The interactions of Canadian ethics consultants with health care managers and governing boards during times of crisis.

BACKGROUND: Health care organizations can be very complex, and are often the setting for crisis situations. In recent years, Canadian health care organizations have faced large-scale systemic medical errors, a nation-wide generic injectable drug shortage, iatrogenic infectious disease outbreaks, and myriad other crises. These situations often have an ethical component that ethics consultants may be able to address. Organizational leaders such as health care managers and governing boards have responsibilities to oversee and direct the response to crisis situations. This study investigates the nature and degree of involvement of Canadian ethics consultants in such situations. METHODS: This qualitative study used semi-structured interviews with Canadian ethics consultants to investigate the nature of their interactions with upper-level managers and governing board members in health care organizations, particularly in times of organizational crisis. We used a purposive sampling technique to identify and recruit ethics consultants throughout Canada. RESULTS: We found variability in the interactions between ethics consultants and upper-level managers and governing boards. Some ethics consultants we interviewed did not participate in managing organizational crisis situations. Most ethics consultants reported that they had assisted in the management of some crises and that their participation was usually initiated by managers. Some ethics consultants reported the ability to bring issues to the attention of upper-level managers and indirectly to their governing boards. The interactions between managers and ethics consultants were characterized by varying degrees of collegiality. Ethics consultants reported participating in or chairing working groups, participating in incident management teams, and developing decision-making frameworks. CONCLUSIONS: Canadian ethics consultants tend to believe that they have valuable skills to offer in the management of organizational crisis situations. Most of the ethics consultants we interviewed believed that they play an important role in this regard.

The use of Ethics Decision-Making Frameworks by Canadian Ethics Consultants: A Qualitative Study.

In this study, Canadian healthcare ethics consultants describe their use of ethics decision-making frameworks. Our research finds that ethics consultants in Canada use multi-purpose ethics decision-making frameworks, as well as targeted frameworks that focus on reaching an ethical resolution to a particular healthcare issue, such as adverse event reporting, or difficult triage scenarios. Several interviewees mention the influence that the accreditation process in Canadian healthcare organizations has on the adoption and use of such frameworks. Some of the ethics consultants we interviewed also report on their reluctance to use these tools. Limited empirical work has been done previously on the use of ethics decision-making frameworks. This study begins to fill this gap in our understanding of the work of healthcare ethics consultants.

Models of Ethics Consultation Used by Canadian Ethics Consultants: A Qualitative Study.

This article describes a qualitative study of models of ethics consultation used by ethics consultants in Canada. We found four different models used by Canadian ethics consultants whom we interviewed, and one sub-variant. We describe (1) the lone ethics consultant model, (1a) the hub-and-spokes sub-variant of this model; (2) the ethics committee model; (3) the capacity-building model; and (4) the facilitated model. Previous empirical studies of ethics consultation describe only two or three of these models.

From framework to the frontline: designing a structure and process for drug supply shortage planning.

Drug shortages are not new; they have been managed through conservation, procurement of alternatives, and redistribution of stock The Sandoz shortage in 2012 has caused a radical reduction of generic injectables. In Newfoundland and Labrador, our response has led to the development of the framework, structure, and process outlined in this paper. The efforts have eased the concerns of clinicians and leaders, as they are aware of the decision-making resource for situations of drug and technology shortage.

Decompressive hemicraniectomy, strokectomy, or both in the treatment of malignant middle cerebral artery syndrome.

