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PubMedDate not supplied

An introduction to case management.

Health-care professionals are constantly being challenged to find innovative ways to maintain quality of care with diminishing resources. Case management has emerged as a viable method of identifying resources and using those resources efficiently while providing the appropriate levels of care. The American Nurses Association defines case management as health assessment and planning, procurement, delivery, coordination, and monitoring to ensure that the multiple needs of the client are met. Organizations that have implemented case management report significant decreases in length of stay and substantial cost savings. The components of a successful case management team include a System Design Team to initiate the process, a Steering Committee to move the process forward, a Case Manager to coordinate and advocate for those patients who fall outside standard protocols or guidelines (critical pathways), an Interdisciplinary Specialty Team to assist in developing critical pathways, identifying variances, and evaluating data and outcomes, and an information system that provides accurate and current information. The ¿team¿ in case management team cannot be emphasized enough--medical staff and health-care providers should be involved in and understand case management practices. Collaboration and cooperation are essential to ensure patient satisfaction, hospital marketability, and presentation of a positive image to the community.

Case Management↗
PubMed2006

Is one-day hospitalization after open pyeloplasty possible and safe?

OBJECTIVES: A critical pathway was developed to determine whether open pyeloplasty could be performed in preadolescent and adolescent children with ureteropelvic junction (UPJ) obstruction with patients safely discharged after a 1-day hospitalization. METHODS: Twenty-six consecutive children who underwent open dismembered pyeloplasty for the treatment of UPJ obstruction and followed a critical pathway for preoperative education, operative management, and postoperative care were evaluated. The patients received a caudal anesthetic for preventive analgesia unless not technically possible and postoperative ketorolac (Toradol) unless contraindicated. A child was required to fulfill five strict criteria to be discharged from the hospital. RESULTS: The 26 patients with UPJ obstruction consisted of 18 boys and 8 girls (age range 2.4 months to 16.7 years). Of the 26 patients, 24 (92%) were discharged on the first postoperative day, with a mean length of hospitalization of 1.1 days (range 1 to 3). All patients younger than 6 years of age (19 patients) were discharged on the first postoperative day. Of the 25 patients who received a caudal block, 24 (96%) were discharged on the first postoperative day. All patients tolerated the procedure well without major complications. CONCLUSIONS: This is the first study, to our knowledge, to describe a detailed critical pathway for open pyeloplasty to treat UPJ obstruction. This enabled all children younger than 6 years of age and more than 90% of all patients to be discharged uniformly on the first postoperative day.

Adolescent↗
PubMedDate not supplied

Acute coronary syndromes: initial evaluation and risk stratification.

Chest pain, the second most frequent presenting complaint in the emergency department (ED), often poses a challenge to the physicians dealing with these patients owing to the wide spectrum of presentation of acute coronary syndromes (ACS). A majority of the patients presenting with chest pain are usually admitted to the hospital for further evaluation and management. Despite the availability of modern-day tools for diagnosis of acute myocardial infarction (AMI), about 5% of patients with AMI are missed in the ED with subsequent associated morbidity and mortality and legal consequences. Several centers have adapted critical pathways derived from American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the management of patients presenting with ACS. We now have some evidence suggesting adherence to the critical pathways derived from ACC/AHA guidelines will optimize the quality of patient care and probably result in better patient outcomes. This article reviews initial evaluation and the importance of risk stratification of the patients presenting with chest pain using the currently available clinical and diagnostic tools. Critical pathways derived from the ACC/AHA guidelines for various presentations of ACS are also reviewed.

Acute Disease↗
PubMed2003

Components of the Rb pathway are critical targets of UV mutagenesis in a murine melanoma model.

Epidemiological studies support a link between melanoma risk and UV exposure early in life, yet the molecular targets of UV's mutagenic actions are not known. By using well characterized murine models of melanoma, we provide genetic and molecular evidence that identifies components of the Rb pathway as the principal targets of UV mutagenesis in murine melanoma development. In a melanoma model driven by H-RAS activation and loss of p19(ARF) function, UV exposure resulted in a marked acceleration in melanoma genesis, with nearly half of these tumors harboring amplification of cyclin-dependent kinase (cdk) 6, whereas none of the melanomas arising in the absence of UV treatment possessed cdk6 amplification. Moreover, UV-induced melanomas showed a strict reciprocal relationship between cdk6 amplification and p16(INK4a) loss, which is consistent with the actions of UV along the Rb pathway. Most significantly, UV exposure had no impact on the kinetics of melanoma driven by H-RAS activation and p16(INK4a) deficiency. Together, these molecular and genetic data identify components of the Rb pathway as critical biological targets of UV-induced mutagenesis in the development of murine melanoma in vivo.

