Not overstepping professional boundaries: the challenging role of nurses in simulated error disclosures

This article provides findings on the role of the nurse in simulated team-based error disclosures. Triangulation of 3 qualitative data sets revealed that a tension exists for nurses in the error disclosure process as they attempt to balance professional boundaries. Study findings point to multilevel strategies including cultural, structural, and educational approaches to enhancing the key roles that nurses need to play in error disclosure to patients and families.     

A randomized trial of transfer for primary angioplasty versus on-site thrombolysis in patients with high-risk myocardial infarction: the Air Primary Angioplasty in Myocardial Infarction study

OBJECTIVES: The Air Primary Angioplasty in Myocardial Infarction (PAMI) study was designed to determine the best reperfusion strategy for patients with high-risk acute myocardial infarction (AMI) at hospitals without percutaneous transluminal coronary angioplasty (PTCA) capability. BACKGROUND: Previous studies have suggested that high-risk patients have better outcomes with primary PTCA than with thrombolytic therapy. It is unknown whether this advantage would be lost if the patient had to be transferred for PTCA, and reperfusion was delayed. METHODS: Patients with high-risk AMI (age >70 years, anterior MI, Killip class II/III, heart rate >100 beats/min or systolic BP <100 mm Hg) who were eligible for thrombolytic therapy were randomized to either transfer for primary PTCA or on-site thrombolysis. RESULTS: One hundred thirty-eight patients were randomized before the study ended (71 to transfer for PTCA and 67 to thrombolysis). The time from arrival to treatment was delayed in the transfer group (155 vs. 51 min, p < 0.0001), largely due to the initiation of transfer (43 min) and transport time (26 min). Patients randomized to transfer had a reduced hospital stay (6.1 +/- 4.3 vs. 7.5 +/- 4.3 days, p = 0.015) and less ischemia (12.7% vs. 31.8%, p = 0.007). At 30 days, a 38% reduction in major adverse cardiac events was observed for the transfer group; however, because of the inability to recruit the necessary sample size, this did not achieve statistical significance (8.4% vs. 13.6%, p = 0.331). CONCLUSIONS: Patients with high-risk AMI at hospitals without a catheterization laboratory may have an improved outcome when transferred for primary PTCA versus on-site thrombolysis; however, this will require further study. The marked delay in the transfer process suggests a role for triaging patients directly to specialized heart-attack centers.     

The incidence, predictors, and outcomes of early reinfarction after primary angioplasty for acute myocardial infarction

OBJECTIVES: We sought to identify the incidence, predictors, and clinical consequences of one-month reinfarction (RE-MI) in patients undergoing primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). BACKGROUND: One-month reinfarction after AMI significantly increases long-term mortality; however, little is known about the incidence and predictors of RE-MI in patients undergoing primary angioplasty. METHODS: We analyzed data from 3,646 patients who underwent primary PCI in the Primary Angioplasty in Acute Myocardial Infarction (PAMI) studies. We studied the incidence, correlates, and clinical outcomes of 30-day RE-MI. RESULTS: Reinfarction within one month of index hospitalization occurred in 77 (2.1%) of patients. In multivariate analysis, admission Killip class >1 (odds ratio [OR] 2.02, 95% confidence interval [CI] 1.09 to 3.76), left ventricular ejection fraction <50% (OR 2.49, 95% CI 1.30 to 4.74), final coronary stenosis >30% (OR 2.57, 95% CI 1.28 to 5.15), and presence of coronary dissection (OR 2.40, 95% CI 1.36 to 4.24) and thrombus (OR 2.36, 95% CI 1.23 to 4.53) on the final angiogram were independent correlates of RE-MI. One-month reinfarction was independently associated with death (OR 7.14, 95% CI 3.28 to 15.5) and ischemic target vessel revascularization (I-TVR) (OR 15.0, 95% CI 8.68 to 26.0) at six months. CONCLUSIONS: We conclude that, although early RE-MI is uncommon in patients treated by primary PCI, it is a significant independent predictor of death and I-TVR at six months. Admission Killip class >1 and left ventricular systolic dysfunction were associated with higher incidence of RE-MI. Our results suggest that optimal revascularization during primary PCI may decrease RE-MI rates.     

Understanding Palliative Care on the Heart Failure Care Team: An Innovative Research Methodology

ContextThere is a growing call to integrate palliative care for patients with advanced heart failure (HF). However, the knowledge to inform integration efforts comes largely from interview and survey research with individual patients and providers. This work has been critically important in raising awareness of the need for integration, but it is insufficient to inform solutions that must be enacted not by isolated individuals but by complex care teams. Research methods are urgently required to support systematic exploration of the experiences of patients with HF, family caregivers, and health care providers as they interact as a care team.ObjectivesTo design a research methodology that can support systematic exploration of the experiences of patients with HF, caregivers, and health care providers as they interact as a care team.MethodsThis article describes in detail a methodology that we have piloted and are currently using in a multisite study of HF care teams.ResultsWe describe three aspects of the methodology: the theoretical framework, an innovative sampling strategy, and an iterative system of data collection and analysis that incorporates four data sources and four analytical steps.ConclusionWe anticipate that this innovative methodology will support groundbreaking research in both HF care and other team settings in which palliative integration efforts are emerging for patients with advanced nonmalignant disease.     

Does Proximal Location of Culprit Lesion Confer Worse Prognosis in Patients Undergoing Primary Percutaneous Coronary Intervention for ST Elevation Myocardial Infarction?

