Promoting Patient Safety and Preventing Medical Error in Emergency Departments

An estimated 108,000 people die each year from potentially preventable iatrogenic injury. One in 50 hospitalized patients experiences a preventable adverse event. Up to 3% of these injuries and events take place in emergency departments. With long and detailed training, morbidity and mortality conferences, and an emphasis on practitioner responsibility, medicine has traditionally faced the challenges of medical error and patient safety through an approach focused almost exclusively on individual practitioners. Yet no matter how well trained and how careful health care providers are, individuals will make mistakes because they are human. In general medicine, the study of adverse drug events has led the way to new methods of error detection and error prevention. A combination of chart reviews, incident logs, observation, and peer solicitation has provided a quantitative tool to demonstrate the effectiveness of interventions such as computer order entry and pharmacist order review. In emergency medicine (EM), error detection has focused on subjects of high liability: missed myocardial infarctions, missed appendicitis, and misreading of radiographs. Some system-level efforts in error prevention have focused on teamwork, on strengthening communication between pharmacists and emergency physicians, on automating drug dosing and distribution, and on rationalizing shifts. This article reviews the definitions, detection, and presentation of error in medicine and EM. Based on review of the current literature, recommendations are offered to enhance the likelihood of reduction of error in EM practice.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74930/1/j.1553-2712.2000.tb00466.x.pd

Repaired tetralogy of Fallot: the roles of cardiovascular magnetic resonance in evaluating pathophysiology and for pulmonary valve replacement decision support

Surgical management of tetralogy of Fallot (TOF) results in anatomic and functional abnormalities in the majority of patients. Although right ventricular volume load due to severe pulmonary regurgitation can be tolerated for many years, there is now evidence that the compensatory mechanisms of the right ventricular myocardium ultimately fail and that if the volume load is not eliminated or reduced by pulmonary valve replacement the dysfunction might be irreversible. Cardiovascular magnetic resonance (CMR) has evolved during the last 2 decades as the reference standard imaging modality to assess the anatomic and functional sequelae in patients with repaired TOF. This article reviews the pathophysiology of chronic right ventricular volume load after TOF repair and the risks and benefits of pulmonary valve replacement. The CMR techniques used to comprehensively evaluate the patient with repaired TOF are reviewed and the role of CMR in supporting clinical decisions regarding pulmonary valve replacement is discussed

Inflammation and Oxidative Stress Are Elevated in the Brain, Blood, and Adrenal Glands during the Progression of Post-Traumatic Stress Disorder in a Predator Exposure Animal Model

This study sought to analyze specific pathophysiological mechanisms involved in the progression of post-traumatic stress disorder (PTSD) by utilizing an animal model. To examine PTSD pathophysiology, we measured damaging reactive oxygen species and inflammatory cytokines to determine if oxidative stress and inflammation in the brain, adrenal glands, and systemic circulation were upregulated in response to constant stress. Pre-clinical PTSD was induced in naïve, male Sprague-Dawley rats via a predator exposure/psychosocial stress regimen. PTSD group rats were secured in Plexiglas cylinders and placed in a cage with a cat for one hour on days 1 and 11 of a 31-day stress regimen. In addition, PTSD group rats were subjected to psychosocial stress whereby their cage cohort was changed daily. This model has been shown to cause heightened anxiety, exaggerated startle response, impaired cognition, and increased cardiovascular reactivity, all of which are common symptoms seen in humans with PTSD. At the conclusion of the predator exposure/psychosocial stress regimen, the rats were euthanized and their brains were dissected to remove the hippocampus, amygdala, and pre-frontal cortex (PFC), the three areas commonly associated with PTSD development. The adrenal glands and whole blood were also collected to assess systemic oxidative stress. Analysis of the whole blood, adrenal glands, and brain regions revealed oxidative stress increased during PTSD progression. In addition, examination of pro-inflammatory cytokine (PIC) mRNA and protein demonstrated neurological inflammatory molecules were significantly upregulated in the PTSD group vs. controls. These results indicate oxidative stress and inflammation in the brain, adrenal glands, and systemic circulation may play a critical role in the development and further exacerbation of PTSD. Thus, PTSD may not be solely a neurological pathology but may progress as a systemic condition involving multiple organ systems