Concept: Causes of death
Homicide is one of the leading causes of death for women aged ≤44 years.* In 2015, homicide caused the death of 3,519 girls and women in the United States. Rates of female homicide vary by race/ethnicity (1), and nearly half of victims are killed by a current or former male intimate partner (2). To inform homicide and intimate partner violence (IPV) prevention efforts, CDC analyzed homicide data from the National Violent Death Reporting System (NVDRS) among 10,018 women aged ≥18 years in 18 states during 2003-2014. The frequency of homicide by race/ethnicity and precipitating circumstances of homicides associated with and without IPV were examined. Non-Hispanic black and American Indian/Alaska Native women experienced the highest rates of homicide (4.4 and 4.3 per 100,000 population, respectively). Over half of all homicides (55.3%) were IPV-related; 11.2% of victims of IPV-related homicide experienced some form of violence in the month preceding their deaths, and argument and jealousy were common precipitating circumstances. Targeted IPV prevention programs for populations at disproportionate risk and enhanced access to intervention services for persons experiencing IPV are needed to reduce homicides among women.
Improvements in our understanding of the role of modifiable risk factors for sudden infant death syndrome (SIDS) mean that previous reassurance to parents that these deaths were unpreventable may no longer be appropriate. This study aimed to learn of bereaved parents' and healthcare professionals' experiences of understanding causes of death following detailed sudden unexpected death in infancy (SUDI) investigations. The research questions were: How do bereaved parents understand the cause of death and risk factors identified during detailed investigation following a sudden unexpected infant death? What is the association between bereaved parents' mental health and this understanding? What are healthcare professionals' experiences of sharing such information with families?
Endotracheal intubation is frequently complicated by laryngeal edema, which may present as postextubation stridor or respiratory difficulty or both. Ultimately, postextubation laryngeal edema may result in respiratory failure with subsequent reintubation. Risk factors for postextubation laryngeal edema include female gender, large tube size, and prolonged intubation. Although patients at low risk for postextubation respiratory insufficiency due to laryngeal edema can be identified by the cuff leak test or laryngeal ultrasound, no reliable test for the identification of high-risk patients is currently available. If applied in a timely manner, intravenous or nebulized corticosteroids can prevent postextubation laryngeal edema; however, the inability to identify high-risk patients prevents the targeted pretreatment of these patients. Therefore, the decision to start corticosteroids should be made on an individual basis and on the basis of the outcome of the cuff leak test and additional risk factors. The preferential treatment of postextubation laryngeal edema consists of intravenous or nebulized corticosteroids combined with nebulized epinephrine, although no data on the optimal treatment algorithm are available. In the presence of respiratory failure, reintubation should be performed without delay. Application of noninvasive ventilation or inhalation of a helium/oxygen mixture is not indicated since it does not improve outcome and increases the delay to intubation.
This review summarizes the most recent clinical and experimental data on the impact of spontaneous breathing in acute respiratory distress syndrome (ARDS).
Road crashes are considered as the eighth leading causes of death. There is a wide disparity in crash severity and law enforcement efficiency among low, medium and high-income countries. It would be helpful to review the crash severity trends in these countries, identify the vulnerable road users and understand the law enforcement effectiveness for coming up with efficient road safety improvement strategies.
Since antiquity, cot death has been explained as accidental suffocation, overlaying, or smothering. Parents were blamed for neglect or drunkenness. A cage called arcuccio was invented around 1570 to protect the sleeping infant. Up to the 19th century, accidents were registered as natural causes of death. From 1830, accidental suffocation became unacceptable for physicians and legislators, and “natural” explanations for the catastrophe were sought, with parents being consoled rather than blamed. Two assumed causes had serious consequences: thymus hyperplasia was irradiated, causing thyroid cancer, and the concept of central apnea was widely accepted, which led to home monitors and distracted from epidemiological evidence. Prone sleeping originated in the 1930s and from 1944, it was associated with cot death. However, from the 1960s, many authors recommended prone sleeping for infants, and many countries adopted the advice. A worldwide epidemic followed, peaking at 2‰ in England and Wales and 5‰ in New Zealand in the 1980s. Although epidemiological evidence was available by 1970, the first intervention was initiated in the Netherlands in 1989. Cot death disappeared almost entirely wherever prone sleeping was avoided. This strongly supports the assumption that prone sleeping has the greatest influence on the disorder, and that the epidemic resulted from wrong advice.
ST-elevation acute myocardial infarction (STEMI) represents one of the leading causes of death. The time of STEMI onset has a circadian rhythm with a peak during diurnal hours, and the occurrence of STEMI follows a seasonal pattern with a salient peak of cases in the winter months and a marked reduction of cases in the summer months. Scholars investigated the reason behind the winter peak, suggesting that environmental and climatic factors concur in STEMI pathogenesis, but no studies have investigated whether the circadian rhythm is modified with the seasonal pattern, in particular during the summer reduction in STEMI occurrence.
High-permeability pulmonary edema is a hallmark of acute respiratory distress syndrome (ARDS) and is frequently accompanied by impaired alveolar fluid clearance (AFC). AP301 enhances AFC by activating epithelial sodium channels (ENaCs) on alveolar epithelial cells, and we investigated its effect on extravascular lung water index (EVLWI) in mechanically ventilated patients with ARDS.
- Journal of neurology, neurosurgery, and psychiatry
- Published over 1 year ago
Survival and causes of death (COD) in multiple sclerosis (MS) provide ultimate endpoints. We aimed to investigate survival and COD in a 60-year population-based MS cohort compared with the general population.
- Journal of urban health : bulletin of the New York Academy of Medicine
- Published over 4 years ago
In the USA, homicide is a leading cause of death for young males and a major cause of racial disparities in life expectancy for men. There are intense debate and little rigorous research on the effects of firearm sales regulation on homicides. This study estimates the impact of Missouri’s 2007 repeal of its permit-to-purchase (PTP) handgun law on states' homicide rates and controls for changes in poverty, unemployment, crime, incarceration, policing levels, and other policies that could potentially affect homicides. Using death certificate data available through 2010, the repeal of Missouri’s PTP law was associated with an increase in annual firearm homicides rates of 1.09 per 100,000 (+23 %) but was unrelated to changes in non-firearm homicide rates. Using Uniform Crime Reporting data from police through 2012, the law’s repeal was associated with increased annual murders rates of 0.93 per 100,000 (+16 %). These estimated effects translate to increases of between 55 and 63 homicides per year in Missouri.