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)

A 71-year-old man was noted to habitually snore loudly at night and have a predisposition to somnolence during the daytime. While dozing during the day, he developed cardiac arrest at the time when snoring stopped, and was resuscitated. By means of a respiration monitor, he was diagnosed as having sleep apnea syndrome (SAS) with a combination of obstructive, central, and mixed type. However, neither respiratory insufficiency nor cardiac insufficiency was observed, and there were no abnormal findings on laboratory tests and bronchoscopy. SAS complicated by cardiac arrest is usually seen in cases with concomitant symptoms such as excessive obesity, hypertension, arrhythmia, right heart insufficiency, secondary polycythemia, or mental disorder. The present case abruptly developed cardiac arrest in the absence of such symptoms. This case therefore suggests the importance of screening tests using a respiration monitor during sleep in subjects who have a loud snore or a predisposition to somnolence during the daytime. Although treatment with UPPP alone had no noticeable effect, UPPP treatment combined with sleeping in the lateral position was effective in the present case. The efficacy rate of UPPP has been reported to be 50 to 60%. The early establishment of a method for precise evaluation of the site of obstruction as well as criteria for appropriate application of UPPP are urgently required.
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PMID:[A resuscitated case of sleep apnea syndrome with cardiac arrest]. 160 64

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

Snoring has only recently come under wide study. Recent research has established the close relationship of severe snoring to sleep apnea in terms of the obstructive pathophysiology. Snoring tends to increase in severity over time and may progress to sleep apnea. Severe snoring may be associated with pulmonary and systemic hypertension, secondary polycythemia, and cardiac arrhythmias.
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PMID:Snoring: clinical implications and treatment. 310 90

Morbid obesity is often associated with severe respiratory insufficiency, commonly known as the pickwickian syndrome. This can be divided into the following two primary breathing disorders which can affect patients alone or in combination: the obstructive sleep apnea syndrome (SAS); and the obesity-hypoventilation syndrome (OHS). Thirty-eight (14 percent) of 263 morbidly obese patients with respiratory insufficiency of obesity underwent gastric surgery for weight reduction. Ten had OHS, nine has SAS, and 19 had both. Of these patients, one died of postoperative complications, one died at five weeks with an inconclusive autopsy, one was lost to follow-up, and the time since surgery was too short (less than three months) in three. A total of 30 patients lost 45 +/- 25 percent (p less than 0.0001) of excess body weight within 3 to 12 months following surgery, when repeat pulmonary studies were done. Most patients continued to lose additional weight until two years, when they had lost 62 +/- 26 percent of excess weight. Nine patients failed initial surgery (gastroplasty); seven of these were successfully converted to gastric bypass. Weight loss was associated with a significant decrease in the percentage of sleep apnea from 44 +/- 15 to 8 +/- 11 (p less than 0.0001). In patients with OHS, the arterial oxygen pressure (PaO2) increased from 53 +/- 9 to 68 +/- 11 mm Hg (p less than 0.0001), and the arterial carbon dioxide tension decreased from 51 +/- 7 to 41 +/- 4 mm Hg (p less than 0.0001). Pulmonary function tests in the patients with OHS revealed significant increases, as a percentage of predicted normal, in the forced vital capacity, forced expiratory volume in one second, expiratory reserve volume, functional residual capacity, and total lung capacity. Secondary polycythemia, defined as a hemoglobin level greater than 16 g/dl associated with a PaO2 less than 60 mm Hg, was noted in 13 of 29 patients with OHS. This fell from 16.9 +/- 1.1 to 14.9 +/- 1.7 g/dl (p less than 0.001) after weight loss and improved pulmonary function.
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PMID:Gastric surgery for respiratory insufficiency of obesity. 372 Mar 90

