Nursing Praxis for Reducing Documentation Burden Within Nursing Admission Assessments.

The purpose of this quality improvement project was to conduct a scholarly assessment of the information collected within the nursing admission encounter and implement content revisions across three pilot medical surgical units. The guiding principles were to preserve regulatory information, identify nurse-sensitive data, and eliminate nonessential information. The goal was to decrease the number of clicks and time expended to document electronically an acute admission encounter by 20% and to project the number of hours returned to patient care as a result of decreasing computer clicks. A second goal was to quantify the projected costs of completing a nursing admission encounter. This quality improvement project leveraged nurse executive competencies to intersect the nursing process to develop a nursing documentation praxis. This author's praxis reduced nursing documentation burden in clicks by 29% and reduced time to document on an admission encounter by 34%. This restored the focus on nurse-patient interactions by returning 1016 hours per year to patient care activities, across three pilot units, as well as quantified the costs of completing a nursing admission assessment to utilize in future cost analysis of nursing tasks.

The Expressions of Hope in the Face of Complex Surgery: Experiences of Patients and Their Loved Ones.

BACKGROUND: Lung volume reduction surgery (LVRS), a reduction in damaged lung tissue in end-stage chronic obstructive pulmonary disease, is a breakthrough surgical procedure requiring months of rigorous screening, testing, and conditioning. Engaging in this process is prolonged and challenging with no research found exploring patients and loved ones' experiences through this demanding process. OBJECTIVE: The purpose was to examine the experience of LVRS for patients and loved ones as they encounter the complex preparation required prior to, during, and throughout the extended convalescence following surgery. METHODS: A mixed-methods approach was used, combining health outcomes with interview data. Participants and loved ones were purposefully selected, invited, and consented during the perioperative phase of LVRS. Quantitative data were obtained via chart review, while qualitative data were gathered through a 2-stage interview process, preoperatively and postoperatively. Qualitative data were analyzed using naturalistic inquiry approaches. RESULTS: Patients and loved ones described difficulties of living with illness during the preoperative phase, and expressed relief and joy for an improved quality of life afterward. The overarching theme uncovered was hope. Preoperatively, hope was coupled with anxiety about the upcoming surgery and potential outcomes, whereas the hope expressed after surgery focused on the future, in particular, a shared future. Statistically significant differences were found in the quality of life measures. CONCLUSION: For both patients and loved ones, LVRS is filled with hope for a more expansive future. Although that future is unclear prior to surgery, clarification and a new normal signals hope for a shared future following LVRS.

See You in 7: improving acute myocardial infarction follow-up care.

Acute myocardial infarction (AMI) follow-up care is a crucial part of the AMI recovery process. The American College of Cardiology's 'See You in 7 Challenge' advocates that all patients discharged with a diagnosis of AMI have a cardiac rehabilitation referral made and outpatient cardiac rehabilitation appointment scheduled to occur within 7 days of hospital discharge. A streamlined AMI cardiac rehabilitation referral and appointment scheduling process was not in place at this urban academic medical centre. To develop the streamlined processes, a Six Sigma project was initiated. Four months before the intervention, 1/38 patients with AMI (2.6%) were scheduled to have the initial outpatient cardiac rehabilitation appointment occur within 7 days of hospital discharge, with an average 18.7 days from hospital discharge to the scheduled initial outpatient cardiac rehabilitation appointment. To reduce the time to this initial appointment, availability of outpatient cardiac rehabilitation appointments was increased, additional staff were trained in appointment scheduling and insurance verification processes and appointments were scheduled prior to hospital discharge. After intervention, the number of patients scheduled to attend an outpatient cardiac rehabilitation appointment within 7 days of hospital discharge improved to 72/79 (91.1%) (two-proportion test, p<0.001). Days from hospital discharge to first scheduled outpatient cardiac rehabilitation appointment were reduced from 18.7 days to 6.3 days (a 66.3% reduction) (Mann-Whitney U test, p<0.01). Initial outpatient cardiac rehabilitation attendance within 7 days of hospital discharge increased from 1/38 (2.6%) to 42/79 (53.2%) (a 50.6% increase) (two-proportion test, p<0.001).

