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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive sleep apnea syndrome (OSAS) is increasingly recognized in the pediatric population. It is characterized by a combination of partial upper airway obstruction and intermittent obstructive apnea that disrupts normal ventilation and sleep. It is estimated to occur in 1-3% of children with a peak age of 2 to 5 years. Common symptoms include habitual snoring, difficulty breathing during sleep, restlessness, and witnessed apnea. Adenotonsillar hypertrophy is the most common associated condition in otherwise normal children, but cranialfacial abnormalities, neuromuscular diseases, and obesity are also predisposing factors. Severe OSAS can have serious neurobehavioral and cardiorespiratory consequences including excessive daytime sleepiness, growth failure, school failure, behavioral problems, cor pulmonale, or even death. Diagnosis is based on data from the history, physical exam, and laboratory studies that confirm the presence and severity of the upper airway obstruction. Polysomnography has been the diagnostic tool of choice. Treatment depends on the severity of symptoms and the underlying anatomic and physiologic abnormalities. Since childhood OSAS is usually associated with adenotonsillar hypertrophy, the majority of cases are amenable to surgical treatment. However, there is increasing pediatric experience with CPAP therapy when tonsillectomy and adenoidectomy are either unsuccessful or inappropriate.
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PMID:Obstructive sleep apnea syndrome (OSAS) in children: diagnostic challenges. 908 30

Our objective was to investigate possible factors implicated in either early death from or scintigraphic resolution of pulmonary embolism. To that end we conducted a retrospective study of 116 patients with either a high likelihood of pulmonary thromboembolism (PTE) diagnosed by scintiscan or with a fair probability of PTE by scintiscan accompanied by a positive phlebograph. The images were taken upon admission, at 7 days, 10 days and 6 months. The factors analyzed were age, sex, trauma, immobility, surgery, obesity, hemiplegia, venous insufficiency, cardiopulmonary disease, neoplasia, chest X-ray and ECG alterations, D(A-a)O2 and size of perfusion defects upon admission and 7 to 10 days later. We performed single-variable analyses and multiple logical regression analyses using perfusion defect at 6 months as the dependent variable. The early mortality rate (13%) was higher in patients with neoplasms, a larger alveolar-arterial index and greater perfusion defects upon admission. Scintiscans became normal in 28%. Multivariate analysis to predict total or partial resolution at 6 months showed that size of perfusion defects at 7 to 10 days was the best predictive factor. A cutoff point was calculated by analyzing the ROC for this factor. Thus, when the defect at 7 to 10 days was equal to or greater than 1 segment, the probability of residual defects remaining after 6 months was twice as great (sensitivity 83%, specificity 57%). In conclusion, early death was more likely in PTE patients with neoplasms, larger defects upon admission and greater alveolar-arterial difference. Scintigrams showed resolution 6 months after admission in 28%. The size of perfusion defects 7 to 10 days after admission was the factor that best predicted total of partial resolution at 6 months.
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PMID:[The prognostic factors for early mortality and for total or partial gammagraphic resolution in venous thromboembolic disease]. 925 67

The goal of this article is to provide a perspective on how research involving the acute and chronic effects of exercise (referred to as "exercise sciences") on the structure and function of organs systems will evolve in the next century. Within the last 30 years, exercise-related research has rapidly transitioned from an organ to a subcellular/molecular focus. Thus future research will continue to be heavily influenced by molecular biology tools, fueled by both emerging technologies (e.g., "gene-chip microarrays") designed to dissect gene function on a macro scale as well as by the completion of the human genome project in which the approximately 80,000 genes comprising humans will be completely sequenced. These successes will drive the emerging fields of functional genomics (the dissecting of a gene's identity and function) and proteomics (the study of the properties of proteins). Funding levels at the National Institutes of Health will likely increase in order to expand these emerging fields as well as provide avenues for translating fundamental knowledge into solving the complexities of a number of degenerative diseases influenced heavily by activity/inactivity factors such as cardiopulmonary disease, diabetes, obesity, and the debilitating disorders associated with aging. Thus there are many challenges facing future exercise scientists who must harness the new technologies and take an aggressive stance in bringing this important field to the forefront.
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PMID:Research in the exercise sciences: where do we go from here? 1064 98