OBJECTIVE: We sought to evaluate the impact of a craniotomy for strokectomy (CS) with bone replacement, decompressive hemicraniectomy (DHC), or DHC with a strokectomy (DHC+S) on outcome after malignant supratentorial infarction. METHODS: We conducted a retrospective cohort study of cases of malignant supratentorial infarction treated by CS (n = 18), DHC (n = 17), or DHC+S (n = 33) at our institution from 2002 to 2008. End points included functional outcome measured by the modified Rankin Scale and incidence of mortality at 1 year. RESULTS: Mean age, gender, side, vessel, and time from ictus to surgery were not statistically different between treatment groups. Stroke volume was significantly higher in the CS group. Operative time and blood loss were significantly higher in the DHC+S group. At 1 year, the median modified Rankin Scale score was 4 and overall survival was 71%. Functional outcomes and mortality for both the CS and DHC+S groups were not significantly different from the DHC group (P = 0.24). After adjusting for patient age, stroke volume, and time to surgery, there was no significant difference in outcome. CONCLUSION: In patients with malignant supratentorial infarction, a strokectomy alone may be equivalent to a decompressive hemicraniectomy with or without brain resection.

Iatrogenic cerebral venous sinus occlusion with flowable topical hemostatic matrix.

OBJECT: The use of commercially available topical hemostatic adjuncts has increased the safety profile of surgery as a whole. Cranial surgery has also benefited from the development of numerous agents designed to permit more rapid achievement of hemostasis. Flowable topical hemostatic agents applied via syringe injection are now commonly employed in many neurosurgical procedures, including cranial surgery. Intravascular use of these strongly thrombogenic agents is contraindicated, but in certain settings, inadvertent intravascular administration can occur, resulting in vascular occlusion, thrombosis, and potential dissemination. To date, there have no reports detailing the presence and incidence of this complication. METHODS: The authors conducted a retrospective review of all cranial surgeries performed at Presbyterian University Hospital by members of the University of Pittsburgh Medical Center's Department of Neurological Surgery between 2007 and 2009. Cases complicated by vascular occlusion due to inadvertent intravascular administration of flowable topical hemostatic matrix (FTHM) were identified and analyzed. RESULTS: Iatrogenic vascular occlusion induced by FTHM was identified in 5 (0.1%) of 3969 cranial surgery cases. None of these events occurred in 3318 supratentorial cases, whereas 5 cases of cerebral venous sinus occlusion occurred in 651 infratentorial cases (0.8%). The risk of accidental vessel occlusion was significantly associated with infratentorial surgery, and all events occurred in the transverse and/or sigmoid sinus. No episodes of inadvertent vascular occlusion occurred during endoscopic surgery. No cases of arterial occlusion were identified. Of the 5 patients with FTHM-related cerebral venous sinus occlusion, none developed long-term neurological sequelae referable to the event. CONCLUSIONS: Inadvertent intravascular administration of FTHM is a rare complication associated with cranial surgery that occurs most commonly during infratentorial procedures around the transverse and/or sigmoid sinuses. Modifications in the choice of when to use an FTHM and the method of application may help prevent accidental venous sinus administration.

Benign perimesencephalic hemorrhage occurring after previous aneurysmal subarachnoid hemorrhage: a case report.

INTRODUCTION: Both aneurysmal subarachnoid hemorrhage and benign perimesencephalic hemorrhage are well-described causes of spontaneous subarachnoid hemorrhage that arise as a result of different pathologic processes. To the best of the authors' knowledge, there have been no reports of both vascular pathologies occurring in the same individual. CASE PRESENTATION: A 51-year-old Caucasian woman with a history of aneurysmal subarachnoid hemorrhage presented five years after her initial treatment with ictal headache, meningismus, nausea and emesis similar to her previous bleeding event. Computed tomographic imaging revealed perimesencephalic bleeding remote from her previously coiled anterior communicating artery aneurysm. Both immediate and delayed diagnostic angiography revealed no residual filling of the previously coiled aneurysm and no other vascular anomalies, consistent with benign perimesencephalic hemorrhage. The patient had an uneventful hospital course and was discharged to home in good condition. CONCLUSIONS: This report for the first time identifies benign perimesencephalic hemorrhage occurring in the setting of previous aneurysmal subarachnoid hemorrhage. The presence of a previously treated aneurysm can complicate the process of diagnosing benign perimesencephalic hemorrhage. Fortunately, in this case, the previously treated anterior communicating artery aneurysm was remote from the perimesencephalic hemorrhage and could be ruled out as a source. The patient's prior aneurysmal subarachnoid hemorrhage did not worsen the anticipated good outcome associated with benign perimesencephalic hemorrhage.

