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

This case report describes 3 patients with Down syndrome and obstructive breathing problems, ages: 5 months, 15 months, and 22 years. The youngest one had normal cardiopulmonary function at birth, but soon developed a pulmonary hypertension. The next had a severe atrioventricular defect and additional pulmonary hypertension and there was little hope for her to survive heart surgery. The oldest one had had apneas since childhood with increasing severity, but was regarded as having normal heart function. All 3 were operated to relieve their breathing obstruction. The 5-month-old boy improved only slightly after an initial UPPP and had to be tracheotomized, which solved his problems. The tracheotomy could be removed when he was one year. The 15-month-old girl was cured of her breathing problems through an A + T and survived her heart surgery one month later. Tonsillectomy and UPPP was performed on the oldest patient. Following surgery, he had an episode of life-threatening bleeding and developed a DIC syndrome, and was critically ill for 18 days. After he recovered, his sleep apnea had improved. Once a myxoedema was diagnosed and treated, he made further progress. These cases stress the significance of early recognition of sleep apnea in children with Down syndrome and the importance of a careful preoperative investigation in collaboration with cardiologists.
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PMID:Down syndrome and sleep apnea--a therapeutic challenge. 183 Nov 85

The symptoms of hypothyroidism are protean and include apathy, somnolence, lethargy, personality change, and intellectual deterioration. Many of these symptoms may be related to hypothyroid-induced sleep disorders. Hypothyroidism is associated with abnormal ventilatory drive, abnormal sleep architecture, and sleep apnea. Central, obstructive, and mixed patterns of sleep apnea are commonly observed in hypothyroidism. A case of severe sleep apnea in a grossly myxedematous patient who improved dramatically following thyroid replacement alone is presented. Myxedema is a reversible cause of sleep apnea, and thyroid function testing should be considered in its diagnostic work-up.
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PMID:Sleep apnea, sleep disorders, and hypothyroidism. 276 18

After irradiation of the neck for a squamous cell carcinoma of the tonsillar pillar and vocal cord, a 71-year-old man presented with a rapidly progressive sleep apnea syndrome. Previous reports describe the condition of patients with obstructive sleep apnea that developed after neck irradiation and secondary to supraglottic edema. Our patient had an obstructive component to his apnea similar to that described in previous cases, but, in addition, he had hypothyroidism. Myxedema is a well-described cause of both obstructive and central apnea. We believe both contributed to his condition. He was successfully treated by placement of a tracheostomy and by thyroid supplementation. In patients who present with sleep apnea after neck irradiation, especially with acute or severe symptoms, the differential diagnosis should include both a central cause from hypothyroidism as well as a peripheral obstructive cause from laryngeal edema.
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PMID:Sleep apnea syndrome after irradiation of the neck. 281

Thyroid deficiency states are now a well recognized cause of the sleep apnea syndrome. The spectrum of disease ranges from mild, asymptomatic hypothyroidism to severe myxedema, and the disorder is associated with both obstructive and central types of sleep apnea. A variety of factors may be involved, including upper airway obstruction with or without obesity, and alterations in ventilatory drive. The definitive therapy is thyroid hormone replacement, which has been shown to diminish or completely eliminate apneic episodes and arterial oxygen desaturation, as well as to effect many improvements in sleep patterns and overall sleep efficiency. The incidence of thyroid deficiency states in patients with sleep apnea syndrome is not known, but it seems reasonable to evaluate thyroid function in all patients. Thyroid replacement therapy seems logical for the treatment of sleep apnea in patients with previously unrecognized subclinical hypothyroidism. Much remains to be learned about the diagnosis and treatment of sleep apnea syndromes associated with thyroid hormone deficiency, and further studies are needed.
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PMID:Sleep apnea and hypothyroidism. 305 27