What Is It Like to Experience Improved Care Coordination Through a Community Outreach Program? A Qualitative, Descriptive Study.

Community-based programs deploying community health workers (CHWs) who collaborate with other entities are beginning to emerge as the US health system evolves. Although these programs have used various evaluation criteria to determine program success, little research has been completed to examine the experiences of program participants as they receive these services. The purpose of this qualitative descriptive study was to describe what it was like to experience the benefit of improved care coordination through a community-based program featuring CHWs, in collaboration with community-based interprofessional providers. Knowing the help I needed emerged as the overarching theme.

Influencing Commitment to BSN Completion: A Pilot Project Using Motivational Interviewing.

The 2010 Institute of Medicine's Future of Nursing report posed recommendations to increase numbers of nurses with baccalaureate degrees or greater to 80%. This project engaged associate degree nurses in motivational interviewing focusing on finding and removing barriers to baccalaureate matriculation and completion. Results indicated a statistically significant influence on attitudes and return-to-school decision making and identified a qualitative theme: "I know more now… I could be a better nurse."

Introduction of the six major genomic deletions of modified vaccinia virus Ankara (MVA) into the parental vaccinia virus is not sufficient to reproduce an MVA-like phenotype in cell culture and in mice.

Modified vaccinia virus Ankara (MVA) has a highly restricted host range in cell culture and is apathogenic in vivo. MVA was derived from the parental chorioallantois vaccinia virus Ankara (CVA) by more than 570 passages in chicken embryo fibroblast (CEF) cells. During CEF cell passaging, six major deletions comprising 24,668 nucleotides occurred in the CVA genome. We have cloned both the MVA and the parental CVA genome as bacterial artificial chromosomes (BACs) and have sequentially introduced the six major MVA deletions into the cloned CVA genome. Reconstituted mutant CVA viruses containing up to six major MVA deletions showed no detectable replication restriction in 12 of 14 mammalian cell lines tested; the exceptions were rabbit cell lines RK13 and SIRC. In mice, CVA mutants with up to three deletions showed slightly enhanced virulence, suggesting that gene deletion in replicating vaccinia virus (VACV) can result in gain of fitness in vivo. CVA mutants containing five or all six deletions were still pathogenic, with a moderate degree of attenuation. Deletion V was mainly responsible for the attenuated phenotype of these mutants. In conclusion, loss or truncation of all 31 open reading frames in the six major deletions is not sufficient to reproduce the specific MVA phenotype of strong attenuation and highly restricted host range. Mutations in viral genes outside or in association with the six major deletions appear to contribute significantly to this phenotype. Host range restriction and avirulence of MVA are most likely a cooperative effect of gene deletions and mutations involving the major deletions.

An innovative approach to standardizing heart failure care: the heart failure support team.

PURPOSE: The purpose of this project was to determine if a comprehensive program of heart failure support using a three-step approach during acute care led by an advanced practice nurse (APN) improves outcomes. The goal was to implement Centers for Medicare and Medicaid Services (CMS) appropriate care recommendations for all patients with heart failure, reducing variation, and increasing quality of care. DATA SOURCES: Retrospective hospital chart reviews demonstrated patients were being admitted with one diagnosis, but ultimately discharged under the heart failure diagnosis-related group (DRG). Because these patients had not been identified as heart failure patients during hospitalization, we discovered an opportunity to improve care through program development. CONCLUSIONS: Once this approach was implemented consistently and sustained, we achieved near-perfect CMS scores. Composite quality scores for patients with heart failure improved from 82.12% to 100%. Electronic tracking of patients after referrals from multiple sources became the keystone of the program, facilitating early identification, teaching, and ongoing patient monitoring. IMPLICATIONS FOR PRACTICE: A comprehensive approach to heart failure support using a team is recommended. However, research is needed to determine if this approach improves quality of life, hospital readmission rates, or lengths of stay for this vulnerable population.

Immediate-early expression of a recombinant antigen by modified vaccinia virus ankara breaks the immunodominance of strong vector-specific B8R antigen in acute and memory CD8 T-cell responses.

