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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case of severe breathing abnormality during sleep in a young man who had had poliomyelitis 20 yr before. His sleep disorder led to respiratory failure and cor pulmonale, which were greatly improved by oxygen therapy. A study of this case and those previously described supports the notion that brainstem damage during acute poliomyelitis is important in the later appearance of sleep-disordered breathing. In addition, such patients usually have mechanical abnormalities involving the thoracic cage and respiratory muscles. These ventilatory restrictions amplify the pathophysiologic effects of abnormal central nervous system control of breathing during sleep, and we suggest that their presence has a key role in the development of sleep apnea syndrome in these patients.
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PMID:Sleep apnea syndrome after poliomyelitis. 684 37

Fourteen children with disordered breathing during sleep (obstructive apnea, obstructive hypopnea, or snoring) and anatomic obstruction of the upper airway were studied. Twelve children had hypertrophied tonsils and adenoids, and two had a deviated nasal septum. No child had sequelae of severe sleep apnea--that is, cor pulmonale, pulmonary hypertension, or alveolar hypoventilation. Results of polysomnographic studies were abnormal in all and revealed that obstructive hypopnea (increased respiratory effort with decreased airflow) was more common than obstructive apnea (increased respiratory effort without airflow). Surgical removal or correction of the upper airway obstructive lesion in 12 children resulted in normal nocturnal respiration. Surgical intervention was declined in two patients, and their symptoms persist. We conclude that surgical removal of upper airway obstructive lesions in children with disturbed nocturnal sleep should not be reserved only for those with serious sequelae of obstructive sleep apnea; considerable benefit is gained in selected patients with mild obstructive sleep apnea or hypopnea.
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PMID:Upper airway obstruction and disordered nocturnal breathing in children. 685 72

Patients with sleep apnea syndrome may present with many types of cardiopulmonary abnormalities. Acute pulmonary edema, however, either as a part, or as the presenting feature, of the sleep apnea syndrome has not been reported to our knowledge. A 20-year-old obese woman with no history of cardiopulmonary disease presented twice to the emergency room because of sudden onset of shortness of breath. Each time her chest roentgenogram showed bilateral pulmonary edema. On nocturnal polysomnographic recording, the patient had obstructive apneic episodes; the longest apneic episode lasted 132 seconds. Complete resolution to her symptoms occurred following tracheostomy.
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PMID:Pulmonary edema as a presenting feature of sleep apnea syndrome. 708 22

Certain patients with chronic obstructive pulmonary disease may be classified as blue bloaters or pink puffers. Recent studies suggest that physiologic changes during sleep contribute to the clinical expression of these syndromes. To investigate this, we monitored four blue bloaters and six pink puffers during one night's sleep to determine the incidence of sleep disordered breathing (SDB) and of arterial oxygen desaturation. There were no significant differences between the two groups for sleep period time, awake oxygen saturation, or the number of episodes of SDB. Blue bloaters had lower baseline oxygen saturations, more episodes of arterial oxygen desaturation, and larger falls in oxygen saturation and spent more time at low levels of oxygen saturation while asleep. We propose that the degree and the duration of sleep hypoxemia of blue bloaters but not of pink puffers may contribute to early pulmonary hypertension and cor pulmonale.
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PMID:Oxygen desaturation during sleep as a determinant of the "Blue and Bloated" syndrome. 722 51

The presenting symptom complex, diagnostic features, and therapeutic alternatives for obstructive and central sleep apnea are discussed in relation to two illustrative patients. Heavy snoring and restlessness during sleep in an obese individual, usually a male, may indicate obstructive apnea. Daytime hypersomnolence, intellectual deterioration, mental depression, impotence, cardiac arrhythmias, cor pulmonale, systemic hypertension, and erythrocytosis are the most common complications. Tracheostomy, the classic form of therapy, can be replaced by pharmacologic intervention in most patients. The clinical presentation of central apnea is less dramatic, but neurological and cardiac complications can occur. Therapy is less well established for this entity. Knowledge of the increased incidence of these disorders and awareness of more subtle complications indicate that sleep apnea should be placed in the differential diagnosis of pulmonary and systemic hypertension, hypersomnolence states, mental deterioration, psychiatric illness, and even insomnia.
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PMID:Diagnosis and therapy of sleep apnea. 722 83

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.
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PMID:Obstructive sleep apnea. 814 53