Resveratrol attenuates behavioral impairments and reduces cortical and hippocampal loss in a rat controlled cortical impact model of traumatic brain injury.

Resveratrol (3,5,4'-trihydroxystilbene) is a plant-derived small molecule that is protective against multiple neurological and systemic insults. To date, no studies have explored the potential for resveratrol to provide behavioral protection in adult animals in the setting of traumatic brain injury (TBI). Using 50 male Sprague-Dawley rats, we employed the controlled cortical impact (CCI) model to ascertain whether post-injury administration of resveratrol would reduce the severity of the well-described cognitive and motor deficits associated with the model. Contusion volumes and hippocampal neuronal numbers were also measured to characterize the tissue and neuronal-sparing properties, respectively, of resveratrol. We found that 100 mg/kg, but not 10 mg/kg, of intraperitoneal resveratrol administered after injury provides significant behavioral protection in rats sustaining CCI. Specifically, rodents treated with 100 mg/kg of resveratrol showed improvements in motor performance (beam balance and beam walking) and testing of visuospatial memory (Morris water maze). Behavioral protection was correlated with significantly reduced contusion volumes, preservation of CA1 and CA3 hippocampal neurons, and protection from overt hippocampal loss as a result of incorporation into the overlying cortical contusion in resveratrol-treated animals. Although the mechanisms by which resveratrol mediates its neuroprotection is unclear, the current study adds to the growing literature identifying resveratrol as a potential therapy for human brain injury.

Tailoring the photoluminescence properties of transition metal phosphonates.

A series of phenylphosphonates, Zn(1-x)Mn(x)(O(3)PC(6)H(5)) x H(2)O, where x = 0, 0.005, 0.25, 0.5, 0.75 and 1.0, has been prepared and their photoluminescence responses studied. The presence of Mn in the sample results in a red emission, whilst when x = 0 the emission is green. Levels of Mn <1 mol% result in an orange emission. Ag(6)(m-O(3)PC(6)H(4)CO(2))(2) has been prepared by hydrothermal reaction of Ag(NO(3)) and m-phosphonobenzoic acid. The material has a 1D channel structure in which the channels are lined with the phenyl groups. Ag(6)(m-O(3)PC(6)H(4)CO(2))(2) shows a green luminescence response to laser excitation, whilst the related Zn material, Zn(3)(m-O(3)PC(6)H(4)CO(2))(2), shows an unusual yellow emission.

Human rights and ethical considerations in oral health research.

Although international agreements set the framework for research ethics, countries vary in their interpretation and execution. The Government of Canada guidelines are based on the Tri-council policy statement: ethical conduct for research involving humans (2005) and the new CIHR guidelines for health research involving Aboriginal people (2007). In this critical review, we address 3 areas of educational value to practitioners who care for the oral health needs of the public, research trainees and research investigators who advance knowledge pertaining to oral health: protection of human study participants, conflicts of interest and investigator integrity. Its main message is that ethical health care should be supported by a strong foundation of ethical research.

Radiation-induced meningioma concealed by shunt valve artifact: case report.

OBJECTIVE: Ventricular shunting is a common neurosurgical procedure. Metal-containing shunt components can cause artifacts on magnetic resonance imaging (MRI), obscuring visualization of the surrounding tissue. We present the case of a radiation-induced meningioma growing around a ventricular catheter that was not noted at an early stage as a result of artifact from an overlying shunt. CLINICAL PRESENTATION: We present the case of a 27-year-old survivor of a childhood medulloblastoma who required ventriculoperitoneal shunting as a consequence of her treatment. As a result of radiation-induced meningiomas that developed in adolescence, the patient was screened biennially via contrasted MRI. Her most recent imaging revealed a new meningioma at the edge of the MRI artifact associated with the shunt valve. A contrasted computed tomographic scan demonstrated a large meningioma with mass effect on the surrounding brain. INTERVENTION: Complete surgical resection of the meningioma was obtained. The ventricular catheter was preserved and the shunt valve replaced with a newer system that is reported to generate less magnetic artifact. CONCLUSION: Artifact from shunt valves or other implanted metallic devices obscures the surrounding tissues on MRI. Patients with significant artifact who are at higher risk for development of intracranial pathology may benefit from periodic imaging through alternate modalities that are not susceptible to magnetic artifact.

