The pathway was a consensus-based guideline for patient management that was intended to be adapted to the care of an individual patient. Prior to the implementation of the clinical pathway, nurses, attending physicians, house staff, and respiratory therapists were trained in its use. The main hospital chart of each patient who was admitted to the pathway had a flowchart that outlined day-to-day guidelines for monitoring and care. Nursing staff were responsible for documenting when a patient's care varied from the pathway, and these variances were entered into a computer database. OUTCOME MEASURES: Use of peak flowmeters, steroids, laboratory studies, radiological studies, and respiratory therapy was assessed by analyzing the patients' electronic billing records. For patients enrolled in the pathway, additional data on process of care were obtained by analyzing the variance database. For both groups, the total charges, length of stay, and rate of readmission to the hospital were measured by use of the billing records. RESULTS: There were no significant differences in the use of steroids or peak flowmeters, average lengths of stay, or total charges between the 2 groups. However, patients in the "pathway group" had significantly lower average charges for laboratory ($26 vs $39; P < .05) and radiology ($32 vs $55; P < .001) services. Variances from the pathway guidelines were most often related to the patients' responses to therapy. CONCLUSIONS: The asthma clinical pathway had no effect on clinical outcomes and small effects on the use of resources. Further development, including physician and nurse training, computer and administrative support, and clinical severity scales, are needed to develop the potential utility of the clinical pathway as a research and quality assurance tool.
OBJECTIVE: The current study describes the short-term outcome of 61 inpatients with anorexia nervosa (AN), utilizing a standardized protocol that could be completed by most patients within the typical length of stay (LOS) in an academic medical center in our geographic area. METHOD: Patients were placed on disorder-specific and medication clinical pathways and completed questionnaires at admission and discharge. Diagnostic, historical, demographic, and treatment-related information was obtained. RESULTS: Treatment was sufficient to resolve acute medical problems, initiate refeeding, and interrupt compensatory behaviors, but continued intensive treatment will be critical to full recovery. Patients were discharged at an average of 85% of ideal body weight (IBW). Twenty patients were discharged against medical advice (AMA). Clinical and demographic variables poorly predicted AMA status. DISCUSSION: Attainable inpatient treatment goals in our care environment appear to be > or = 80% IBW at discharge, resolution of acute medical problems, and interruption of compensatory behaviors. Future research should examine whether shorter LOS increases readmission rates or long-term costs.
BACKGROUND: Oleoyl-estrone elicits powerful slimming effects on lean and obese rats, sparing protein, lowering appetite and maintaining energy expenditure. Leptin synthesis is markedly reduced by oleoyl-estrone. However, this effect is not observed in the obese Zucker fa/fa rats; these rats do not fully respond to leptin but they lose fat under oleoyl-estrone treatment. AIM OF THE STUDY: To determine the role of leptin in the conversion of estrone to fatty-acyl estrone in white adipose tissue both in vivo in Zucker lean and obese rats, and in vitro. METHODS: Two series of experiments were performed: a) Growth and differentiation of 3T3L1 preadipocytes into adipocytes followed by incubation with tritium-labeled estrone in the medium in the presence/absence of 1 nM leptin, and estimation of the incorporation of label into estrone and estrone ester fractions of cell extracts. b) Zucker lean (Fa/?) [ZL] and obese (fa/fa) [ZO] rats were injected i.v. with carrier-free oleoyl-estrone in chylomicra-sized liposomes, then euthanized after 10 min. Free and esterified estrone were measured in blood, liver, muscle, skin, white adipose tissue (WAT), and brown adipose tissue (BAT). RESULTS: In the first study, in a 72-h incubation, adipocytes took up 20-27% of the medium estrone. In the leptin(-) controls, 47% of the label in the cell fraction was in the form of estrone esters and 45% as free estrone; in the leptin(+) cells, 71% of the label was in the estrone ester fraction and 24% was free estrone. In the second study, a large part of the injected tritium-label remained in the ZO blood, with only a small part remaining in ZL. In ZL 39% of the label was found in the tissues in the form of free estrone, and in ZO only 22%; in both cases about half of it was in WAT. Plasma free estrone levels were 0.3 +/- 0.1 nM in ZL and 0.5 +/- 0.3 nM in ZO, and esterified estrone was 242 +/- 99 nM for ZL and 201 +/- 29 nM for ZO. Plasma leptin levels were 1.73 +/- 0.16 ng/ml in ZL and 61.0 +/- 1.4 ng/ml in ZO. CONCLUSION: The presence of an infact leptin pathway is critical for the uptake and synthesis of estrone esters as well as for the plasma acyl-estrone turnover. The presented results show a direct relationship between oleoyl-estrone and leptin in the WAT. A fully functional leptin pathway is needed for the synthesis of acyl-estrone and the removal of free estrone from the bloodstream, as well as for the disposal of excess circulating oleoyl-estrone. This has a direct bearing on human and animal obesity, since estrone induces increases in fat deposition.