To date, a paucity of information is available on the optimal management of obstructive sleep apnea in Down syndrome, which may have particularly important implications in this already vulnerable patient population. The objective of this study was to evaluate prospectively the results of a new surgical approach for the treatment of obstructive sleep apnea. Patients with Down syndrome and obstructive sleep apnea underwent preoperative and postoperative polysomnography and clinical and radiologic evaluation to determine prospectively the efficacy of sleep apnea surgery. Statistical testing of apnea index, respiratory disturbance index, and lowest oxygen saturation were compared by means of paired t tests. Seven children (five boys, two girls) from 3 to 12 years of age were subjected to a management protocol that included an aggressive surgical approach to the treatment of obstructive sleep apnea. Clinical symptoms and signs of obstructive sleep apnea, apnea index, respiratory disturbance index, lowest oxygen saturation, and surgical morbidity were the main outcome measures. Surgical treatment consisted of a combination of soft-tissue and skeletal alterations including tongue reduction (n = 6), tongue hyoid advancement (n = 4), uvulopalatopharyngoplasty (n = 7), and maxillary or midface advancement (n = 2). Polysomnography was obtained preoperatively and postoperatively in six patients. One patient was intubated preoperatively. Mean preoperative apnea index and respiratory disturbance index were 34.00 and 52.46 compared with mean postoperative values of 1.62 and 6.46, respectively. Clinically, all patients were improved symptomatically in terms of snoring, noisy breathing, and oxygen requirements. The one patient who had been intubated preoperatively for respiratory failure was extubated successfully but later developed recurrent tricuspid regurgitation and was found to have fixed pulmonary hypertension with cor pulmonale. This patient represented the only treatment failure and underwent tracheostomy. An aggressive surgical approach aimed at correcting all anatomic abnormalities associated with upper airway obstruction was applied successfully to the treatment of obstructive sleep apnea in Down syndrome. We suggest periodic polysomnography in patients with Down syndrome, especially if there is unexplained deterioration in mental capacity or other signs and symptoms of obstructive sleep apnea. Surgical treatment should address both the soft-tissue abnormalities and the skeletal deformities such as midface retrusion. Preoperative cardiac ultrasonography is important to determine the presence of right-sided heart failure, which may be an indication for cardiac catheterization to determine pulmonary venous pressures.
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PMID:Down syndrome: identification and surgical management of obstructive sleep apnea. 904 80

A 54-year-old man presented 54 months after a successful heart transplant with cor pulmonale secondary to obstructive sleep apnoea/hypopnoea syndrome (SAHS). This unusual cause of reversible graft failure following heart transplantation is presented in this case report.
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PMID:Sleep apnoea/hypopnoea syndrome: a potential cause of graft failure following heart transplantation. 958 29

Ventricular hypertrophy is associated with an increased risk of cardiovascular death and cardiac events. In response to a haemodynamic load, ventricular hypertrophy may either be eccentric (dilation in response to volume overload) or concentric (increase in wall thickness in response to pressure overload). Ventricular hypertrophy increases with age, weight, blood pressure, and the presence of cardiovascular disease. It is greater in men than in women when adjusting for other variables. Echocardiography is the best method for accurate quantification of left ventricular mass and for detecting right ventricular hypertrophy. In obstructive sleep apnoea there are reports of both eccentric and concentric hypertrophy of the left ventricle. However, many of these reports have failed to control for patient weight or age. More recent reports indicate that much of the hypertrophy of the left ventricle reported in obstructive sleep apnoea can be related to patients' age, blood pressure, or size. However, right ventricular hypertrophy appears to be distinctly associated with the presence and severity of obstructive sleep apnoea. Right ventricular hypertrophy secondary to obstructive sleep apnoea may be the substrate for the eventual development of cor pulmonale and right heart failure. Its pathophysiological significance and potential use as a marker of severe OSA requires further investigation. Further investigation into left ventricular hypertrophy and sleep apnoea must control for the potentially confounding variables listed above and will require population-based and/or carefully matched case control studies.
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PMID:Ventricular hypertrophy in sleep apnoea. 1060 97

Sleep has well-recognized effects on breathing, including changes in central respiratory control, airways resistance, and muscular contractility, which do not have an adverse effect in healthy individuals but may cause problems in patients with COPD. Sleep-related hypoxemia and hypercapnia are well recognized in COPD and are most pronounced in rapid eye movement sleep. However, sleep studies are usually only indicated in patients with COPD when there is a possibility of sleep apnea or when cor pulmonale and/or polycythemia are not explained by the awake PaO(2) level. Management options for patients with sleep-related respiratory failure include general measures such as optimizing therapy of the underlying condition; physiotherapy and prompt treatment of infective exacerbations; supplemental oxygen; pharmacologic treatments such as bronchodilators, particularly ipratropium bromide, theophylline, and almitrine; and noninvasive positive pressure ventilation.
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PMID:Impact of sleep in COPD. 1067 75


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