No description available.

Background: Compassion Fatigue (CF) describes the emotional, spiritual, intellectual and physical exhaustion that results from untreated distress among nurses, stemming from exposure to traumatic events and work environment stressors. Comprised of Burnout (BO), Secondary Traumatic Stress (STS) and Compassion Satisfaction (CS), CF results when BO and STS outweigh CS. CF leads to physical and emotional problems including fatigue, hopelessness, anger, and an increased use of sick days. For hospitals, this means poor morale, increased medication errors and higher turnover. Objective: The purpose of this study was to determine the prevalence and severity of CF risk among the nursing staff at Maricopa Medical Center (MMC).Design: Descriptive study completed to determine: 1) What is the prevalence and severity of CF risk among nurses at MMC; and 2) compared to nurses with low CF risk, do nurses with high CF risk have differences in demographic and workplace characteristics? Setting: Maricopa Medical Center between April 14, 2015 and May 26, 2015 Participants: 315 full-time nurses at MMC in Phoenix. Measurements: Nurses were surveyed using the Professional Quality of Life Scale-5 (ProQOL-5) measuring the three components of CF: BO, STS and CS. Results: 46% of nurses reported moderate to high risk of CF. Nurses who worked in Labor and Delivery, Psychiatric Annex/Desert Vista, Emergency Departments, Intensive Care Units and Rapid Response units reported the highest risk. Risk increased significantly after their first year working at MMC. More frequent job changes outside of MMC correlated with lower risk profiles. Lower risk was seen in nurses with advanced degrees. Trends indicated that younger nurses, Clinical Resource Leaders, and nurses who had taken nine or more sick days in the previous six months were more at risk. Conclusion: Almost half of nurses were at moderate to high risk of CF. Unique findings were reported, including possible links between CF risk and job changes, and years working at a single facility. These links were previously unstudied. It was determined that the focus of interventions should be on nurses who work in the units most at risk and on new hire nurses, regardless of their years of nursing experience.

Traumatic Brain Injury (TBI) accounts for 1,000,000 hospital admissions in the European Union every year and is the leading cause of death in individuals under 45 years of age in both Europe and the United States. This thesis examines the consequences to both the brain and lung following TBI using the lateral fluid percussion injury (FPI) in an in-vivo murine model. In the murine FPI model, alongside cerebral inflammation (associated with neuronal damage and the infiltration of inflammatory cells), there is significant neutrophil accumulation within the pulmonary interstitium 6 and 24 hours after TBI. This was associated with pulmonary haemorrhage and increased vascular permeability. In an attempt to reduce pulmonary injury, 17-DMAG, an HSP90 inhibitor, was applied but proved to be nonprotective. Since patients with TBI show increased susceptibility to bacterial infection, microaspiration and ventilator-induced lung injury, a double-hit model was established whereby mice first received the head injury and then received a lung injury. This demonstrated worse lung injury following intra-tracheal administration of hydrochloric acid after TBI. Depleting neutrophils with an anti-LY-6G depleting antibody improved outcome in this model, indicating increased susceptibility to damage was neutrophil dependent. To test whether neutrophil accumulation within the pulmonary interstitium was specifically related to brain injury, lung tissue following other distant organ injury such as renal ischemia-reperfusion injury (IRI) and renal transplantation were assessed. Significant pulmonary interstitial neutrophil accumulation was seen following both models and was associated with significant pulmonary haemorrhage. Inducing HSP70 activity with an HSP90 inhibitor was shown to be protective by reducing the degree of pulmonary haemorrhage in these models. In an attempt to identify the mechanisms behind neutrophil accumulation in TBI, renal IRI and renal transplantation, ICAM-1 (CD54), a marker of the reverse transmigration of neutrophils was investigated. No differences in ICAM-1 expression were seen following TBI, indicating that another mechanism must be responsible. This mechanism is the focus of on going work within the laboratory. Hypoxia is believed to contribute towards the development of secondary brain injury however little is known regarding its direct contribution. Working alongside chemists at the University of Edinburgh, a number of novel fluorescent hypoxia probes were designed and tested, but none proved to be able to detect hypoxia in-vitro. In conclusion, this thesis has demonstrated that following mild TBI, the lungs are “primed” with a massive interstitial neutrophil influx and that a subsequent micro aspiration of acid induces exaggerated lung injury. The mechanism by which this occurs is the focus of on-going investigation. Pulmonary sequestration of neutrophils is also a predominant feature of other distant organ injuries.