Efficient T-cell responses against recombinant antigens expressed by vaccinia virus vectors require expression of these antigens in the early phase of the virus replication cycle. The kinetics of recombinant gene expression in poxviruses are largely determined by the promoter chosen. We used the highly attenuated modified vaccinia virus Ankara (MVA) to determine the role of promoters in the induction of CD8 T-cell responses. We constructed MVA recombinants expressing either enhanced green fluorescent protein (EGFP) or chicken ovalbumin (OVA), each under the control of a hybrid early-late promoter (pHyb) containing five copies of a strong early element or the well-known early-late p7.5 or pS promoter for comparison. In primary or cultured cells, EGFP expression under the control of pHyb was detected within 30 min, as an immediate-early protein, and remained higher over the first 6 h of infection than p7.5- or pS-driven EGFP expression. Repeated immunizations of mice with recombinant MVA expressing OVA under the control of the pHyb promoter led to superior acute and memory CD8 T-cell responses compared to those to p7.5- and pS-driven OVA. Moreover, OVA expressed under the control of pHyb replaced the MVA-derived B8R protein as the immunodominant CD8 T-cell antigen after three or more immunizations. This is the first demonstration of an immediate-early neoantigen expressed by a poxviral vector resulting in superior induction of neoantigen-specific CD8 T-cell responses.

Antiviral CD8 T cells recognize borna disease virus antigen transgenically expressed in either neurons or astrocytes.

Borna disease virus (BDV) can persistently infect the central nervous system (CNS) of mice. The infection remains nonsymptomatic as long as antiviral CD8 T cells do not infiltrate the infected brain. BDV mainly infects neurons which reportedly carry few, if any, major histocompatibility complex class I molecules on the surface. Therefore, it remains unclear whether T cells can recognize replicating virus in these cells or whether cross-presentation of viral antigen by other cell types is important for immune recognition of BDV. To distinguish between these possibilities, we used two lines of transgenic mice that strongly express the N protein of BDV in either neurons (Neuro-N) or astrocytes (Astro-N). Since these animals are tolerant to the neo-self-antigen, we adoptively transferred T cells with specificity for BDV N. In nontransgenic mice persistently infected with BDV, the transferred cells accumulated in the brain parenchyma along with immune cells of host origin and efficiently induced neurological disease. Neurological disease was also observed if antiviral T cells were injected into the brains of Astro-N or Neuro-N but not nontransgenic control mice. Our results demonstrate that CD8 T cells can recognize foreign antigen on neurons and astrocytes even in the absence of infection or inflammation, indicating that these CNS cell types are playing an active role in immune recognition of viruses.

Pathogenic potential of borna disease virus lacking the immunodominant CD8 T-cell epitope.

Borna disease virus (BDV) is a highly neurotropic, noncytolytic virus. Experimentally infected B10.BR mice remain healthy unless specific antiviral T cells that infiltrate the infected brain are triggered by immunization. In contrast, infected MRL mice spontaneously mount an antiviral T-cell response that can result in meningoencephalitis and neurological disease. The antiviral T cells may, alternatively, eliminate the virus without inducing disease if they are present in sufficient numbers before the virus replicates to high titers. Since the immune response of H-2(k) mice is directed mainly against the epitope TELEISSI located in the viral nucleoprotein N, we generated BDV mutants that feature TQLEISSI in place of TELEISSI. We show that adoptive transfer of BDV N-specific CD8 T cells induced neurological disease in B10.BR mice persistently infected with wild-type BDV but not with the mutant virus expressing TQLEISSI. Surprisingly, the mutant virus replicated less well in adult MRL wild-type mice than in mutant mice lacking mature CD8 T cells. Furthermore, when MRL mice were infected with the TQLEISSI-expressing BDV mutant as newborns, neurological disease was observed, although at a lower rate and with slower kinetics than in mice infected with wild-type virus. These results confirm that TELEISSI is the major CD8 T-cell epitope in H-2(k) mice and suggest that unidentified minor epitopes are present in the BDV proteome which are recognized rather efficiently by antiviral T cells if the dominant epitope is absent.

