RESUMEN
OBJECTIVE: The emergency department (ED) is a demanding environment, and critical events have been identified as contributors to stress. Debriefing is a possible intervention for staff, but there is little information regarding formulation and implementation. A needs assessment was conducted to describe the emotions of pediatric ED (PED) staff following critical events and assess opinions regarding debriefing. METHOD: This mixed methods study used convergent design for triangulation. After critical cases, PED staff members were given the Peritraumatic Distress Inventory (PDI). Additionally, a questionnaire with 2 open-ended questions on debriefing was administered. Themes were extracted from the questionnaire using directed content analysis. RESULTS: A total of 719 responses were collected for 142 critical cases. Physical reactions were often endorsed in the PDI, and these reactions were mirrored in the qualitative data, which included physiological responses such as stress, adrenaline high, anxiety, fatigue, and overwhelm. Helplessness and grief were 2 of the emotional PDI items frequently endorsed, which were reflected in the qualitative strand by themes such as helplessness, sadness, disheartenment, and regret. There was considerable variability between critical cases such that not every critical case elicited a desire for a debrief. CONCLUSIONS: PED staff report measurable levels of stress after critical patient cases that warrant follow-up. Formal debriefing immediately after critical patient cases with specific caveats may be valuable for the reduction of stress. Any formal debriefing program will need to balance various goals with attention to the session length, setting, and timing.
Asunto(s)
Emociones , Pesar , Niño , Humanos , Evaluación de Necesidades , Encuestas y CuestionariosRESUMEN
Cerebral amyloid angiopathy (CAA) is a vascular lesion associated with Alzheimer's disease (AD) present in up to 95% of AD patients and produces MRI-detectable microbleeds in many of these patients. It is possible that CAA-related microbleeding is a source of pathological iron in the AD brain. Because the homeostasis of copper, iron, and zinc are so intimately linked, we determined whether CAA contributes to changes in the brain levels of these metals. We obtained brain tissue from AD patients with severe CAA to compare to AD patients without evidence of vascular amyloid-ß. Patients with severe CAA had significantly higher non-heme iron levels. Histologically, iron was deposited in the walls of large CAA-affected vessels. Zinc levels were significantly elevated in grey matter in both the CAA and non-CAA AD tissue, but no vascular staining was noted in CAA cases. Copper levels were decreased in both CAA and non-CAA AD tissues and copper was found to be prominently deposited on the vasculature in CAA. Together, these findings demonstrate that CAA is a significant variable affecting transition metals in AD.
Asunto(s)
Enfermedad de Alzheimer/metabolismo , Encéfalo/metabolismo , Angiopatía Amiloide Cerebral/metabolismo , Cobre/metabolismo , Hierro/metabolismo , Zinc/metabolismo , Anciano , Anciano de 80 o más Años , Enfermedad de Alzheimer/patología , Biomarcadores/metabolismo , Encéfalo/patología , Angiopatía Amiloide Cerebral/patología , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
Reports that iron, zinc and copper homeostasis are in aberrant homeostasis are common for various neurodegenerative diseases, particularly for Huntington's disease, Parkinson's disease, and Alzheimer's disease. Manipulating the levels of these elements in the brain through the application of chelators has been and continues to be tested therapeutically in clinical trials with mixed results. Much of the data indicating that these metals are abnormally concentrated in Alzheimer's disease and Parkinson's disease brain tissue was generated through the analysis of post-mortem human tissue which was archived in formalin. In this study, we evaluated the effect of formalin fixation of brain on the levels of three important transition metals (iron, copper, and zinc) by atomic absorption spectroscopy. Paired brain specimens were obtained at autopsy for each case; one was conserved by formalin archival (averaging four years), the other was rapidly frozen. Both white and grey matter samples were analyzed and the concentrations of iron and zinc were found to decrease with fixation. Iron was reduced by 40% (P < 0.01), and zinc by 77% (P < 0.0001); copper concentrations increased by 37% (P < 0.05) by the paired T-test. The increase in copper is likely due to contamination from trace copper in the formalin. These results indicate that transition metal data obtained from fixed tissue may be heavily distorted and care should be taken in interpreting this data.
Asunto(s)
Química Encefálica/efectos de los fármacos , Cobre/análisis , Fijadores/farmacología , Formaldehído/farmacología , Hierro/análisis , Zinc/análisis , Enfermedad de Alzheimer/fisiopatología , Artefactos , Congelación , HumanosRESUMEN
Neuroimaging with iron-sensitive MR sequences [gradient echo T2* and susceptibility-weighted imaging (SWI)] identifies small signal voids that are suspected brain microbleeds. Though the clinical significance of these lesions remains uncertain, their distribution and prevalence correlates with cerebral amyloid angiopathy (CAA), hypertension, smoking, and cognitive deficits. Investigation of the pathologies that produce signal voids is necessary to properly interpret these imaging findings. We conducted a systematic correlation of SWI-identified hypointensities to tissue pathology in postmortem brains with Alzheimer's disease (AD) and varying degrees of CAA. Autopsied brains from eight AD patients, six of which showed advanced CAA, were imaged at 3T; foci corresponding to hypointensities were identified and studied histologically. A variety of lesions was detected; the most common lesions were acute microhemorrhage, hemosiderin residua of old hemorrhages, and small lacunes ringed by hemosiderin. In lesions where the bleeding vessel could be identified, ß-amyloid immunohistochemistry confirmed the presence of ß-amyloid in the vessel wall. Significant cellular apoptosis was noted in the perifocal region of recent bleeds along with heme oxygenase 1 activity and late complement activation. Acutely extravasated blood and hemosiderin were noted to migrate through enlarged VirchowRobin spaces propagating an inflammatory reaction along the local microvasculature; a mechanism that may contribute to the formation of lacunar infarcts. Correlation of imaging findings to tissue pathology in our cases indicates that a variety of CAA-related pathologies produce MR-identified signal voids and further supports the use of SWI as a biomarker for this disease.