Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of a 3-year-old child with Prader-Willi syndrome who had severe sleep disordered breathing with daytime hypersomnolence. His daytime blood gases showed type II respiratory failure. He was effectively treated with continuous positive airway pressure (CPAP) and has used this form of therapy for 2 years now with improvement in daytime somnolence, improved mental acuity and normalisation of daytime blood gases.
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PMID:Prader-Willi syndrome with sleep disordered breathing: effect of two years nocturnal CPAP. 1137 May 8

We report a case of a 73-year-old woman with chronic respiratory failure in association with syringohydromyelia and sleep apnea. She was initially intubated and mechanically ventilated. Weaning from the ventilator was only successful after nasal intermittent positive airway pressure therapy was started. A normalization of arterial blood gas exchange could be achieved.
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PMID:Intermittent positive airway pressure by nasal mask as a treatment for respiratory insufficiency in a patient with syringomyelia. 1196 33

We prospectively studied sleep disordered breathing in 50 consecutive patients (39 males) with chronic obstructive pulmonary disease (COPD) with chronic respiratory failure (CRF) (n=33) and without CRF (n=17) by performing polysomnography. Patients with CRF had a lower mean nocturnal oxygen saturation (SaO2 %) (88.6+/-6.7 vs. 96.3+/-0.8; p=0.0001) and a lower minimal nocturnal SaO2 (73.6+/-12.0 vs. 84.3+/-7.3; p=0.002) compared to those without CRF, suggesting that patients with CRF tend to have more severe drops in nocturnal SaO2. Patients with CRF also had a lower FEV1 (% predicted) (p=0.01) and PEFR (% predicted) (p=0.031) compared to those without CRF suggesting an indirect relation to the oxygen saturation. Other pulmonary functions were comparable between both the groups. Among patients with and without CRF, the total sleep time (minutes); the rapid eye movement (REM) stage (% of total sleep time); the non-rapid eye movement (NREM) stage (% of total sleep time) were comparable (p=NS). Only three of the 50 patients with COPD had a significant (>5) apnea-hypopnea index (AHI) (total no. of apneas + total no. of hypopneas/ total sleep time [(hours) = AHI] and these three patients had a mean BMI = 27.7 which was higher than the mean BMI of the whole group (21.1). The AHI was comparable in patients with and without respiratory failure. Multiple regression analysis revealed a positive correlation between AHI and the neck circumference (r=0.41; p=0.005) and BMI (r=0.31; p=NS). There was a small but statistically insignificant negative correlation between AHI and neck length (r= -0.28; p=NS). We conclude that, BMI per se contributes to the AHI and nocturnal desaturation in patients with COPD.
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PMID:Sleep disordered breathing in chronic obstructive pulmonary disease. 1202 59

Sleep disordered breathing with or without nocturnal hypercapnic hypoventilation is a common complication of respiratory muscle weakness in childhood neuromuscular disorders. Nocturnal hypercapnic hypoventilation as a sign of respiratory muscle fatigue, portends a particularly poor prognosis. We aimed at identifying daytime predictors of sleep disordered breathing at its onset and sleep disordered breathing with nocturnal hypercapnic hypoventilation. Forty-nine children and adolescents (11.3+/-4.4 years) with progressive neuromuscular disorders were studied with inspiratory vital capacity, peak inspiratory pressure, arterial blood gases, polysomnography, and a ten-item symptoms questionnaire. Daytime respiratory function was prospectively compared with polysomnographic variables. Sleep disordered breathing was found in 35/49 patients (71%). Twenty-four (49%) had sleep disordered breathing with nocturnal hypercapnic hypoventilation. Inspiratory vital capacity and peak inspiratory pressure, but not symptom score, correlated with sleep disordered breathing and severity of nocturnal hypercapnic hypoventilation. Sleep disordered breathing-onset was predicted by inspiratory vital capacity<60% (sens. 97%, spec. 87%). Sleep disordered breathing with nocturnal hypercapnic hypoventilation was predicted by inspiratory vital capacity<40% (sens. 96%, spec. 88%) and PaCO(2)>40 mmHg (sens. 92%, spec. 72%,). Sleep disordered breathing can reliably be predicted from simple daytime respiratory function tests, which, if applied systematically, will improve recognition of nocturnal respiratory failure.
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PMID:Daytime predictors of sleep disordered breathing in children and adolescents with neuromuscular disorders. 1256 9