A persistent change in subcellular distribution of calcineurin following fluid percussion injury in the rat.

Calcineurin, a neuronally enriched, calcium-stimulated phosphatase, is an important modulator of many neuronal processes, including several that are physiologically related to the pathology of traumatic brain injury. The effect of moderate, central fluid percussion injury on the subcellular distribution of this important neuronal enzyme was examined. Animals were sacrificed at several time points post-injury and calcineurin distribution in subcellular fractions was assayed by Western blot analysis and immunohistochemistry. A persistent increase in calcineurin concentration was observed in crude synaptoplasmic membrane-containing fractions. In cortical fractions, calcineurin immunoreactivity remained persistently increased for 2 weeks post-injury. In hippocampal homogenates, calcineurin immunoreactivity remained increased for up to 4 weeks. Finally, immunohistochemical analysis of hippocampal slices revealed increased staining in the apical dendrites of CA1 neurons. The increased staining was greatest in magnitude 24 h post-injury; however, staining was still more intense than control 4 weeks post-injury. The data support the conclusion that fluid percussion injury results in redistribution of the enzyme in the rat forebrain. These changes have broad physiological implications, possibly resulting in altered cellular excitability or a greater likelihood of neuronal cell death.

Identification and characterization of heterogeneous neuronal injury and death in regions of diffuse brain injury: evidence for multiple independent injury phenotypes.

Diffuse brain injury (DBI) is a consequence of traumatic brain injury evoked via rapid acceleration-deceleration of the cranium, giving rise to subtle pathological changes appreciated best at the microscopic level. DBI is believed to be comprised by diffuse axonal injury and other forms of diffuse vascular change. The potential, however, that the same forces can also directly injure neuronal somata in vivo has not been considered. Recently, while investigating DBI-mediated perisomatic axonal injury, we identified scattered, rapid neuronal somatic necrosis occurring within the same domains. Moving on the premise that these cells sustained direct somatic injury as a result of DBI, we initiated the current study, in which rats were intracerebroventricularly infused with various high-molecular weight tracers (HMWTs) to identify injury-induced neuronal somatic plasmalemmal disruption. These studies revealed that DBI caused immediate, scattered neuronal somatic plasmalemmal injury to all of the extracellular HMWTs used. Through this approach, a spectrum of neuronal change was observed, ranging from rapid necrosis of the tracer-laden neurons to little or no pathological change at the light and electron microscopic level. Parallel double and triple studies using markers of neuronal degeneration, stress, and axonal injury identified additional injured neuronal phenotypes arising in close proximity to, but independent of, neurons demonstrating plasmalemmal disruption. These findings reveal that direct neuronal somatic injury is a component of DBI, and diffuse trauma elicits a heretofore-unrecognized multifaceted neuronal pathological change within the CNS, generating heterogeneous injury and reactive alteration within both axons and neuronal somata in the same domains.

Inability to evoke a long-lasting protective immune response to respiratory syncytial virus infection in mice correlates with ineffective nasal antibody responses.