Animals↗
PubMed1991

ICAM-1-dependent pathway is critically involved in the pathogenesis of adjuvant arthritis in rats.

Intercellular adhesion molecule 1 (ICAM-1) plays important roles in immune responses. In order to examine whether ICAM-1 is involved in pathogenesis of adjuvant arthritis (AA), we investigated the effect of anti-ICAM-1 mAb, 1A29, on AA in rats. In vivo administration of 1A29 exerted a very strong suppressive effect on the development of arthritis and induced a marked reduction of inflammatory parameters. 1A29 suppressed the Ag-specific proliferative response of lymph node cells from AA rats, suggesting that the mAb blocked the Ag recognition phase. The study using adoptive transfer of AA revealed that 1A29 completely inhibited production of arthritogenic lymphocytes in donors and partially suppressed progression of arthritis in recipients caused by these lymphocytes. These findings indicated that the inhibitory effect of 1A29 on development of arthritis was at least twofold, i.e., 1) interference with cell-cell interaction between APC and T cells, which resulted in abrogation of effector cell generation; and 2) blocking of effector cell migration to inflammatory lesions. These results indicated that ICAM-1-dependent pathway is critically involved in the pathogenesis of AA. The data support the concept that ICAM-1-dependent pathways are important in chronic inflammatory disease.

Animals↗
PubMed1983

Rapid and economical identification and antimicrobial susceptibility test methodology for urinary tract pathogens.

To decrease the time and cost of processing urine cultures, we devised a critical pathway to identify and perform antibiotic susceptibility tests on commonly isolated microbial pathogens within 6 h of growth detection. The strategy was based on eliminating expensive kits and automated procedures when not required. A pathway utilizing a statistical matrix and three rapid biochemical tests required to identify the most common pathogen, Escherichia coli, was developed. This species, which represented 82% of urinary isolates, was identified in 1 h for less than 10% the cost of a commercial kit. The specificity of the 1-h E. coli identification battery was greater than or equal to 99.9% with a sensitivity of 93%. In addition, this critical pathway, adapting published methods, permitted the identification of other enteric pathogens, the group D streptococci, and Pseudomonas aeruginosa within 4 to 6 h. Furthermore, it accounted for other microbes that required longer periods of incubation. The pathway also included a rapid disk diffusion sensitivity test. Utilizing the critical pathway strategy, 76% (E. coli frequency of 0.82 X E. coli sensitivity of 0.93) of all urinary pathogens were identified within 1 h, and 98% were identified within 4 h with an antibiotic sensitivity test available within 6 h after the observation of growth. Costs were reduced from 2.5 to 5.0 times. This methodology is applicable to other specimen types.

Anti-Bacterial Agents↗
PubMed1999

Cyclic GMP pathway is critical for inducing long-term sensitization of nociceptive sensory neurons.

Noxious stimulation can trigger persistent sensitization of somatosensory systems that involves memory-like mechanisms. Here we report that noxious stimulation of the mollusc Aplysia produces transcription-dependent, long-term hyperexcitability (LTH) of nociceptive sensory neurons that requires a nitric oxide (NO)-cyclic GMP-protein kinase G (PKG) pathway. Injection of cGMP induced LTH, whereas antagonists of the NO-cGMP-PKG pathway prevented pinch-induced LTH. Co-injection of calcium/cAMP-responsive-element (CRE) blocked both pinch-induced LTH and cAMP-induced LTH, but antagonists of protein kinase A (PKA) failed to block pinch-induced LTH. Thus the NO-cGMP-PKG pathway and at least one other pathway, but not the cAMP-PKA pathway, are critical for inducing LTH after brief, noxious stimulation.

Animals↗
PubMed2004

The vascular endothelial growth factor (VEGF)/VEGF receptor 2 pathway is critical for blood vessel survival in corpora lutea of pregnancy in the rodent.

