Patients' experiences and perceptions of dignity in end-of-life care in emergency departments: A qualitative study.

AIMS: To explore and understand the experiences of patients with advanced illness in relation to dignity during end-of-life care in emergency departments. DESIGN: Qualitative study based on Gadamer's hermeneutics. METHODS: Between September 2019 and February 2020, 16 in-depth interviews were carried out with advanced illness patients who attended emergency departments. The participants were informed priorly and signed informed consent. The data were analysed using an inductive strategy for finding emerging themes. The Consolidated Criteria for Reporting Qualitative Research was used for writing the study's report. RESULTS: In the data analysis process, two main themes emerged that glean the experiences of patients in relation to dignity during end-of-life care in emergency departments. 'Dignity as an individual's attribute' and 'Acting with dignity: Dignity as a behavioural attribute'. CONCLUSION: Patient dignity in end-of-life care is centred around the principle of control (of oneself, one's death and one's emotions). The strategies required for patients to preserve their dignity can be somewhat incompatible with the dynamics and objectives of healthcare professionals who work in emergency departments. IMPACT STATEMENT: The dignity of patients with advanced illness who attend emergency departments is a relevant issue that merits being addressed from the patients' perspective. Participants have identified that dignity is a way of being and behaving in the face of illness. Emergency departments need to respect end-of-life patients' desires by supporting and accompanying them, avoiding therapeutic obstinacy. We recommend care to be centred on patients' well-being, to respect their autonomy and decision-making processes, and to allow prompt referrals to palliative care services. PATIENT OR PUBLIC CONTRIBUTION: Managers from the Emergency Departments participated in the study design and patients' recruitment. Patients' relatives were informed about the study's aim, and they contributed to the development of the interview protocol.

Promoting dignified end-of-life care in the emergency department: A qualitative study.

BACKGROUND: Preservation of a dying person's dignity in the emergency department (ED) is fundamental for the patient, his/her relatives and healthcare professionals. The aim of this study was to explore and interpret physicians' and nurses' experiences regarding conservation of dignity in end-of-life care in dying patients in the ED. METHODS: A qualitative study based on the hermeneutic phenomenological approach, was carried out in the emergency department of two general hospitals. A total of 16 nurses and 10 physicians participated in the study. Data collection included 12 individual in-depth interviews and 2 focus groups. RESULTS: The findings revealed that two themes represent the practices and proposals for the conservation of dignity in the emergency department: dignified care in hostile surroundings and the design of a system focused on the person's dignity. CONCLUSION: Dignifying treatment, redesigning environmental conditions, and reorienting the healthcare system can contribute to maintaining dignity in end-of-life care in the ED.

Signaling mechanisms of interferon gamma induced apoptosis in chromaffin cells: involvement of nNOS, iNOS, and NFkappaB.

Previous work of our group stated that exogenously added and endogenous nitric oxide (NO) generated by cytokines induce apoptosis in chromaffin cells. In this work, we investigate the specific regulation of the NO synthase (NOS) isoforms, inducible NOS (iNOS) and neuronal NOS (nNOS), and their particular participation in cell death induced by interferon gamma (IFNgamma). Lipopolysaccharide (LPS) and IFNgamma increase iNOS expression, with no effect on nNOS expression. On the other hand, dexamethasone increases basal nNOS expression but decreases LPS + IFNgamma-induced iNOS expression. IFNgamma-induced cell death was abolished by W-1400, a specific iNOS inhibitor, but only partially by nNOS inhibitors [N-omega-propyl- L-arginine (N-PLA), 3-Bromo-7-nitroindazol (7-NI), L-methyl thiocitrulline and N-methyl L-arginine], indicating the main iNOS participation in chromaffin cell death. IFNgamma and LPS induce nuclear factor kappaB (NFkappaB) translocation to the nucleus, a process implicated in activation of iNOS expression, as inhibition of NFkappaB translocation, by SN50, decreased iNOS expression. In addition, IFNgamma and LPS induce (847)SernNOS phosphorylation, inhibiting nNOS activity. Both processes, nNOS phosphorylation and iNOS expression induced by LPS + IFNgamma, are regulated by Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathway, as IFNgamma increases (727)STAT-3 phosphorylation and specific inhibitors of JAK/STAT pathway, such as AG490, inhibited both processes. Taken together, these results support the hypothesis of an inactivating phosphorylation of nNOS by IFNgamma, via JAK/STAT, in bovine chromaffin cells. Low NO concentrations achieved by this event, would activate NFkappaB translocation, increasing iNOS expression and generating, this last, high apoptotic NO concentrations.

Mechanisms of nitric oxide-induced apoptosis in bovine chromaffin cells: Role of mitochondria and apoptotic proteins.

The aim of this work was to establish the possible involvement of mitochondria in the apoptotic event triggered by nitric oxide (NO) in chromaffin cells. Using bovine chromaffin cells in primary culture and several NO donors (SNP, SNAP, and GSNO) at apoptotic concentrations (50 microM-1 mM), we have shown that NO induces a time-dependent decrease in the mitochondrial transmembrane potential (DeltaPsi(m)), which correlates with the appearance of hypodiploid cells. Disruption in DeltaPsi(m) is followed by cytochrome c release to the cytosol, which in turn precedes caspase 3 activation. In this mechanism participates the Bcl-2 protein family, because NO donors downregulate the expression of anti-apoptotic members of the family such as Bcl-2 and Bcl-XL, and increase the expression of pro-apoptotic members, Bax and Bcl-Xs, inductors of cytochrome c release to cytosol. Different cell signaling pathways seem to regulate Bax induction and Bcl-2 inhibition because decreased Bcl-2 levels are detected later than enhanced Bax expression. The tumour suppressor protein p53 is also upregulated in a very early phase (30 min) of the NO-induced apoptosis and may be responsible for the further induction of Bax expression. Finally, the translocation of NF-kappaB to the nucleus seems to be another early event in NO-induced apoptosis and it may be involved in the regulation of p53 expression. These results support strongly the participation of mitochondrial mechanisms in NO-induced apoptosis in chromaffin cells and suggest that these cells may be good models for the investigation of molecular basis of neurodegeneration and neuroprotection.