Obesity is a well-known cause of upper airway narrowing, respiratory failure and resulting hypoxemia and hypercapnia, and cardiac arrhythmias during sleep. Obese patients are prone to snore loudly and to develop obstructive sleep apnea syndrome and also obesity-hypoventilation syndrome. Repeated nocturnal upper airway obstruction may cause respiratory failure and cor pulmonale and frequent awakenings, and result in nocturnal choking, with daytime drowsiness, somnolence and irritability. The purpose of this article is to review the evidence for these accepted facts and to consider a variety of new information that relates to the pathogenesis, symptomatology and treatment of sleep disorders caused by obesity.
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PMID:Sleep-related Disorders in the Obese. 1076 3

Based on a case report, we offer brief guidelines on the perioperative management of patients with Sleep-Apnea-Syndrome (SAS) who present with a high incidence of a difficult airway and a high risk of respiratory depression during the perioperative period. A 39 year old male patient with a body mass index of 34.22 kg/m2 and receiving continuous-positive-airway-pressure-(CPAP) therapy for known SAS was scheduled for elective plastic surgery. After induction of anaesthesia and direct laryngoscopy no adequate airway could be established and the patient became hypoxic, hypercapnic and developed hypotension and bradycardia. With the use of a laryngeal mask airway the patient was stabilized and did not show neurologic sequale after immediate awakening. The following fiberoptic intubation of the awake patient, still showing tendency of upper airway obstruction, confirmed the difficult anatomical structures. The subsequent general anesthesia was uneventful. The patient received CPAP therapy and was monitored during the first postoperative night in the Intensive Care Unit. He made an uneventful recovery. He was advised to have regional anaesthesia or planned fiberoptic intubation, where possible, in the case of further anesthetic intervention. SAS has major implications for the anaesthesiologist and whenever patients exhibiting the high risk factors (obesity, male sex, history of intense snoring, impaired daytime performance, nonrefreshing daytime naps) are presented for surgery this condition should be considered. Elective surgery should be postponed until after adequate examination and treatment when necessary. Patients with SAS should always be suspected of having cardiopulmonary dysfunctions such as hypertension, cardiac dysrhythmia or cor pulmonale. It is most important to avoid sedative premedication, to initiate CPAP therapy preoperatively, to encourage regional anaesthesia if possible and to ensure close monitoring over the complete perioperative period. Planned fiberoptic intubation, preferably with surgical personnel available for an emergency airway, is a safe method for the induction of anaesthesia. Postoperatively, patients are at high risk from respiratory depression, even in the awake state. Postoperative opioid analgesia, no matter what route, should only be given under close monitoring. Independently of regional or general anaesthesia there is an increased risk of respiratory depression in the middle of the first postoperative week, suspected to be caused by the catching up on lost REM-sleep, due to shifts in the normal sleep pattern during the first postoperative days.
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PMID:[Induction of anesthesia for a patient with sleep apnea syndrome]. 1084 May 41

Some patients with obesity show chronic hypercapnia while awake. Such patients are referred to as obesity hypoventilation syndrome(OHS). Particularly, patients with profound obesity who have clinical features of sleep disordered breathing, hypersomnolence, cor pulmonale and so on represent the Pickwickian syndrome. The mechanisms of hypoventilation in OHS are multifactorial. The level of the blunted chemosensitivity, mechanical impairments of the respiratory system, the severity of the sleep-disordered breathing, and chronic hypoxemia may be important determinants of chronic hypoventilation. In this paper, the characteristics of pulmonary functions in obesity and the possible mechanisms of hypoventilation in patients with OHS were reviewed. Furthermore, the definition of OHS and descriptions of thr severity of OHS as recommended by Respiratory Failure Research Committee of Japanese Ministry of Health and Welfare are introduced.
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PMID:[Obesity and obesity hypoventilation syndrome]. 1094 42