We report a 47-year-old man with facioscapulohumeral muscular dystrophy (FSHD) presenting with sinus dysfunction. He became unable to roll over and stand up at the age of 42, but he could still walk. Facial muscle involvement, scapular winging, asymmetrical involvement, funnel chest, and the absence of contractures were typical of FSHD. Electrocardiogram (ECG) and cardiac echogram showed the overload of both right atrium and ventricle. On Holter ECG, transient P wave inversion and P-P interval elongation (maximally 2.4 seconds) repeatedly appeared mainly during sleep. There was no bundle branch block, atrioventricular junctional rhythm, or increase of premature ventricular beats. Vital capacity was decreased (0.62 L, 16% of the predicted value). Arterial blood gas analysis showed hypercapnia and hypoxia which aggravated during sleep (PaCO2 87.3Torr, PaO2 41.5Torr). Sleep apnea was not observed. Intracardiac ECG was not performed and he died 2 weeks later. In FSHD, sinus node dysfunction may become distinct especially in the setting of respiratory failure.
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PMID:[Facioscapulohumeral muscular dystrophy with sinus dysfunction]. 1271 90

Sleep hypoventilation (SH) may be important in the development of hypercapnic respiratory failure in chronic obstructive pulmonary disease (COPD). The prevalence of SH, associated factors, and overnight changes in waking arterial blood gases (ABG), were assessed in 54 stable hypercapnic COPD patients without concomitant sleep apnoea or morbid obesity. Lung function assessment, anthropomorphic measurements, and polysomnography with ABG measurement before and after sleep were conducted in all patients. Transcutaneous carbon dioxide tension (Pt,CO2) was measured in sleep, using simultaneous arterial carbon dioxide tension (Pa,CO2) for in vivo calibration and to correct for drift in the sensor. Of the patients, 43% spent > or = 20% of sleep time with Pt,CO2 > 1.33 kPa (10 mmHg) above waking baseline. Severity of SH was best predicted by a combination of baseline Pa,CO2, body mass index and per cent rapid-eye movement (REM) sleep. REM-related hypoventilation correlated significantly with severity of inspiratory flow limitation in REM, and with apnoea/hypopnoea index. Pa,CO2 increased mean+/-SD 0.70+/-0.65 kPa (5.29+/-4.92 mmHg) from night to morning, and this change was highly significant. The change in Pa,CO2 was strongly correlated with severity of SH. Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease, and related to baseline arterial carbon dioxide tension, body mass index and indices of upper airway obstruction. Sleep hypoventilation is associated with significant increases in arterial carbon dioxide tension night-to-morning, and may contribute to long-term elevations in arterial carbon dioxide tension.
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PMID:Sleep hypoventilation in hypercapnic chronic obstructive pulmonary disease: prevalence and associated factors. 1279 91

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

Sleep is characterized by a profound change of load and capacity of the respiratory system. Load increases due to a rise in upper and lower airway resistance. Capacity decreases due to reduced chemosensitivity, a decrease in muscle activity and minute ventilation. Whereas these changes do not lead to relevant blood gas changes and do not disturb sleep in healthy subjects, patients with respiratory diseases frequently show the first symptoms of their disease during sleep. Pulmonary diseases in which sleep plays an important role are asthma, COPD, hypercapnic respiratory failure, sleep disordered breathing, the overlap-syndrome and cystic fibrosis. Medical history should include sleep and complaints during the night. In asthmatics peak-flow measurements during the night may provide valuable information. In all other disorders mentioned, nocturnal ambulatory recording of respiration and arterial oxygen saturation often allow the detection of relevant disorders of breathing during sleep. If ambulatory monitoring reveals relevant pathology, then further evaluation and treatment in the sleep laboratory are warranted.
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PMID:[Relevance of sleep for patients with lung diseases]. 1534 Jun 96

We report a 36 years male, admitted to the hospital for progressive respiratory failure. Chest X ray and CT scan were normal. On admission, a severe bradycardia and slow intellectual activity were noted. Serum thyroid function tests showed a TSH over 150 microU/ml and T3 of 75 ng/ml. Thyroid substitution therapy was associated with a progressive improvement of respiratory function. Diaphragmatic dysfunction, central hypoventilation, airway obstruction, sleep apnea and pleural effusion have been previously reported in patients with hypothyroidism. Therefore, we recommend to measure TSH in patients with unexplained respiratory failure.
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PMID:[Global respiratory failure as the presentation form of hypothyroidism. Report of one case]. 1537 58

A patient with chronic heart failure and chronic respiratory failure (CRF) underwent ambulatory polysomnography at home. She was found dead on the morning after the recording. The tracings confirmed severe sleep apnea syndrome. After 8 h of incessant Cheyne-Stokes respiration during sleep, respiratory arrest occurred, followed 7 min later by asystole. This report illustrates a case of respiratory drive failure during sleep as the mode of death in a patient with heart failure, sleep apnea syndrome, and CRF.
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PMID:Death during polysomnography of a patient with cheyne-stokes respiration, respiratory acidosis, and chronic heart failure. 1553 47


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