Hypertonic saline (HS) is an accepted treatment for traumatic brain injury (TBI). However, the behavioral and cognitive consequences following HS administration have not thoroughly been examined. Recent preclinical evidence has suggested that nicotinamide (NAM) is beneficial for recovery of function following TBI. The first study compared the behavioral and cognitive consequences of HS and NAM as competitive therapeutic agents for the treatment of TBI. Following controlled cortical impact (CCI), bolus administrations of NAM (500 mg/kg), 7.5% HS, or 0.9% saline vehicle (1.0 mL/kg) were given at 2, 24, and 48 hrs post-CCI. Behavioral results revealed that animals treated with NAM and HS showed significant improvements in beam walk and locomotor placing compared to the Vehicle group. The Morris water maze (MWM) retrograde amnesia test was conducted on day 12 post-CCI and showed that all groups had significant retention of memory compared to injured, Vehicle-treated animals. Working memory was also assessed on days 18-20 using the MWM. The NAM and Vehicle groups quickly acquired the task; however, HS animals showed no acquisition of this task. Histological examinations revealed that the HS-treated animals lost significantly more cortical tissue than either the NAM or Vehicle-treated animals. HS-treated animals showed a greater loss of hippocampal tissue compared to the other groups. In general, NAM showed a faster rate of recovery than HS without this associated tissue loss. Study 1 suggested that future research into HS should include drug injection time course studies. Multiple injections may be responsible for the notable tissue damage. Therefore, it is possible that fewer injections will result in comparable behavioral recovery and less tissue damage that was observed. Due to the detrimental effects of 7.5% HS on cognition and hippocampal tissue following multiple administration in study 1, the proposed second study sought to study the behavioral and cognitive effects of HS using either single or multiple injection regime. The proposed study entailed a lengthier testing schedule than in study 1 and included the same histological examination to compare the different dosages. Additionally, edema formation was measured 24 hours following each drug endpoint in order to delineate the possible underlying mechanism of the observed deficits. In Study 2, HS tended to improve function on motor, sensorimotor and neurological tasks. Although this was a trend on all tests, animals treated with a single administration of HS overall performed better on all tasks compared to those receiving double or multiple injections. In the retrograde amnesia test, although not significant, the Sham, HS-2, and HS-24 animals showed improvement; whereas, the Vehicle and HS-48 animals showed no improvement in performance. This could possibly be linked to the additional hippocampal tissue loss that was noted in the HS-48 animals. In the working memory paradigm, the HS-2 and Vehicle groups had longer latencies to reach the platform than did the Sham group. However, after the first testing day, there were no significant differences between any of the groups. All animals treated with HS performed at the same rate and their performance either stayed the same over the three day testing period or became worse. It appears these animals were unable to learn and improve in the new memory acquisition task which is comparable to the results found in study 1. In study 1, there were again no observed hippocampal volume differences between the Sham and Vehicle-treated animals. However, there was extensive hippocampal tissue damage observed in all of the HS groups. Furthermore, animals treated with a single administration of HS had less hippocampal loss than those with double or multiple doses. Those animals receiving more than one dose of HS lost significantly more hippocampal tissue than the Vehicle group. The results of study 2 are comparable, and support, the results of study 1. Both studies support the strengths and weakness of HS therapy following TBI. Although there are potential benefits of HS therapy, there are also detrimental risks involved. Cognitive and structural damage could possible occur if the dosage amounts are not closely studied and monitored. Although the use of HS may be beneficial to reduce ICP following TBI, it appears that the use of HS may also lead to direct or indirect tissue loss possibly by chronic cellular dehydration. Stronger or more delineated effects may be noticed using higher doses or concentrations of HS in future studies. However, due to the nature of these results, caution should be advised with the use of all therapeutic usage of HS until further detailed studies are conducted.

