Books on the topic 'Work injury causing death'

This text is an update of a classic work on diagnosing the cause of coma, with the addition of new sections on the treatment of comatose patients. The first chapter provides an up-to-date review on the brain mechanisms that maintain a conscious state in humans and how lesions that damage these mechanisms cause loss of consciousness or coma. The second chapter reviews the neurological examination of the comatose patient, which provides the basis for determining whether the patient is suffering from a structural brain injury causing the coma or from a metabolic disorder of consciousness. The third and fourth chapters review the pathophysiology of structural lesions causing coma and the specific disease states that result in coma. Chapter 5 is a comprehensive treatment of the many causes of metabolic coma. Chapter 6 review psychiatric causes of unresponsiveness and how to identify and treat them. Chapters 7 and 8 review the overall emergency treatment of comatose patients, followed by the treatment of specific causes of coma. Chapter 9 examines the long-term outcomes of coma, including the minimally conscious state and the persistent vegetative state, how they can be distinguished, and their implications for eventual useful recovery. Chapter 10 reviews the topic of brain death, the standards for examination of a patient that are required to make the determination of brain death, and the ethics of diagnosis and treatment of patients who, by definition, have no way to approve of or communicate about their wishes.

Recent research has provided important insights on the long-term outcomes of patients who develop acute kidney injury (AKI) in the setting of critical illness. Large epidemiologic studies have demonstrated compelling associations between episodes of AKI and progressive kidney disease and death, respectively, although such studies do not establish causality due to the potential for confounding. Whether AKI is intrinsically toxic or a mere by-product of serious comorbidities (e.g. prior chronic kidney disease, heart failure, diabetes), there is no doubt that AKI survivors are a high-risk group who would likely benefit from close post-discharge follow-up. Recent studies have shown that a minority of patients with AKI receive specialized nephrology follow-up after discharge, suggesting an opportunity for quality improvement. Emerging research is evaluating factors that predict chronic kidney disease, end-stage renal disease, and death among AKI survivors. This work will, it is hoped, suggest new targets for prevention and treatment, with the goal of enhancing the likelihood of recovery following AKI.

Falls in the elderly are very common, and their frequency increases with aging. At a personal level, falls are associated with a subsequent fear of falling, a decline in function, increased nursing home placement, and increased use of medical services, and complications resulting from falls represent the leading cause of death from injury in geriatric population. At the more global level, falls in the elderly are associated with increased use of medical services and increased cost directly to the patient and also indirectly, if we add the number of hours of work lost by caregivers who will assume care of that elderly person after the fall. This chapter covers the definition and relevance of falls in the elderly population; etiology and risk factors for falls; evaluation and management; and assessment for and correction of risk factors. Integrative management approaches discussed in this chapter are movement and exercise, nutrition and supplements, and hormone replacement.

The prevention of disease at a population health level rather than an individual health level is aimed at reducing causes of ‘preventable’ death and, under the auspices of public health and epidemiology, is an integral part of primary, secondary, and tertiary care. Classification of death is usually according to the type of primary disease or injury. However, there are a number of recognized risk factors for death, and modifications in behaviour or risk factors can substantially reduce preventable causes of death and the associated healthcare and economic burden of chronic disease management. According to the WHO, hundreds of millions of people from infancy to old age suffer from preventable chronic respiratory diseases, there are over four million deaths annually from preventable respiratory diseases, and common respiratory disorders (e.g. lower respiratory tract infections, chronic obstructive pulmonary disease, lung cancer, and tuberculosis) account for approximately 20% of all deaths worldwide. This chapter discusses the prevention of respiratory disease, covering diseases associated with smoking (one of the biggest risk factors associated with preventable deaths), air pollution, and other lifestyle factors associated with respiratory disease; changes in legislation concerning smoking and work-related respiratory disease; and, finally, the prevention of respiratory diseases through the use of immunization and screening tools.

This book conducts a cultural analysis of the labor of the news fixer—the locally based media employee who helps international correspondents research stories, set up interviews, translate foreign languages, and navigate unfamiliar regions. Foreign reporters often say that their work would be impossible without these local news assistants. Yet, fixers are among some of the most exploited and persecuted people contributing to the production of international news. Targeted by militant groups, by their own governments, or even by their own neighbors, fixers must often engage in a precarious balancing act between appeasing their community members and pleasing the correspondents who visit from faraway. Though foreign news outlets routinely depend upon news fixers’ insider awareness of politically tense situations in order to keep their own reporters safe in the field, fixers themselves continually face detainment, injury, and death. Even so, international news organizations almost never provide their fixers with hazardous environment training or medical insurance. What is more, fixers rarely receive professional credit from the reporters who hire them, suggesting that their often life-threatening labor is deeply undervalued. Drawing upon 75 interviews with fixers from 39 different countries, this book argues that although fixers’ labor is essential to international news reporting, it is still relegated to the shadows of the international news industry.

The Oxford Handbook of Behavioral Emergencies and Crisesincludes the most up-to-date and valuable research on the evaluation and management of arguably the most challenging patients faced by mental health practitioners—that is, individuals who are at high risk of suicide or other-directed violence or of becoming the victims of interpersonal violence. The outcome with such cases can be serious injury or death, and there can be negative consequences for the patient, and also for the patient’s family and friends, for the clinician, and for the clinic or medical center. This book presents a framework for learning the skills to assess and work competently with these patients. The book has sections dealing with such critical incidents in children, adolescents, adults, and the elderly. There are sections to aid clinicians with conditions that need to be distinguished from behavioral emergencies; on treating patients or clients who have ongoing chronic risk of harming themselves or others; and on legal and ethical risk management as well as psychological risk management for the clinician in the event of a negative outcome. The book examines interrelated aspects of the major behavioral emergencies; for example, the degree to which interpersonal victimization may lead an individual to later suicidal or violent behavior; or the degree to which suicidal individuals and violent individuals may share certain cognitive characteristics. It also presents a method for reducing the clinician’s stress and acquiring skill in working with high-risk people.

Behind heart disease and cancer, medical error is now listed as one of the leading causes of death. Of the medical errors that lead to injury and death, diagnostic failure is regarded as the most significant. Generally, the majority of diagnostic failures are attributed to the clinicians directly involved with the patient, and to a lesser extent, the system in which they work. In turn, the majority of errors made by clinicians is due to decision making failures manifested by various departures from rationality. Of all the medical environments in which patients are seen and diagnosed, the emergency department is the most challenging. It has been described as a ‘wicked’ environment where illness and disease may range from minor ailments and complaints to severe, life-threatening disorders. The Cognitive Autopsy is a novel strategy towards understanding medical error and diagnostic failure in 42 clinical cases with which the author was directly involved or became aware of at the time. Essentially, it describes a cognitive approach towards root cause analysis of medical adverse events or near misses. Whereas root cause analysis typically focuses on the observable and measurable aspects of adverse events, the cognitive autopsy attempts to identify covert cognitive processes that may have contributed to outcomes. In this clinical setting, no cognitive process is directly observable but must be inferred from the behaviour of the individual clinician. The book illustrates unequivocally that chief among these cognitive processes are cognitive biases and other flaws in decision making, rather than knowledge deficits.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.