CD8 T cells require gamma interferon to clear borna disease virus from the brain and prevent immune system-mediated neuronal damage.

Borna disease virus (BDV) frequently causes meningoencephalitis and fatal neurological disease in young but not old mice of strain MRL. Disease does not result from the virus-induced destruction of infected neurons. Rather, it is mediated by H-2(k)-restricted antiviral CD8 T cells that recognize a peptide derived from the BDV nucleoprotein N. Persistent BDV infection in mice is not spontaneously cleared. We report here that N-specific vaccination can protect wild-type MRL mice but not mutant MRL mice lacking gamma interferon (IFN-gamma) from persistent infection with BDV. Furthermore, we observed a significant degree of resistance of old MRL mice to persistent BDV infection that depended on the presence of CD8 T cells. We found that virus initially infected hippocampal neurons around 2 weeks after intracerebral infection but was eventually cleared in most wild-type MRL mice. Unexpectedly, young as well as old IFN-gamma-deficient MRL mice were completely susceptible to infection with BDV. Moreover, neurons in the CA1 region of the hippocampus were severely damaged in most diseased IFN-gamma-deficient mice but not in wild-type mice. Furthermore, large numbers of eosinophils were present in the inflamed brains of IFN-gamma-deficient mice but not in those of wild-type mice, presumably because of increased intracerebral synthesis of interleukin-13 and the chemokines CCL1 and CCL11, which can attract eosinophils. These results demonstrate that IFN-gamma plays a central role in host resistance against infection of the central nervous system with BDV and in clearance of BDV from neurons. They further indicate that IFN-gamma may function as a neuroprotective factor that can limit the loss of neurons in the course of antiviral immune responses in the brain.

The functional avidity of virus-specific CD8+ T cells is down-modulated in Borna disease virus-induced immunopathology of the central nervous system.

Borna disease virus (BDV) infection of the central nervous system (CNS) leads to severe neurological symptoms in susceptible MRL mice. The disease is mainly mediated by CD8+ T cells specific for the immunodominant epitope TELEISSI in the BDV nucleoprotein. In this study, TELEISSI/MHC class I tetramers were used to directly visualize antigen-specific CD8+ T cells. We found that on average approximately 30% of the ex vivo analyzed CD8+ T cells in the CNS of diseased mice were specific for TELEISSI. Unexpectedly, the frequency of tetramer-reactive brain-derived CD8+ T cells doubled following overnight culture in the absence of antigen. The majority of CD8+ T cells showed enhanced tetramer binding without up-regulation of T cell receptor surface expression. The frequency of IFN-gamma-secreting CD8+ T cells after antigen-specific stimulation was higher in overnight cultures than in freshly isolated BDV-specific brain lymphocytes, and enhanced tetramer binding correlated with elevated sensitivity to lower levels of peptide antigen in cytotoxicity assays. These results indicate that the functional avidity of virus-specific CD8+ T cells was down-modulated in vivo. Thus, quantification of tissue-infiltrating CD8+ T cells by the tetramer technique must be interpreted with caution as it may underestimate the real frequency of antigen-specific CD8+ T cells.

Vaccine-induced protection against Borna disease in wild-type and perforin-deficient mice.

Borna disease virus (BDV) can persistently infect the central nervous system and induce CD8+ T-cell-mediated neurological disease in MRL mice. To determine whether specific immune priming would prevent disease, a prime-boost immunization protocol was established in which intramuscular injection of a recombinant parapoxvirus expressing BDV nucleoprotein (BDV-N) was followed by intraperitoneal infection with vaccinia virus expressing BDV-N. Immunized wild-type and perforin-deficient mice remained healthy after intracerebral infection with BDV and contained almost no virus in the brain at 5 weeks post-challenge. Immunization failed to induce resistance against BDV in mice lacking mature CD8+ T cells. Immunization of perforin-deficient mice with a poxvirus vector expressing mutant BDV-N lacking the known CD8+ T-cell epitope did not efficiently block multiplication of BDV in the brain and did not prevent neurological disease, indicating that vaccine-induced immunity to BDV in wild-type and perforin-deficient mice resulted from the action of CD8+ T cells.