While participation in youth sports bolster a myriad of health benefits, it can also pose a risk to the athlete's health from the increasing prevalence of repetitive mild traumatic brain injuries (TBI), often referred to as concussions. The adverse effects from repeated traumatic blows give a combination of acute symptoms, which may potentially develop into long-term complications. There is little known about the epidemiology of concussions, and thus the development of an animal model would help enhance our understanding of this potentially debilitating injury. An appropriate animal model should mimic the conditions of how concussions occur, in that there is not an invasive method to induce the injury and follows the same biomechanics. In our adolescent repetitive mild TBI model, we utilized a free-falling weight to deliver the traumatic blow to anesthetized mice that allowed free head rotation after impact. The injured group received one hit daily over the course of three days. The mice then underwent several behavioral tests to analyze the cognitive deficits, and the pathology of the tissue was analyzed via silver, Hematoxylin and Eosin (H&E), and Fluoro Jade-B staining. The injured mice developed both short- and long-term memory and spatial learning deficits, symptoms commonly found in concussed athletes, but failed to show deficits in anxiety and depression tests. The Fluoro Jade-B, silver and H&E staining resulted in negative signals for cell death. This study properly demonstrates repetitive mild TBIs in an adolescent mice model.

Thesis (M.A.)--Boston University / Sports-related concussions are a very large public health concern and have only recently been brought into the national spotlight, thanks largely to the increased media coverage following the deaths of several current and former players of the National Football League (NFL). This problem extends not only to professional athletes, but reaches down through college, high school and to our youth athletes as well. The symptoms resulting from concussion are diverse and include both acute and long-term effects, and could have particularly debilitating effects on the developing brains of young athletes. Various neurocognitive deficits, as well as neurodegenerative diseases such as chronic traumatic encephalopathy (CTE) have been associated with concussions. Research about both the short and long-term effects of concussions has been growing in recent years, and will continue to grow as advanced neuroimaging tools and biomarkers become better developed. This will improve diagnostic capabilities, result in better prognoses, as well as treatments and prevention. This review analyzes current literature in order to evaluate the lasting impacts of sports-related concussions. By showing the effects of sports-related concussions, especially on the developing brain, policy changes aimed at the prevention of concussion in sports will be suggested, specifically in terms of mitigating the adverse effects of concussions on brain development.

OBJECTIVES: (1) to investigate trends in non-traumatic dental visits (NTDV) to hospital-based emergency departments (ED) in Rhode Island (RI) and to compare them with those for other ambulatory sensitive care conditions (ACSC); (2) to examine the effect of expansion of Medicaid coverage on the rate NTDV to ED; (3) and to examine community-level factors associated with NTDVs. METHODS: Data for ED visits in 2005–2014 were obtained from RI hospital discharge data and annual population estimates from the U.S.Census Bureau, and were used to calculate annual visit rates. Medicaid enrollment report for the calendar years 2013 and 2014 were used to calculate monthly enrollment and an interrupted time series analysis was used to examine the effect of expansion of Medicaid coverage on visit rates. Zip code was used as a unit of analysis for community-level factor analysis, 2010 data. A negative binomial regression model with log link was performed. RESULTS: From January 2005 to December 2014, the annual average number of ED NTDV was 7440, accounting for 1.4–2.1% of all ED visits each year, there was a slight but not statistically significant decrease in the NTDV rate between 2005 and 2014. Visits for asthma also declined slightly, but the decrease was statistically significant. There were statistically significant increases in ED visit rates for diabetes and back pain. The NTDV rate increased by 34.8/100,000 enrollees per month immediately and significantly after expansion, amounting to more than 1000 additional ED visits. ED visits for asthma and back pain declined immediately after the expansion of coverage, but not significantly so. Community-level factors associated with NTDVs were higher level of poverty and communities with younger population (more individuals aged 20–34 years) which had significantly higher ED NTDV rates. CONCLUSION: RI NTDVs slightly declined, but still accounts for around 1.6% of ED visits. Medicaid expansion under the ACA, caused an immediate increase in NTDVs to ED, that might be attributed to the increased number of Medicaid enrollees, with no change in the workforce. Among community-level factors, high poverty level and high percent of young population had the highest impact on visit rates. / 2019-09-26T00:00:00Z

Traumatic brain injury (TBI) is a major health problem affecting the adult and pediatric population. Scientists and clinicians are working diligently to discover possible therapeutics for the treatment of TBI. Two possible treatments to deal with TBI include sleep and the administration of progesterone. Yet, there are conflicting results from studies regarding the efficacy of either treatment. Sleep appears to reduce neuroinflammation and reduce axonal damage in the brain following TBI. Sleep deprivation, however, may have neuroprotective effects after TBI. Progesterone has also been shown to have neuroprotective effects following TBI. But, there are no sufficient data from animal studies to determine if progesterone is an effective therapeutic. More research studies will have to be conducted to further understand the role of sleep and progesterone in alleviating TBI.

