PREHOSPITAL TROPONIN TESTING PROTOCOL FOR ACCELERATED DIAGNOSIS AND EARLY INTERVENTION IN CHEST PAIN PATIENTS

Non-ST elevation acute coronary syndromes (NSTE-ACS) have significant morbidity and mortality rates despite the progress made in diagnosis and management and represent a significant public health burden in the United States. Lengthy diagnostic algorithms contribute to emergency department over-crowding, increased health care costs, and adverse patient outcomes. A troponin assay instituted earlier in the diagnostic pathway of patients with chest pain suspected of NSTE-ACS will reduce time to definitive diagnosis and medical intervention. This will improve patient outcomes, decrease emergency department crowding through improved ED workflow, and reduce the economic burden. The Star Model of Knowledge Transformation was used to guide an understanding of the cycles, nature, and characteristics of knowledge of NSTE-ACS, organize previous and current concepts of improving care, and provided the framework to guide design, implementation, evaluation and sustainability. The Prehospital Troponin Testing Protocol (PHTTP) instituted a point-of-care troponin assay in the ambulances of the Plainview Fire-EMS department and used this value in an accelerated diagnostic pathway in the Covenant Plainview Emergency Department. The PHTTP reduced the time to first troponin from 79 minutes (1.32 hours) to 22 minutes (0.37 hours) and time to disposition of patients from 191.00 minutes (3.18 hour) to 150.04 minutes (2.50 hours). Time to first troponin was reduced by 47.00 minutes (0.78 hours) and length of stay was reduced by 40.96 minutes (0.67 hours). The prehospital scene time was increased by 1 minute which was not statistically significant

The contribution of environmental exposure to the etiology of autism spectrum disorder

Autism spectrum disorder (ASD) is a neurodevelopmental condition of heterogeneous etiology. While it is widely recognized that genetic and environmental factors and their interactions contribute to autism phenotypes, their precise causal mechanisms remain poorly understood. This article reviews our current understanding of environmental risk factors of ASD and their presumed adverse physiological mechanisms. It comprehensively maps the significance of parental age, teratogenic compounds, perinatal risks, medication, smoking and alcohol use, nutrition, vaccination, toxic exposures, as well as the role of extreme psychosocial factors. Further, we consider the role of potential protective factors such as folate and fatty acid intake. Evidence indicates an increased offspring vulnerability to ASD through advanced maternal and paternal age, valproate intake, toxic chemical exposure, maternal diabetes, enhanced steroidogenic activity, immune activation, and possibly altered zinc-copper cycles and treatment with selective serotonin reuptake inhibitors. Epidemiological studies demonstrate no evidence for vaccination posing an autism risk. It is concluded that future research needs to consider categorical autism, broader autism phenotypes, as well as autistic traits, and examine more homogenous autism variants by subgroup stratification. Our understanding of autism etiology could be advanced by research aimed at disentangling the causal and non-causal environmental effects, both founding and moderating, and gene-environment interplay using twin studies, longitudinal and experimental designs. The specificity of many environmental risks for ASD remains unknown and control of multiple confounders has been limited. Further understanding of the critical windows of neurodevelopmental vulnerability and investigating the fit of multiple hit and cumulative risk models are likely promising approaches in enhancing the understanding of role of environmental factors in the etiology of ASD.peerReviewe