The ATR-Claspin-Chk1 pathway is critical for turning on the cellular response to DNA damage and replication stress. Five recent reports uncover new mechanisms controlling the recovery phase of the checkpoint response, and introduce crucial roles for Claspin, Rad17 phosphorylation and the ubiquitin proteasome pathway in Chk1 signaling.
The human immunodeficiency virus-1 (HIV-1), the causative agent of autoimmune deficiency syndrome (AIDS) is a major health problem world-wide. Central to HIV infection is the transactivator protein Tat, that plays a critical role in the nucleus during the HIV infectious cycle, by binding the transactivation-responsive region (TAR) and thereby enhancing transcriptional elongation. Tat appears to gain nuclear entry through a novel mechanism, independent of the normal cellular importin/Ran-dependent pathways, and regulated by a cytoplasmic retention mechanism. Since blocking Tat nuclear import is likely to prevent HIV infection, detailed delineation of Tat's nuclear import pathway is critical to assessing its viability as a therapeutic target. Other feasible anti-HIV therapies include approaches to inhibit Tat-TAR interaction.
Identification of alternative pathways of caspase activation is an important step to develop new antitumor treatments. We report here the result of a screening with a small chemical library, the Developmental Therapeutics Program-National Cancer Institute "challenge set," on cells expressing mutated caspase-9. We have identified two molecules capable of activating an apoptosome-independent apoptotic pathway. These compounds, named F6 and G5, target the ubiquitin-proteasome system by inhibiting the ubiquitin isopeptidases. We have shown that F6 and G5 induce a rather unique apoptotic pathway, which includes a Bcl-2-dependent but apoptosome-independent mitochondrial pathway with up-regulation of the BH3-only protein Noxa, stabilization of the inhibitor of apoptosis antagonist Smac, but also the involvement of the death receptor pathway. Noxa plays an important role in the induction of mitochondrial fragmentation and caspase activation, whereas the death receptor pathway becomes critical in the absence of a functional apoptosome. This study suggests that screening of chemical libraries on cancer cells with defined mutations in apoptotic key elements can lead to the identification of compounds that are useful to characterize alternative pathways of caspase activation.
BACKGROUND: Inequalities of service use across ethnic groups are important to policy makers, service providers and service users. AIMS: To identify ethnic variations in pathways to specialist mental health care, continuity of contact, voluntary and compulsory psychiatric in-patient admissions; to assess the methodological strength of the findings. METHOD: A systematic review of all quantitative studies comparing use of mental health services by more than one ethnic group in the UK. Narrative analysis supplemented by meta-analysis, where appropriate. RESULTS: Most studies compared Black and White patients, finding higher rates of in-patient admission among Black patients. The pooled odds ratio for compulsory admission, Black patients compared with White patients, was 4.31 (95% CI 3.33-5.58). Black patients had more complex pathways to specialist care, with some evidence of ethnic variations in primary care assessments. CONCLUSIONS: There is strong evidence of variation between ethnic groups for voluntary and compulsory admissions, and some evidence of variation in pathways to specialist care.