The vascular endothelial growth factor (VEGF)/VEGF receptor 2 (VEGFR-2) pathway regulates proliferation, survival, and permeability of vasculature. This pathway is active during the formation of a corpus luteum, a highly vascularized, endocrine organ with a short life span during the nonpregnant state. In the pregnant state, the life span of corpora lutea is much longer because they play a critical role in supporting pregnancy development. We hypothesized that the VEGF/VEGFR-2 pathway plays a critical role in regulating angiogenic events in the corpora lutea of pregnancy. Injection of the neutralizing anti-VEGFR-2 antibody DC101 (ImClone Systems, Inc., New York, NY) on embryonic d 3.5 (preimplantation) or 6.5 (postimplantation) disrupts function of the corpora lutea of pregnancy in CD1 mice, as evidenced by a decrease in organ size, regression of luteal vessels, and a fall in progesterone secretion within 24 h postinjection. Inhibition of the VEGFR-2 caused removal of endothelial cells, mostly through endothelial cell detachment from the vascular basement membrane. Luteal steroid-producing epithelial cells were eliminated through apoptosis secondary to vasculature becoming dysfunctional. Disruption of luteal function caused arrest of embryonic development. The effect of antibody is specific to the ovary, because pregnancy progresses normally in ovariectomized, progesterone-replaced animals treated with anti-VEGFR-2 antibody. Embryonic blood vessels were not affected directly by the antibody, because it did not reach the embryo. Administration of an antibody against VE-cadherin (E4G10), which specifically blocks endothelial proliferation, did not disrupt luteal function and pregnancy development. Thus, VEGFR-2-mediated endothelial cell signals are critical to maintain functionality of luteal blood vessels during pregnancy. Potential clinical applications of inhibitors of the VEGF/VEGFR-2 pathway include emergency contraception and medical treatment of ectopic and abnormal intrauterine pregnancies.

Animals↗
PubMed2005

Bilateral extravesical ureteral reimplantation in toilet trained children: Is 1-day hospitalization without urinary retention possible?

PURPOSE: Bilateral extravesical ureteral reimplantation has been associated with urinary retention. We developed a critical pathway and modification of surgical technique to determine whether the bilateral extravesical procedure could be performed in toilet trained children with patients discharged home after a 1-day hospitalization and without urinary retention. MATERIALS AND METHODS: A total of 50 consecutive toilet trained children were evaluated after undergoing bilateral extravesical ureteral reimplantation using a modified technique that limits ureteral dissection, ureteral mobilization and detrusor dissection to as distally as possible so that a 5:1 ratio of tunnel length to ureteral diameter can be accomplished. No surgical dissection occurs in proximity to the obliterated umbilical artery, nor is the artery ligated. Patients follow a strict postoperative critical pathway, and parents receive extensive preoperative and postoperative education. A child is required to fulfill 5 strict criteria to be discharged from the hospital. RESULTS: Patient age ranged from 1.9 to 12.8 years (mean 4.9), with 37 girls and 13 boys participating. All patients were discharged home on postoperative day 1. All patients were able to void postoperatively without any instances of urinary retention. None of the children had acute urinary tract infections or required rehospitalization. All patients had radiographic resolution of the vesicoureteral reflux on postoperative voiding cystourethrogram. CONCLUSIONS: To our knowledge this is the first study to demonstrate that bilateral extravesical ureteroneocystostomy can be performed in selected patients without postoperative urinary retention and with uniform hospital discharge in 1 day. The critical pathway and limited dissection extravesical approach are essential for this success.

Child↗
PubMed1997

Inhibition of the defense system stimulating interleukin-12 interferon-gamma pathway during critical Illness.

Interleukin-12 (IL-12) and interferon-gamma (IFN-gamma) exert protective effects during experimental endotoxemia through upregulation of cellular immunity and phagocytic functions. They are part of a positive regulatory feedback loop that enhances the production of the other. Because critically ill patients show a marked suppression of T-cell and macrophage functions with a high susceptibility to infection, potential defects in the immunity/inflammation upregulating IL-12 IFN-gamma pathway were studied. As an ex vivo model of endotoxemia, lipopolysaccharide (LPS) stimulated whole blood from 25 critically ill patients and 12 healthy individuals was incubated with either recombinant human (rh) IL-12 or rhIFN-gamma, respectively. IFN-gamma dose-dependently (P < .05) increased the release of IL-12 p40 and p70 into LPS-stimulated whole blood from healthy humans without effect in whole blood from critically ill patients. RhIL-12 p70 enhanced (P < .05) the secretion of IFN-gamma in controls, while it was ineffective in LPS-stimulated whole blood from critically ill patients. The observed inhibition of the IL-12 IFN-gamma pathway is not specific to LPS, since Staphylococcus aureus Cowan strain I (SAC)-stimulated whole blood from critically ill patients showed similar suppression. The secretion of IL-12 and IFN-gamma was less reduced in critically ill patients when using isolated cultures of adherent cells or lymphocytes. Although preculture of whole blood from healthy humans with IL-10, but not with IL-4, mimicked suppression of the IL-12 IFN-gamma pathway similar to that observed during critical illness, the release of antiinflammatory reacting cytokines (IL-4, IL-10, transforming growth factor [TGF]-beta 1) was decreased into LPS-stimulated whole blood from critically ill patients. These results indicate at least two mechanisms responsible for dramatic disturbances of the IL-12 IFN-gamma pathway during critical illness: (1) deactivation of IL-12 and IFN-gamma producing leukocytes in vivo early after the primary insult, and (2) presence of serum suppressive factors different from IL-4, IL-10, or TGF-beta 1. Because IL-12 and IFN-gamma upregulate essential immune functions, the marked inhibition of IL-12 and IFN-gamma release may be pivotal for high susceptibility of critically ill patients to infection.