Long-lasting protective antibody is not normally generated in children following primary respiratory syncytial virus (RSV) infection, frequently leading to reinfection. We used the BALB/c mouse model to examine the role of the nasal-associated lymphoid tissue and the bone marrow in the generation of RSV-specific long-lasting plasma cells, with a view to further understanding the mechanisms responsible for the poorly sustained RSV antibody levels following primary infection. We show here that substantial numbers of RSV-specific plasma cells were generated in the bone marrow following challenge, which were maintained thereafter. In contrast, in the nasal-associated lymphoid tissue, RSV-specific plasma cell numbers waned quickly both after primary infection and after challenge and were not maintained at a higher level after boosting. These data indicate that the inability to generate a robust local mucosal response in the nasal tissues may contribute substantially to the likelihood of subsequent reinfection and that the presence of serum anti-RSV antibody without local protection is not enough to protect against reinfection.

Caspase-3-mediated cleavage of amyloid precursor protein and formation of amyloid Beta peptide in traumatic axonal injury.

Immunohistochemical studies demonstrate accumulation of the beta-amyloid precursor protein (APP) within injured axons following traumatic brain injury (TBI). Despite such descriptions, little is known about the ultimate fate of accumulating APP at sites of traumatic axonal injury (TAI). Recently, caspase-3-mediated cleavage of APP and subsequent Abeta deposition was linked to apoptotic neuronal death pathways in hippocampal neurons following ischemic and excitotoxic brain injury. Given that (1) APP is known to accumulate within traumatically injured axons, (2) caspase-3 activation has been demonstrated in traumatic axonal injury (TAI), and (3) recent studies have identified a caspase-3 cleavage site within APP, we initiated the current investigation to determine whether caspase-3-mediated cleavage of APP occurs in TAI. We further assessed whether these events were found in relation to Abeta peptide formation. To this end, we employed antibodies targeting APP, the caspase-3-mediated breakdown product of APP proteolysis, and the Abeta peptide. Rats were subjected to impact acceleration TBI (6 h to 10 days survival), and their brains were processed for single-label bright field and multiple double-label immunofluorescent paradigms using the above antibodies. By 12 h postinjury, caspase-3-mediated APP proteolysis (CMAP) was demonstrated within the medial lemniscus (ML) and medial longitudinal fasciculus (MLF) in axons undergoing TAI, identified by their concomitant APP accumulation. Immunoreactivity for CMAP persisted up to 48 h postinjury in the ML and MLF, but was notably reduced by 10 days following injury. Further, CMAP was colocalized with Abeta formation in foci of TAI. The current study demonstrates that caspase-3 cleavage of APP occurs in TAI and is associated with formation of Abeta peptide. These findings are of interest given recent epidemiological studies supporting an association between TBI and later risk for AD development.

Traumatically induced axotomy adjacent to the soma does not result in acute neuronal death.

Traumatic axonal injury (TAI), a consequence of traumatic brain injury (TBI), results from progressive pathologic processes initiated at the time of injury. Studies attempting to characterize the pathology associated with TAI have not succeeded in following damaged and/or disconnected axonal segments back to their individual neuronal somata to determine their fate. To address this issue, 71 adult male Sprague Dawley rats were subjected to moderate central fluid percussion injury and killed between 30 min and 7 d after injury. Antibodies to the C terminus of beta-amyloid precursor protein (APP) identified TAI in continuity with individual neuronal somata in the mediodorsal neocortex, the hilus of the dentate gyrus, and the dorsolateral thalamus. These somata were followed with immunocytochemical markers of neuronal injury targeting phosphorylated 200 kDa neurofilaments (RMO-24), altered protein translation (phosphorylated eukaryotic translation initiation factor 2 alpha), and cell death [terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)], with parallel electron microscopic (EM) assessment. Despite the finding of TAI within 20-50 micrometer of the soma, no evidence of cell death, long associated with proximal axotomy, was seen via TUNEL or routine light microscopy/electron microscopy. Rather, there was rapid onset (<6 hr after injury) subcellular change associated with impaired protein synthesis identified by EM, immunocytochemical, and Western blot analyses. When followed 7 d after injury, these abnormalities did not reveal dramatic progression. Rather, some somata showed evidence of potential reorganization and repair. This study demonstrates a novel somatic response to TAI in the perisomatic domain and also provides insight into the multifaceted pathology associated with TBI.