Despite significant progress in breast cancer treatment, mammary tumours still represent the second most frequent cause of cancer-related death in women in the US, with > 211,000 new cases in 2005; however, an expanding range of options for early diagnosis and more reliable risk assessment offers new alternatives for disease control by cancer prevention. Completed large studies with the classical selective estrogen receptor modulator (SERM) tamoxifen have demonstrated that preventing breast cancer pharmacologically is now possible. Novel SERMs, aromatase inhibitors and gonadotropin-releasing hormone agonists targeting hormonal pathways are being tested in clinical trials, revealing the potential for dramatic reductions in tumour incidence with minimal side effects; however, SERMs and aromatase inhibitors are effective only against estrogen receptor-positive tumours, thus chemopreventive drugs targeting other critical signalling pathways (such as retinoids, selective COX inhibitors and tyrosine kinase inhibitors) may provide a means to prevent estrogen receptor-negative breast cancer. In the future, hormonal and estrogen receptor-independent agents may be combined to prevent the development of all mammary tumours. This article reviews the current and novel strategies for breast cancer prevention.
After discovering that stroke patients were receiving care on 18 different units within the hospital, St. Luke's Medical Center in Milwaukee developed its first cross-unit clinical pathway, targeted at cerebrovascular accident (CVA) patients. Implemented in October 1996, the five-day CVA pathway has cut length of stay by 1.6 days while maintaining a patient satisfaction rating of 94%. Nurse clinicians developed five key outcomes for the CVA pathway, including visits from speech therapy, a physiatry referral, a severity assessment, patient education, and patient consultation on the details of the discharge plan.
The quality movement has gone through three phases in this century. The first, quality assurance, emphasized reacting to problems and identifying "bad apples." The second, quality improvement, shifted the focus from individuals to processes but still retained a reactive problem-solving approach to improving the quality of products and services. The third phase, quality management, has gained strength in other industries over the years. The article presents a quality management, or "next generation quality," model for health care centered on clinical pathways as core clinical processes that are continuously improved and monitored through an improved version of variance management systems called the gateway model.
The first two goals of health care must always be quality care and achievement of patient outcomes. In today's health care environment, these goals are achieved with an eye on the financial picture. Cost-saving efforts by decreasing LOS, decreasing the use of ICUs, and lowering laboratory and radiologic expenses without affecting the quality of care are requirements in today's setting. The process of creating a clinical pathway for patients undergoing CEA can help to examine your care and determine evidence-based practice.
AIM: To evaluate the impact on the clinical service of incorporating cardiac troponin T (cTnT) measurement into the existing chest pain care pathway in our district general hospital. METHODS: We randomised 200 consecutive patients admitted with acute chest pain, but without ST elevation on ECG, either to our existing chest pain care pathway (pathway 1) or to a new pathway incorporating semi-quantitative cTnT measurement (pathway 2). RESULTS: In comparison with pathway 1, in pathway 2 there was a strong trend towards reduced length of stay (3.13 v 4.36 days, p=0.08), and reduced usage of low molecular weight heparin (LMWH) (4.59 v 5.45 doses per patient, p=0.05). The number of cardiac events at three months in care pathway 1 (14/92) and care pathway 2 (22/108) did not significantly differ, p=0.34. In patients with atypical chest pain, there was a tendency for cardiologists to discharge earlier (1.75 v 2.03 days, p=0.07) and use less LMWH (2.04 v 2.97 doses, p=0.06) than general physicians. CONCLUSION: In this study, incorporation of cTnT measurement into a chest pain care pathway resulted in a strong trend towards reduced length of hospital stay and LMWH usage.
The Clinical Care Costing Method (CCCM for the Home Health Care Classification (HHCC) System provides an innovative way to determine the cost of clinical nursing practice. This costing methodology consists of three major nursing indicators--Care Components, Actions and Outcomes. These three indicators require Clinical Care Pathways (CCP) to document, track, and code clinical care using the HHCC System. The clinical care costs and/or resources are derived from the time and frequencies of the Action Types for the specific nursing interventions performed by the different type of health care providers to achieve the Outcomes and resolve the Care Component that are used to classify nursing diagnoses/patient problems. This method can also be used to deter-mine the reimbursement for nursing care services retrospectively and once validated prospectively. The Clinical Pathway data provide the evidence that the nursing interventions achieve the desired outcomes.