Down-Regulation↗
PubMed2001

Effects of heptachlor epoxide on components of various signal transduction pathways important in tumor promotion in mouse hepatoma cells. Determination of the most sensitive tumor promoter related effect induced by heptachlor epoxide.

The effects of the organochlorine (OC) liver tumor promoter heptachlor epoxide (HE; 0, 0.1, 1, 10, and 50 microM) on several cellular tumor promoter-sensitive parameters were studied in mouse 1c1c7 hepatoma cells in an effort to identify the most sensitive biomarker for OC promoter exposure and the critical pathway and target of OC promoters. The levels of Ca2+ in the endoplasmic reticulum (ER) store, connexin43 (Cx43), PLCgamma(1), nPKCvarepsilon, and AP-1 DNA binding in nucleus were studied to screen for effects induced by submicromolar HE levels. While all the parameters tested elicited effects, particulate PLCgamma(1) and AP-1 DNA binding were found to be the most sensitive parameters affected by HE on both dose and temporal bases. Their levels were increased with 10- to 100-fold lower HE concentrations than were required to affect nPKCvarepsilon or Cx43. Further, with the lower HE dosages, particulate PLCgamma(1) and nuclear AP-1 were positively modulated by HE after 1 h versus 3 or 72 h for nPKCvarepsilon and Cx43. Ca2+ store depletion was probably the third most sensitive parameter, after AP-1 and PLCgamma(1). These results suggest the tyrosine kinase growth factor receptor pathway is the probable critical pathway for HE-induce tumor promotion with the critical target most likely being upstream of PLCgamma(1) and AP-1. This work also demonstates that upon exposure to a tumor promoter such as HE, many hepatocellular effects or changes result, suggesting that a cellular-program shift occurs similar to that described by the resistant hepatocyte model after exposure to a carcinogen or enzyme inducer.

Animals↗
PubMed2004

Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis.

To analyze the role of the classical and alternative pathways of complement activation in the effector phase of arthritis, we have induced arthritis in C3- and factor B (FB)-deficient (C3(-/-) and FB(-/-)) DBA/1J mice using well-defined monoclonal IgG2b and IgG2a antibodies to type II collagen. In control DBA/1J mice, severe swelling of the joints, destruction of cartilage and erosion of bone developed very rapidly with a 100% incidence and a peak on days 7-10. Although 75% of C3(-/-) mice developed arthritis, the clinical severity was very mild and the onset was delayed. Severity of arthritis in FB(-/-) mice ranked intermediate in comparison with C3(-/-) and control mice with an incidence of 100%. Immunohistochemical analysis of the inflamed joints demonstrated substantial reduction in macrophage and neutrophilic leukocyte infiltration in both C3(-/-) and FB(-/-) mice, thereby confirming the clinical findings. We conclude that both the classical and the alternative pathways of complement activation are involved in the effector phase of arthritis.

Animals↗
PubMed2001

Cardiovascular critical event pathways for the progression of heart failure; a report from the ATLAS study.

AIMS: To determine the sequence of critical cardiovascular events in the progression of heart failure, and whether aetiology or high-dose vs low-dose lisinopril affected these pathways. METHODS AND RESULTS: This was a post-hoc investigation of the ATLAS database, which comprised 3164 patients with chronic heart failure, randomized to low- (2.5-5.0 mg. day(-1)) or high-dose (32.5-35.0 mg. day(-1)) lisinopril, followed up for a median of 46 months. Two-thirds (64.3%) of patients had heart failure attributed to ischaemic heart disease. During the study, most patients (61.1%) had at least one cardiovascular hospitalization and 42.5% of all patients died: most deaths (88.2%) were cardiovascular. Nearly half (49.7%) of the cardiovascular deaths were considered sudden and 45.2% of cardiovascular deaths occurred as the first cardiovascular event. A third (30.2%) of deaths resulted from heart failure and were generally preceded by hospitalization, either for heart failure (85.5%), myocardial ischaemic events (21.7%) or arrhythmias (18.0%). Compared with low-dose, high-dose lisinopril was associated with a lower risk of death or hospitalization for any reason (P=0.002) and death or hospitalization with worsening heart failure (P<0.001). High-dose lisinopril delayed the time to all-cause mortality and hospitalization for chronic heart failure by 7.1 months. CONCLUSIONS: Vascular and arrhythmic events may not only be important precipitants of sudden death, but were also seen to contribute to the progression of heart failure. A reduction in vascular events, as well as benefits on ventricular remodelling, could account for the decrease in death or hospitalization with high-dose lisinopril.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

STAT-4 mediated IL-12 signaling pathway is critical for the development of protective immunity in cutaneous leishmaniasis.