ST segment elevation myocardial infarction (STEMI) from proximally located culprit lesion is associated with greater myocardium at jeopardy. In STEMI patients treated with thrombolytics, proximal culprit lesions are known to have worse prognosis. This relation has not been studied in patients undergoing primary percutaneous coronary intervention (PCI). In 3,535 STEMI patients with native coronary artery occlusion pooled from the primary angioplasty in myocardial infarction database, we compared in-hospital and 1-year outcomes between those with proximal (n = 1,606) versus non-proximal (n = 1,929) culprit lesions. Patients with proximal culprits were more likely to die and suffer major adverse cardiovascular events (MACE) during the index hospital stay (3.8% vs 2.2%, P = 0.006; 8.2% vs 5.8%, P = 0.0066, respectively) as well as during 1-year follow-up (6.9% vs 4.5%, P = 0.0013; 22% vs 17%, P = 0.003, respectively) compared to those with non-proximal culprits. After adjustment for baseline differences, proximal culprit was independently predictive of in-hospital death (adjusted odds ratio% 1.58, 95% confidence intervals, CI 1.05-2.40) and MACE (OR 1.41, CI 1.06-1.86), but not 1-year death or MACE. In addition, proximal culprit was independently associated with higher incidence of ventricular arrhythmias and sustained hypotension during the index hospitalization. The univariate impact of proximal culprit lesion on in-hospital death and MACE was comparable to other adverse angiographic characteristics, such as multivessel disease and poor initial thrombolysis in myocardial infarction flow, and greater than that of anterior wall STEMI. In conclusion, proximal location of the culprit lesion is a strong independent predictor of worse in-hospital outcomes in patients with STEMI undergoing primary PCI.     

Abbreviated exposure to cuprizone is sufficient to induce demyelination and oligodendrocyte loss

Cuprizone intoxication is one of several animal models used to study demyelination and remyelination. Early treatment protocols exposed mice to cuprizone for 6 weeks to induce demyelination; however, more recent reports have varied exposure times from 4 to 5 weeks. The goal of this study was to determine the minimal exposure of cuprizone in C57BL/6 mice that would induce a pathology of robust demyelination and gliosis similar to that described for a 5‐ or 6‐week treatment. We found that an abbreviated insult of only 2 weeks of exposure to cuprizone induced significant demyelination 3 weeks later (5‐week time point) but was somewhat variable. Three weeks of exposure to cuprizone produced extensive demyelination by week 5, equivalent to that observed with 5 weeks of exposure. The depletion of mature oligodendrocytes, as well as microglia and astrocyte accumulation, showed trends similar to those with 5‐week exposure to cuprizone. Once mature oligodendrocytes are perturbed after a 3‐week treatment, the progression to demyelination occurs without requiring further exposure. Furthermore, the early removal of cuprizone did not accelerate remyelination, suggesting that other sequences of events must follow before repair can occur. Thus, a short, “hit and run” CNS insult triggers a cascade of events leading to demyelination 2–3 weeks later. © 2012 Wiley Periodicals, Inc.     

Photobiomodulation Therapy Attenuates Hypoxic-Ischemic Injury in a Neonatal Rat Model

Photobiomodulation (PBM) has been demonstrated as a neuroprotective strategy, but its effect on perinatal hypoxic-ischemic encephalopathy is still unknown. The current study was designed to shed light on the potential beneficial effect of PBM on neonatal brain injury induced by hypoxia ischemia (HI) in a rat model. Postnatal rats were subjected to hypoxic-ischemic insult, followed by a 7-day PBM treatment via a continuous wave diode laser with a wavelength of 808 nm. We demonstrated that PBM treatment significantly reduced HI-induced brain lesion in both the cortex and hippocampal CA1 subregions. Molecular studies indicated that PBM treatment profoundly restored mitochondrial dynamics by suppressing HI-induced mitochondrial fragmentation. Further investigation of mitochondrial function revealed that PBM treatment remarkably attenuated mitochondrial membrane collapse, accompanied with enhanced ATP synthesis in neonatal HI rats. In addition, PBM treatment led to robust inhibition of oxidative damage, manifested by significant reduction in the productions of 4-HNE, P-H2AX (S139), malondialdehyde (MDA), as well as protein carbonyls. Finally, PBM treatment suppressed the activation of mitochondria-dependent neuronal apoptosis in HI rats, as evidenced by decreased pro-apoptotic cascade 3/9 and TUNEL-positive neurons. Taken together, our findings demonstrated that PBM treatment contributed to a robust neuroprotection via the attenuation of mitochondrial dysfunction, oxidative stress, and final neuronal apoptosis in the neonatal HI brain.     

"Stop the noise!" From voice to silence

Nurses are frequently portrayed in the literature as being silent about ethical concerns that arise in their practice. This silence is often represented as a lack of voice. However, in our study, we found that nurses who responded to questions about moral distress were not so much silent as silenced. These nurses were enacting their moral agency by engaging in diverse, multiple and time-consuming actions in response to situations identified as morally distressing with families, colleagues, physicians, educators or managers. In many situations, they took action by contacting other healthcare team members, making referrals and coordinating care with other departments such as home care and hospice, as well as initiating contact with groups such as professional regulatory bodies or unions. Examining the relationship between ethical climate, moral distress and voice offers insights into both the meaning and impact of being silenced in the workplace.