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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The obesity-hypoventilation syndrome (or alveolar hypoventilation in the obese) is a new name for an old syndrome, Pickwickian syndrome. It is defined as chronic alveolar hypoventilation (PaO(2)<70 mmHg, PaCO(2) > 45 mmHg) in obese patient with a body mass index > 30 kg/m(2) who have no other respiratory disease explaining the gas anomalies. The large majority of obese subjects are not hypercapnic, even in case of severe obesity. There are three principal causes explaining alveolar hypoventilation in obese subjects: high cost of the work of respiration, dysfunction of the respiratory centers, repeated episodes of nocturnal obstructive apnea. The obesity-hypoventilation syndrome is generally found in males aged over 50 years. Exercise-induced breathlessness is a constant finding. Diagnosis is often made after an episode of severe respiratory failure. Associated diseases favored by obesity are frequent: diabetes, high blood pressure, heart disease. By definition, there is a hypoxemia-hypercapnia syndrome persisting after an acute episode. Spirography usually demonstrates moderate volume restriction. Pulmonary hypertension is frequent but not constant. Obesity-hypoventilation syndrome must be distinguished from obstructive sleep apnea, although the two conditions are often associated. Obstructive sleep apnea may be absent in certain patients with obesity-hypoventilation syndrome (we have had several cases) and inversely, obesity is not observed in certain patients with obstructive apnea. It should be recalled that the term Pickwickian syndrome designates obesity-hypoventilation syndrome (with or without obstructive apnea) and not obstructive sleep apnea syndrome.
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PMID:[Alveolar hypoventilation in the obese: the obesity-hypoventilation syndrome]. 1208 46

Obstructive sleep apnea, obesity-related hypoventilation - a hypoventilation which is independent of apneas and increased by sleep -, and hypoxemia related to local ventilation-perfusion disorders are the main mechanisms of respiratory failure occurring during acute respiratory decompensation following an often minimal triggering event. Non-invasive ventilation has been found to be an effective treatment, particularly with a ventilator capable of maintaining positive expiratory and pressure. The level of the expiratory positive airway pressure must be adapted to cure episodes of obstructive apnea or hypopnea. The level of the inspiratory positive airway pressure (pressure support ventilator), or the tidal volume (volume-controlled ventilator) must be adapted to correct the residual hypoventilation. These adaptations can be made by proper assessment of nocturnal SaO(2) recordings. In particularly severe cases, use of endotracheal ventilation may be necessary to control a state of shock or consciousness disorders incompatible with the patient cooperation necessary for non-invasive ventilation.
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PMID:[Acute respiratory failure in obesity]. 1208 50

The obstructive sleep apnea syndrome (OSAS) is caused by an intermittent and repetitive obstruction of the upper respiratory tract during sleep, which leads to a complete (apnea) or partial (hypopnea) block of air flow. It is quite prevalent, being seen in 4-6% of males and 2% of females. Structural abnormalities present in the upper respiratory tract and obesity are the fundamental etiological factors. Clinical manifestations are due to sleep fragmentation and oxygen desaturation which cause the apnea. Day hypersomnia, snoring and episodes of apnea described by the spouse are the three basic symptoms. The diagnosis is based on polysomnography, which can be substituted for a night cardiorespiratory polygraphy. It has an important morbimortality rate, mainly due to traffic and labor accidents, ischemic heart disease and chronic respiratory failure. The treatment is multifactorial. First, eliminating alcohol and hypnotic drugs. Obesity, which is almost always present, must also be corrected. Structural abnormalities of the upper respiratory tract may require a surgical solution. The treatment preferred nowadays is the application of a nasal continuous positive airway pressure (CPAP) while the patient is asleep. It should be considered for those symptomatic patients with an apnea-hypopnea index over 30, or if the index is below 30, than when a respiratory insufficiency or cardiovascular risk factors are present. In some cases surgical procedures may be considered, such as uvulopalatopharyngoplasty.
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PMID:[Obstructive sleep apnea syndrome]. 1219 5

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39

This article considers the evaluation of patients prior to institution of long-term ventilation (LTV). LTV has evolved from a concept of necessity ventilation to a more satisfactory approach of preventive LTV, enabled by the impressive development of noninvasive mechanical ventilation (NIV). Due to its convenience and efficacy, and its safety compared with invasive ventilation, NIV has rapidly gained popularity among patients with chronic respiratory failure (CRF) requiring intermittent ventilatory assistance. Evaluation of candidates for LTV involves clinical and laboratory evaluations and sleep monitoring. It includes consideration of the etiology of CRF, be it restrictive lung disease, chronic obstructive pulmonary disease, obesity or other cause, and considers the feasibility of LTV as well as its desirability.
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PMID:Evaluation of candidates for long-term ventilation. 1248 64