Recent studies have demonstrated that two IL-12 signaling pathways, a STAT 4 - dependent and STAT4 - independent, are involved in the development of a Th1-like response. To determine their roles in the development of protective immunity against Leishmania major, we monitored progression of cutaneous Leishmania major infection in STAT4-deficient mice (STAT4-/-) compared to similarly infected wild-type (STAT4+/+) mice. Although the onset of lesion growth was delayed in STAT4-/- mice during the early phase of infection, these mice eventually developed large, non-healing lesions, whereas STAT4+/+ mice resolved their lesions. As infection progressed, both STAT4+/+ and STAT4-/- mice infected with L. major displayed similar titers of Leishmania-specific IgG1 and IgE but later produced lower IgG2a. On days 20 and 40 post-infection, Leishmania antigen-stimulated lymphnode cells from STAT4-/- mice produced significantly lower amounts of IFN-gamma than those from STAT4+/+ mice as measured by enzyme-linked immunosorbent assay. There was no significant difference, however, in IL-4 and IL-12 production between the two groups. These results indicate that STAT4-mediated IL-12 signaling is critical for the development of protective Th1 response following L. major infection in genetically resistant mice. Additionally, they demonstrate that, although genetically resistant mice lacking STAT4 signaling pathway develop large, non-healing lesions, they do not default towards a Th2-like response.

Animals↗
PubMedDate not supplied

The CQI pathway.

The use of CQI to identify issues, processes, and methods of quality management was a favorable learning experience for the Botsford General rehabilitation staff. They experienced improved interdepartmental communication and enhanced understanding of the roles and responsibilities of other disciplines, as well as the overall CQI process. The use of the CQI process accomplished the objective of decreasing the length of stay of patients with amputations by 6 to 8 days, thereby reducing costs. Use of flowcharting to outline a typical patient stay from admission to discharge helped to clarify potential problems, eliminate unnecessary steps, and reduce documentation time. Although rehabilitation services are currently exempt from diagnosis-related group application, in order to maintain cost efficiency and service effectiveness, it behooves us to continually track and stay in line with the competition. In light of anticipated health care reforms, the rehabilitation industry must be proactive in its management of service delivery with an emphasis on functional outcomes. Botsford General's success with using a critical pathway for the amputee program as part of a program evaluation system will lead to the development of critical pathways for additional diagnoses.

Algorithms↗
PubMed2000

Mutational analysis of the CTNNB1 and APC genes in uterine endometrioid carcinoma.

Despite recent studies, the molecular genetic events responsible for the development of uterine endometrioid carcinoma (UEC) remain incompletely characterized. Mutations in the beta-catenin (CTNNB1) gene have been recently reported in a small percentage of UECs and in the endometrioid variant of ovarian carcinoma suggesting that the Wnt signal transduction pathway is involved in the development of female genital tract tumors with endometrioid morphology. The Wnt pathway is a critical pathway in the development of colorectal cancer (CRC) with mutations occurring in the beta-catenin (CTNNB1) or adenomatous polyposis coli (APC) genes in 10 to 15% and 85% of cases, respectively. Because UEC and CRC share other molecular genetic alterations and histologic features and previous studies of UEC have not reported an analysis of the APC gene, we chose to further elucidate the role of the Wnt pathway in UEC. To this end, we analyzed 32 cases of UEC for mutations of the CTNNB1 and APC genes. Mutations of CTNNB1 were present in six of 32 (18%) cases: four grade 1 carcinomas, one grade 2, and one grade 3 carcinoma. Five missense mutations were identified, three involving Ser/Thr phosphorylation sites and two adjacent to a Ser phosphorylation site. One case contained a deletion encompassing codons 34 to 37, which includes a Ser phosphorylation site. No mutations resulting in truncation of the APC protein were found. Our results support a role for the Wnt signaling pathway via mutation of CTNNB1, but not APC, in the development of a subset of UECs.

Blotting, Western↗