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Recently, the World Health Organization declared a pandemic mediated by the novel A H1N1 influenza virus. Soon after the first report from Mexico, the disease arrived in Chile, where it spread quickly from south to north, mimicking cold weather progression through the country. Between May and September 2009, 366,624 cases of H1N1 were reported; 12,248 were confirmed by real-time reverse-transcription polymerase chain reaction and 1562 were hospitalized. One hundred thirty-two deaths were attributable to the infection, creating a death rate of 0.78 per 100,000 inhabitants. Common comorbidities were present in 59%, including obesity, chronic obstructive pulmonary disease, hypertension, type II diabetes, and congestive heart failure. Nine percent were pregnant. Severe disease developed early; the median time to admittance was 5 days, and the most common clinical manifestations were cough, fever, dyspnea, and myalgia. Mean acute physiology and chronic health evaluation II and sequential organ failure assessment scores were 14 and 5, respectively. Highlighted laboratory data were lactate dehydrogenase and creatine kinase elevation, leukocytosis in 50%, elevated creatinine in a 25%, and thrombocytopenia in 20%. Severe respiratory failure requiring high-frequency oscillatory ventilation and extracorporeal membrane oxygenation as sophisticated modes of respiratory support was seen in 17%. Acute renal failure occurred in 25% of the intensive care unit patients, with death rates near 50%. Health systems reinforced outpatient guards with extra staff and extension of the duty schedules. Antivirals were supplied free for medically diagnosed cases. Admissions for severe cases were prioritized, reconverting hospital beds into advanced care ones; a central coordination station rationed their assignment. Recommendations for small hospitals include adding ventilators, using videoconferences, providing tutorial activity from experts, developing guidelines for disease management, and outlining criteria for transport.
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PMID:Influenza A pandemics: clinical and organizational aspects: the experience in Chile. 1993 12

We report the pathological and virological findings of the first autopsy case of the 2009 pandemic influenza (A/H1N1pdm) virus infection in Japan. A man aged 33 years with chronic heart failure due to dilated cardiomyopathy, mild diabetes mellitus, atopic dermatitis, bronchial asthma, and obesity died of respiratory failure and multiple organ dysfunction syndrome. Macroscopic examination showed severe pulmonary edema and microscopically the lung sections showed very early exudative-stage diffuse alveolar damage (DAD). Immunohistochemistry revealed proliferation of the influenza (A/H1N1pdm) virus in alveolar epithelial cells, some of which expressed SAalpha2-3Gal on the cell surface. Influenza (A/H1N1pdm) virus genomic RNA and mRNA were also detected in alveolar epithelial cells. Real-time PCR revealed 723 copies/cell in the left lower lung section from which the influenza (A/H1N1pdm) virus was isolated. Electron microscopic analysis revealed filamentous viral particles in the lung tissue. The concentrations of various cytokines/chemokines in the serum and the autopsied lung tissue were measured. IL-2R, IL-6, IL-8, IL-10, IFN-alpha, MCP-1, and MIG levels were elevated in both. These findings indicated a case of viral pneumonia caused by influenza (A/H1N1pdm) virus infection, showing characteristic pathological findings of the early stage of DAD.
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PMID:The first autopsy case of pandemic influenza (A/H1N1pdm) virus infection in Japan: detection of a high copy number of the virus in type II alveolar epithelial cells by pathological and virological examination. 2009 68

If the H1N1 pandemic worsens, there may not be enough ventilated beds to care for all persons with respiratory failure. To date, researchers who explicitly discuss the ethics of intensive care unit admission and the allocation of ventilators during an influenza pandemic have based criteria predominantly on the principles of utility and efficiency, that is, promoting actions that maximize the greatest good for the greatest number of people. However, haphazardly applying utility and efficiency potentially disadvantages marginalized populations who might be at increased risk of severe reactions to H1N1. In Canada, Aboriginals represent 3% of Canadians, yet 11% of H1N1 cases requiring hospitalization involve Aboriginal persons. Aboriginal persons suffer from high rates of obesity due to socio-economic inequalities. Obesity is also a risk factor for severe H1N1 reactions. Yet, since obesity is found to increase the duration of stay in ventilated beds and a long stay is not considered an optimal use of ventilators, applying the principles of utility and efficiency may magnify existing social inequalities. Although promoting utility and efficiency is important, other ethical principles, such as equity and need, require thoughtful consideration and implementation. Furthermore, since public resources are being used to address a public health hazard, the viewpoints of the public, and specifically stakeholders who will be disproportionately affected, should inform decision-makers. Finally, giving attention to the needs and rights of marginalized populations means that ventilators should not be allocated based on criteria that exacerbate the social injustices faced by these groups of people.
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PMID:Contextualizing ethics: ventilators, H1N1 and marginalized populations. 2010 34