The pathophysiology of traumatic brain injury (TBI) includes perturbations to energy metabolism. Improving our understanding of cerebral energy metabolism will lead to strategies that improve clinical outcomes. For the studies in my thesis I used microdialysis to deliver carbon-13 labelled substrates to the human brain. I combined this with nuclear magnetic resonance (NMR) spectroscopy of interstitial fluid sampled from the brain to interrogate glucose, lactate and tricarboxylic acid (TCA) cycle metabolism. Study I: I defined the optimal parameters for quantitative proton and carbon-13 NMR of cerebral microdialysates. Study II: I measured baseline microdialysate metabolite concentrations for brain and muscle and investigated the influence of muscle activity and cerebral catheter placement in grey or white matter on metabolite concentrations. Study III: I used 1,2-13C2 glucose to measure glycolysis and pentose phosphate pathway activity. Glycolysis is the dominant lactate-producing pathway but the pentose phosphate pathway also contributes and is increased in some TBI patients. Study IV: I used arterio-venous gradients to measure glucose and lactate delivery to the brain. There are periods after injury when lactate is imported from the circulation despite relatively high brain lactate levels suggesting up-regulation of lactate transport. Study V: I followed the metabolism of 3-13C lactate and demonstrated that lactate is metabolised by the TCA cycle. This occurs in both normal and injured brain but not in muscle. Study VI: I used 2,3-13C2 succinate to investigate the role of the TCA cycle in producing metabolites that are exported into the interstitium. The TCA cycle is found to be a source of lactate. Succinate delivered to the brain improves redox and enhances glutamate uptake into cells. The implications of the findings in my thesis on existing knowledge of cerebral metabolism are discussed. Strategies that might potentiate cerebral metabolism and improve clinical outcomes are suggested.

Traumatic Brain Injury (TBI) is a leading cause of death and disability in the United States for which there are no federally approved pharmacological treatments. Preclinical trials with nicotinamide (NAM) and progesterone (Prog) treatment demonstrate beneficial neuroprotection and recovery of function following TBI. The primary goal of this study was to assess both neuroprotection and recovery of function in an animal model of TBI after combination treatment of both NAM and Prog. Animals received a cortical contusion injury over the sensorimotor cortex and were treated with either nicotinamide (75 mg/kg, i.p. NAM loading dose, 12 mg/kg/hr NAM, s.c. over 72 hrs), Prog (10 mg/kg Prog, i.p. over 72 hrs), NAM and Prog(75 mg/kg, i.p. NAM loading dose, followed by continuous infusion of 12 mg/kg/hr NAM, s.c. over 72 hrs; 10 mg/kg Prog, i.p. over 72 hrs) or Vehicle (75 mg/kg, i.p. sterile saline loading dose, followed by continuous infusion 12 mg/kg/hr sterile saline, s.c. over 72 hrs; 10 mg/kg peanut oil, i.p. over 72 hrs), and compared to a craniotomy only (Sham) group. Following this regimen they were assessed in a battery of behavioral (fine and gross motor, sensory, and cognitive) tasks or a histological assessment at 24 hrs post-injury assessing lesion cavity size, degenerating neurons, and reactive astrocytes. Our results replicate the beneficial effects of treatment with either NAM or Prog demonstrating significant improvements in recovery of function, and a reduction in lesion cavitation, degenerating neurons and reactive astrocytes 24 hours post-injury. The combination treatment of NAM and Prog led to a significant improvement in both neuroprotection at 24 hrs post-injury and recovery of function in sensorimotor related tasks when compared to each individual treatment (NAM or Prog). It is suggested here that further preclinical trials using NAM and Prog as a combination treatment should be done to identify any drug interactions, pharmacokinetics, and a new window of opportunity and proper dosing of this combination treatment.