A 52-year-old man with myxedema was evaluated for anterior chest pain that was considered to be compatible with myocardial ischemia. The night after admission he developed extreme bradycardia, hypotension, and apneic episodes lasting up to 25 s. Continuous positive airway pressure and administration of medroxyprogesterone acetate prevented further episodes and relieved much of the somnolence and lethargy that had contributed to the evidence for myxedema. Alveolar hypoventilation caused by decreased sensitivity to carbon dioxide, inadequate central neural drive, peripheral muscle force, and obesity all may have contributed to the apnea. Chest pain has not recurred, and results of electrocardiography have remained normal following full thyroid hormone replacement. The early recognition of myxedema causing sleep apnea will allow specific treatment to avoid the cardiovascular risks related to prolonged apnea and will help avoid confusion with other etiologies of cardiovascular abnormalities.
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PMID:Extreme bradycardia during sleep apnea caused by myxedema. 363 55

Three cases of hypersomnolence, snoring and documented sleep apnea are reported. All three patients were profoundly myxedematous, both clinically and biochemically. Polygraphic studies during sleep documented the presence of repetitive episodes of obstructive sleep apnea in all three patients. These were accompanied by arterial oxygen desaturation. After becoming euthyroid following the administration of the l-thyroxine all patients underwent a repeat evaluation in the sleep laboratory. These studies revealed nearly complete resolution of obstructive sleep apnea in all patients. In addition, several sleep parameters showed marked improvement. These data strongly suggest that the presence of profound daytime sleepiness in hypothyroid patients could be indicative of a potentially lethal complication of myxedema, obstructive sleep apnea.
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PMID:Myxedema and obstructive sleep apnea. 723 72

The pertinent literature on the prevalence, clinical manifestations and pathogenic mechanisms of sleep apnoea (SA) in endocrine diseases, namely acromegaly, Cushing syndrome, hypothyroidism and diabetes mellitus was reviewed. An increased prevalence is well documented in patients with active and treated acromegaly. While most authors report peripheral obstruction, due to hypertrophy of tongue and pharyngeal tissues, to be the cause of SA in acromegaly, some findings argue for a role of hormone-induced changes of central respiratory control. SA is also more common in hypothyroidism, especially when myxedema is present. The associated edema and myopathy appear to be of pathogenic importance. Thyroxin substitution is frequently effective for the treatment of SA but nCPAP can be necessary initially and in some patients even after remission of clinical signs of hypothyroidism. In Cushing disease and syndrome, parapharyngeal fat accumulation can cause SA, but no epidemiological information is available. In non insulin dependent diabetes (NIDDM), obesity is the common risk factor for both, nocturnal hypoxia and insulin resistance. In IDDM, the development of autonomic neuropathy may predispose to SA. Where treatment of the underlying endocrine disease is unable cure the associated SA, nCPAP is usually the treatment of first choice. More prospective studies are clearly needed to establish prevalences and resolve the controversies regarding pathogenesis.
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PMID:Sleep apnoea in endocrine diseases. 961 23

The case is presented of a 48-year old, slightly overweight, brachymorphic male affected by undiagnosed myxedema, admitted for nocturnal dyspnea present for several years but worsened in the last few weeks. At the age of 19, a paranoid schizophrenia diagnosis was indicated leading to repeated admissions to psychiatric hospitals and continued pharmacological therapy. His sensorium was lucid albeit with a slight psycho-motor slowing down; pharyngeal edema and macroglossia were also apparent, blood O2 saturation was 97%. After the first emergency exams, a hypothyroid condition associated with multinodular goiter and tracheal dislocation was found. Administration of triiodothyronine p.o. and hydrocortisone i.v. was thus initiated. In the doubt of sleep apnea syndrome (SAS) occurrence, pulse oximetry was performed, but after 7 hours, the patient suddenly deceased. Data showed waves of deep O2 desaturation secondary to periods of prolonged apnea. A literature review shows that such a case has never been reported. A posteriori analysis of the patient's clinical management indicates that the obstructive form of SAS, associated with myxedema is a condition which needs to be promptly diagnosed; due to the possible seriousness of its functional evolution, the need for intensive or sub-intensive therapy, with continuous nasal airway positive pressure or with oro-tracheal intubation and assisted ventilation, should be carefully taken into consideration; continuous cardiac monitoring should also be carried out, given the risk for acute coronary complications and ventricular arrhythmias in the early phases of substitutive therapy with thyroid hormone.
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PMID:[Sudden death by sleep apnea syndrome associated with myxedema. A case report and a review of the literature]. 1073 43