Hypoxic-ischemic brain damage often results from a combination of cardiogenic and respiratory failure. Whether or not hypoxia in the absence of ischemia is injurious to the brain has been a topic of research. An example of hypoxia without ischemia is found in obstructive sleep apnea (OSA), which causes recurrent nocturnal oxygen desaturations. Furthermore, it is a pervasive problem in the general population, particularly in people with common disorders such as obesity or diabetes. Mounting evidence in the past decade indicates that cerebrovascular disease, specifically stroke, and neurobehavioral consequences, including excessive daytime sleepiness and cognitive deficits, are prevalent in people with OSA, at great costs to the individual well-being, public health, and the economy. Investigation of the two disease associations poses similar and unique challenges. Predictors of these sequelae need to be better defined. The apnea-hypopnea index, the most common measure of OSA, has proven to be variably related to stroke and cognitive impairment. The role of individual markers, whether they are comorbidities or differences in inherent cognitive reserve, also is incompletely understood. This review discusses the burgeoning literature on the neurological and neurobehavioral sequelae of OSA and highlights the future avenues of research in the field.
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PMID:Neurological and neurobehavioral sequelae of obstructive sleep apnea. 2013 Mar 57

The prevalence of obesity is increasing. The mortality and morbidity among obese intensive care unit (ICU) patients has been a matter of concern. Most of the retrospective studies performed have yielded contradictory results. Recently, two large prospective studies showed that respiratory failure, length of mechanical ventilation and ICU acquired infections were increased in obese patients. Obesity was, however, not associated with increased mortality. The results were confirmed by a meta-analysis which showed that obesity was associated with increased morbidity but not with increased mortality.
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PMID:[Obesity is not associated with an increased mortality in critical disease and intensive care]. 2015 3

As the pandemic of 2009 H1N1 influenza A virus progressed, more patients required hospitalisation. The objective of this study is to describe the characteristics and clinical course of hospitalised patients with 2009 H1N1 virus infection in Chile. This was a prospective, observational study of 100 consecutive hospitalised patients with RT-PCR-confirmed 2009 H1N1 influenza A, admitted to Puerto Montt General Hospital (Puerto Montt, Chile). Information was obtained regarding contact history, demographics, laboratory values and clinical course. The primary reason for hospitalisation was pneumonia, in 75% of patients. Rapid influenza A test was positive in 51% of patients. Prior exposure to 2009 H1N1 virus was documented in 21% of patients. Clinical failure, documented in 18% of cases, was characterised by respiratory failure and acute respiratory distress syndrome. Failure was more common in patients with obesity, tachypnoea, confusion and multilobar infiltrates. When evaluating a patient hospitalised with influenza-like illness, a negative rapid test for influenza A or negative contact with a suspected case should not alter physicians' considerations regarding the likelihood of 2009 H1N1 virus infection. Patients with 2009 H1N1 virus infection with obesity, tachypnoea, confusion and multilobar infiltrates should be closely monitored since they are at high risk for clinical failure.
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PMID:Characteristics of hospitalised patients with 2009 H1N1 influenza in Chile. 2018 21