A 24-year-old obese woman was found dead in her boyfriend's apartment in his absence. She had been admitted to the hospital six times previously because of diminished consciousness, respiratory failure, and pneumonia. A diagnosis of obesity-sleep apnea (Pickwickian) syndrome was made. An autopsy showed that she had an extremely small larynx, intra-alveolar hemorrhage, edema, pulmonary lymphocyte infiltration, and severe focal myocardial fibrosis. No fresh myocardial lesion, coronary arterial lesion, or findings of heart failure were seen. The woman's elder sister had also died of the same disease at the age of 23. The cause of death was diagnosed as respiratory failure and pneumonia with the sleep-apnea syndrome as the underlying cause of death. Although no autopsy reports of the sleep-apnea syndrome have been published in the field of forensic pathology, this syndrome is a predominant cause of sudden death in obese persons and could be a hidden cause of accidental death in such persons.
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PMID:Obesity-sleep apnea (Pickwickian) syndrome: autopsy findings and a medicolegal review. 1293 64

Individuals with Prader-Willi syndrome (PWS) generally survive into adulthood. Common causes of death are obesity related cor pulmonale and respiratory failure. We report on a case series of eight children and two adults with unexpected death or critical illness. Our data show age-specific characteristics of PWS patients with fatal or life-threatening illnesses. Under the age of 2 years, childhood illnesses in general were associated with high fever and rapid demise or near-demise. Hypothalamic dysfunction likely plays a role in exaggerated fever response, but also perhaps in central regulation of adrenal function. Below average sized adrenal glands were found in three children, which raises the possibility of unrecognized adrenal insufficiency in a subset of individuals with PWS and emphasizes the vital role of autopsy. The tub drowning death of an adult patient could be related to central hypersomnia, which has been reported in PWS. We suggest that increased risk for critical illness be considered in the discussion of anticipatory guidance for the care of infants with PWS. Since a number of children died while hospitalized, particularly close observation of PWS children who are ill enough to warrant hospital admission is recommended.
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PMID:Unexpected death and critical illness in Prader-Willi syndrome: report of ten individuals. 1469 14

We report on three male infants with de novo terminal deletions of chromosome 9q34.3. The clinical features are compared to the nine cases described in the literature. Case 1 and 3 were ascertained following the use of subtelomeric FISH to screen for a chromosomal anomaly, case 2 was confirmed by FISH probe following detection of a 9q deletion on standard karyotyping. Deletions in this region result in severe developmental delay, a distinct facial phenotype, cardiac anomalies, obesity, and respiratory failure, which may result in premature death. The delineation of the 9q deletion phenotype will aid diagnosis and genetic counseling as subtelomere FISH screening becomes more widely available.
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PMID:Three patients with terminal deletions within the subtelomeric region of chromosome 9q. 1563 79

Age at diagnosis, Body Mass Index and physical morbidity in children and adults with the Prader-Willi syndrome: The medical findings of a population of 54 Prader-Willi patients with a molecular confirmed diagnosis are discussed. In the age group aged 18 or younger, a reasonably good control of weight as measured by Body Mass Index (BMI) is found. This is probably due to the fact that diagnosis was made at an early age and intensive diet management was started early. Despite their relatively low BMI, these children remain at high risk for developing scoliosis requiring active treatment (28% of the children). Adults (older than 18) diagnosed at the age of 10 or later have a high risk for developing obesity and obesity related health problems such as hypertension (38%), non-insulin dependant diabetes mellitus (11%) and cardio respiratory failure (16%).
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PMID:Age at diagnosis, body mass index and physical morbidity in children and adults with the Prader-Willi syndrome. 1565 14

The development of respiratory failure is common in patients with neuromuscular disorders that involve the respiratory muscles. However, the high incidence of sleep-related breathing problems in this population is less well known. In patients with neuromuscular disease, nocturnal breathing abnormalities frequently precede respiratory failure during wakefulness by months or even years. These nocturnal breathing problems are caused by multiple factors, including diaphragm and upper airway muscle weakness, scoliosis, obesity, and central respiratory control problems. Advances in the understanding of the links between sleep-disordered breathing and the development of daytime dysfunction and respiratory failure has revolutionized the management of these individuals. Mask positive pressure therapy is now available to improve both quality of life and longevity for these individuals. The lack of correlation between daytime testing and the severity of nocturnal breathing abnormalities makes it difficult to predict the presence of sleep-disordered breathing. Further, patients may not always be aware of symptoms associated with sleep-disordered breathing, even if specifically questioned. However, simple bedside measurements of vital capacity and inspiratory muscle strength can provide useful guides for when nocturnal respiratory monitoring is indicated.
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PMID:Sleep abnormalities associated with neuromuscular disease: pathophysiology and evaluation. 1608 13


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