A 58-yr-old man with primary alveolar hypoventilation, central sleep apnea, and secondary polycythemia failed to improve when treated with respiratory stimulant medications, including oxtriphylline, acetazolamide, and medroxyprogesterone. In contrast, after institution of treatment with low-flow nocturnal oxygen, there was a marked decrease in the number and duration of sleep apneas, and an increase in the level of ventilation during sleep. These changes were sustained during 5 months of nocturnal oxygen therapy. The improvement produced by oxygen may have been due to the fact that the patient had no demonstrable ventilatory response to hypoxia during wakefulness, and therefore may have developed hypoxic brainstem depression during sleep. The findings suggest that oxygen therapy during sleep may be beneficial in patients with primary alveolar hypoventilation and central sleep apnea who demonstrate no ventilatory response to hypoxia during wakefulness.
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PMID:Beneficial effect of oxygen in primary alveolar hypoventilation with central sleep apnea. 709 88

25 patients with idiopathic erythrocytosis (absolute increase in red cell mass without conventional criteria of primary polycythaemia or known underlying cause) have been further studied for evidence of primary or secondary polycythaemia. Additional non-conventional criteria used were: platelet distribution width, platelet nucleotide ratio, serum erythropoietin, clinical evidence of ischaemic vascular disease and erythroid culture variables in serum-free system. All had been used in an earlier study in score form to assist in the diagnosis of primary polycythaemia. These patients were also newly assessed for the presence of hypoxia (supine oximeter values, history suggestive of sleep apnoea), for renal lesions and for splenic enlargement (impalpable) by ultrasound or computerized tomography. 7 patients had erythroid culture scores suggesting primary polycythaemia but the addition of non-culture criteria did not result in any scores more strongly predictive of primary polycythaemia. Supine oximeter values < 92% suggested hypoxaemia as the mechanism of polycythaemia in 3 patients in whom it had not previously been suspected. Some splenic enlargement (impalpable) was demonstrated in 6 patients, only 1 of whom had erythroid culture scores suggesting primary polycythaemia. 12 patients had confirmed, raised erythropoietin levels. We conclude that idiopathic erythrocytosis refers to a heterogenous group of patients. Features of primary or secondary polycythaemia may be demonstrated in some of them by additional new study techniques. The raised erythropoietin values found in half the patients were unexpected.
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PMID:Idiopathic erythrocytosis--additional new study techniques suggest a heterogenous group. 792 59

Two patients with obstructive sleep apnoea are presented. Both had marked hypoxaemic polycythaemia treated for many years with phlebotomies before a proper diagnosis was established. Diagnosis of obstructive sleep apnoea and introduction of CPAP treatment resulted in clinical improvement and regression of polycythaemia. In secondary polycythaemia differential diagnosis should include obstructive sleep apnoea.
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PMID:[Marked polyglobulia in patients with obstructive sleep apnoea]. 941 24

Splenic infarction is rare, resulting from occlusion of the splenic artery or its branches. Its aetiology is complex and multifactorial involving various vascular and thrombotic diseases, thus, misdiagnosis or missed diagnosis is common. Here, the case of a 45-year old male patient diagnosed with splenic infarction caused by secondary erythrocytosis associated with obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is reported. The patient presented with 10 days of abdominal distension and pain that worsened after eating, and had developed to include nausea, vomiting and fever. The patient had a history of night snoring for over 10 years without treatment, a diagnosis of chronic pulmonary heart disease and secondary polycythaemia 5 years previously, and diagnosis of OSAHS 1 year previously. He had not received previous non-invasive ventilation or oxygen therapy. Enhanced upper abdomen computed tomography (CT) showed splenic infarction, bone marrow cytology suggested secondary polycythaemia, and sleep polysomnography revealed severe OSAHS. Low molecular-weight heparin, ceftriaxone, fluid and oxygen treatment gradually relieved abdominal distension and pain. Enhanced CT showed splenic infarction improvement. The present case highlights that splenic embolism should not be ignored as a potential complication of OSAHS.
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PMID:Splenic infarction associated with obstructive sleep apnoea/hypopnoea syndrome: a case report. 3305 Jul 67