An adult man was brought into the emergency department after deliberate ingestion of dinitrophenol: an agent that uncouples mitochondrial oxidative phosphorylation. The patient rapidly developed a hyper-metabolic state with fever, respiratory failure and died within a few hours after admission. Dinitrophenol is used in the manufacture of dyes, pesticides and explosives. Sub-acute poisoning is associated with weight-loss and the substance had been prescribed for this purpose during the 1930s in the United States before being banned due to serious side effects. Although remaining unlicensed as a drug, dinitrophenol is widely available through mail-order websites and online pharmacies, which promote it as an anti-obesity treatment. This case highlights the need for awareness of possibly increasing rates of accidental poisoning with a growing obesity prevalence and availability of this unlicensed drug through the internet. Additionally, we discuss the use of dantrolene in dinitrophenol poisoning and question whether current Toxbase/UK National Poison Information Service treatment guidelines regarding the indication and dosing of this drug, the only relatively specific treatment in dinitrophenol poisoning presently recommended, could be revised.
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PMID:'Fatal 2,4-dinitrophenol poisoning... coming to a hospital near you'. 2051 42

Congenital central hypoventilation syndrome (CCHS) is a rare disorder with uncertain nosology that usually presents early in life. The syndrome is characterized by ventilatory response impairment to carbon dioxide and may result in respiratory failure at birth. Recent reports have identified a similar clinical presentation beyond infancy called late-onset central hypoventilation syndrome (LO-CHS) as a disease continuum of CCHS with similar and overlapping pathophysiology. However, some have proposed that the syndrome accompanied by hypothalamic dysfunction (HD) be classified as a distinct clinical entity, LO-CHS/HD. To the best of our knowledge, the case reported herein is the oldest case of LO-CHS/HD in childhood, at 13 years old. He suffered from recurrent pulmonary edema, acute convulsive seizures, hypersomnia, hyperphagia, obesity, impaired glucose tolerance test, and hypercapnia, diagnosed as LO-CHS/HD, and was successfully treated with nasal bi-level positive airway pressure.
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PMID:A case of late-onset central hypoventilation syndrome with hypothalamic dysfunction: through a new phenotype. 2056 Feb 60

Daytime hypercapnia that develops in morbidly obese individuals in the absence of concurrent lung or neuromuscular disease is referred to as the obesity hypoventilation syndrome (OHS). The characteristic polysomnographic (PSG) abnormality is marked sleep hypoxemia. Although the likelihood of hypoventilation increases with increasing body mass index (BMI), it is too simplistic to think of this disorder arising merely from chest wall restriction due to excess weight. Rather, this is a disorder which emerges when the compensatory mechanisms that normally operate to maintain ventilation appropriate for the level of obesity are impaired. OHS develops from a complex interaction between abnormal respiratory function, sleep disordered breathing and diminished respiratory drive. Irrespective of the mechanisms underlying the development of this disorder, early recognition of the problem and institution of effective therapy is important to reduce the significant clinical and societal repercussions of OHS. While therapy directed at improving sleep disordered breathing is effective in reversing daytime respiratory failure, it is not universally successful and information regarding longer term clinical outcomes is limited. Attention to weight reduction strategies are also necessary to reduce comorbid conditions and improve quality of life, but data regarding how successful and sustained this is in obesity hypoventilation are sparse.
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PMID:Obesity hypoventilation syndrome--the big and the breathless. 2129 2

Sleep hypoventilation is seen in patients with neuromuscular disease, as well as in those with obesity hypoventilation syndrome (OHS), which is defined as the combination of obesity, chronic hypercapnia, and hypoxemia during wakefulness that is aggravated during sleep. In 90% of cases, OHS is accompanied by obstructive sleep apnea. The diagnosis of OHS is based on hypoventilation and pulmonary hypertension that cannot be explained by alterations in pulmonary function. The mortality of patients with OHS is greater than is that of obese patients without hypoventilation. The principal neuromuscular diseases associated with OHS are the muscular dystrophies. The progression to chronic respiratory failure results from respiratory muscle weakness and impaired airway secretion clearance, causing atelectasis and pneumonia. With a decrease of greater than 50% in respiratory muscle strength, there is a reduction in VC. Cough peak flow < 160 L/min is associated with impaired airway secretion clearance, and values near 270 L/min indicate the need for assisted cough techniques. Obstructive sleep apnea usually worsens sleep hypoventilation. Noninvasive ventilation during sleep can improve survival, symptoms, and hypoventilation during wakefulness, as well as being able to improve pulmonary function in patients with neuromuscular disease. Patients with OHS can require oxygen therapy.
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PMID:[Sleep hypoventilation]. 2094 82


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