Sleep-disordered breathing is a prevalent condition associated with impairment of daytime function and may predispose individuals to metabolic abnormalities independent of obesity. The primary objective of this study was to determine the metabolic consequences and community prevalence of sleep-disordered breathing in mildly obese, but otherwise healthy, individuals. One hundred and fifty healthy men, without diabetes or cardiopulmonary disease, were recruited from the community. Measurements included polysomnography, a multiple sleep latency test, an oral glucose tolerance test, determination of body fat by hydrodensitometry, and fasting insulin and lipids. The prevalence of sleep-disordered breathing, depending on the apnea-hypopnea index (AHI) cutoff, ranged from 40 to 60%. After adjusting for body mass index (BMI) and percent body fat, an AHI gt-or-equal, slanted 5 events/h was associated with an increased risk of having impaired or diabetic glucose tolerance (odds ratio, 2.15; 95% CI, 1.05-4.38). The impairment in glucose tolerance was related to the severity of oxygen desaturation (DeltaSa(O(2))) associated with sleep-disordered breathing. For a 4% decrease in oxygen saturation, the associated odds ratio for worsening glucose tolerance was 1.99 (95% CI, 1.11 to 3.56) after adjusting for percent body fat, BMI, and AHI. Multivariable linear regression analyses revealed that increasing AHI was associated with worsening insulin resistance independent of obesity. Thus, sleep-disordered breathing is a prevalent condition in mildly obese men and is independently associated with glucose intolerance and insulin resistance.
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PMID:Sleep-disordered breathing and insulin resistance in middle-aged and overweight men. 1187 3

Compared with open procedures, laparoscopic surgery is safe with a low incidence of complications. In rare circumstances, however, intraoperative complications such as acute pulmonary edema have been reported. The patient described herein is a 59-year-old woman with obesity, gastroesophageal reflux disease, and chronic obstructive pulmonary disease who developed acute congestive heart failure (CHF) and cardiomegaly immediately following laparoscopic cholecystectomy. She required emergent reintubation, diuresis, and admission to the intensive care unit for postoperative mechanical ventilation. Potential causes of pulmonary edema associated with laparoscopic surgery (extreme Trendelenburg position, venous carbon dioxide embolism, absorption of crystalloid irrigation fluid, cardiopulmonary disease, adverse drug reactions, negative pressure [postobstructive pulmonary edema]) were considered. A process of exclusion revealed that the hemodynamic changes induced by insufflation with an intra-abdominal pressure of 20 mm Hg were the most likely causes of the CHF. Suggestions to prevent occurrence of CHF are tight control of hemodynamics with use of invasive monitoring in high-risk patients and gentle, slow insufflation of the abdomen to an intra-abdominal pressure of 15 mm Hg or less. Intraoperative and/or postoperative CHF should be treated with diuretics, intravenous nitroglycerin, arterial vasodilators, and/or inotropic agents as needed.
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PMID:Acute congestive heart failure after laparoscopic cholecystectomy: a case report. 1277 45

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

Ongoing research in obstructive sleep apnea (OSA) suggests strong associations with cardiopulmonary disorders. There is an abundance of studies describing physiological pathways in OSA that acutely impact the cardiovascular system. These mechanisms, if proven to carry over into the daytime hours, could form the basis for clinical disease. The challenge remains in disentangling these mechanistic processes from the many comorbid conditions often present in patients with OSA. Examples include male gender, obesity, and diabetes mellitus, all of which exert their own influence on the development of cardiopulmonary disease. This review discusses some of the physiological mechanisms associated with disordered breathing during sleep and explores putative cardiopulmonary disease associations.
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PMID:Cardiopulmonary consequences of obstructive sleep apnea. 1605 15


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