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)

Pulmonary edema due to upper airway obstruction can be observed in a variety of clinical situations. The predominant mechanism is increased negative intrathoracic pressure, although hypoxia and cardiac and neurologic factors may contribute. Laryngospasm associated with intubation and general anesthesia is a common cause of pulmonary edema in children. However, only seven cases of pulmonary edema presumably due to laryngospasm have been reported in adolescents and adults. Five of the seven had other risk factors for upper airway obstruction, and in four, the diagnosis of "laryngospasm" could be explained by other factors. Patients with underlying risk factors for upper airway obstruction, such as a forme fruste of sleep apnea or nasopharyngeal abnormalities, appear to be at increased risk for the development of pulmonary edema in the setting of intubation and anesthesia. This form of pulmonary edema usually resolves rapidly without the need for aggressive therapy or invasive monitoring.
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PMID:Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction. Are certain patients at increased risk? 378 Mar 26

A 4-week-old infant experienced prolonged central sleep apnea requiring resuscitation. At 6 months of age he developed episodic obstructive apnea (diagnosed as laryngospasm by direct laryngoscopy) with an abnormal EEG and a normal computed tomography (CT) scan, and at 14 months of age he developed hemiparesis due to a gemistocytic astrocytoma grade III-IV. Following removal of the mass, he has had occasional seizure activity, but no further episodes of obstructive apnea.
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PMID:Astrocytoma in an infant with prolonged apnea. 742 32

A 33-year-old male was scheduled for tonsillectomy and pharyngoplasty due to sleep apnea syndrome. The intubation was uneventful following induction with thiamylal and vecuronium. Anesthesia was maintained with O2-N2O-sevoflurane. No complications were observed during the 90 min operation. After the termination of the anesthesia, a hyperadrenergic state was observed: arterial pressure and heart rate rose to 230/135 mmHg and 135 bpm, respectively. Immediately after extubation, he developed dyspnea with tracheal tag and stridor, and became cyanotic despite the use of a simple oxygen mask and assisted ventilation. Laryngospasm was suspected. The patient was reintubated and suctioned; pink, frothy sputum was not obtained. Arterial blood gases 5 minutes after reintubation revealed a pH of 7.24, Pao2 86 mmHg (FIo2 1.0), and Paco2 54 mmHg. Chest X-ray 30 minutes after reintubation revealed bilateral diffuse alveolar infiltration. The diagnosis was interstitial pulmonary edema. The patient was ventilated mechanically by applying a positive end-expiratory pressure of 5cm H2O, and furosemide and dopamine were administered intravenously. The patient was extubated the next day, and discharged from hospital ten days later. We considered that the lung edema was induced by the severe negative pressure generated by inspirating against a closed upper airway, as well as by the hyperadrenergic state and severe hypoxemia observed during and after extubation.
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PMID:[Pulmonary edema due to acute airway obstruction immediately after tracheal extubation]. 985 97

Permanent tracheotomy was the first surgical procedure proposed for the treatment of severe obstructive sleep apnoea syndrome and is still the only surgical option that ensures, even in very severe cases, complete elimination of apnoea and, in turn, clinical remission. Improved knowledge of the causes of obstructive sleep apnoea syndromes and the increasing therapeutic options (instrumental, medical and surgical) have resulted in cases requiring tracheotomy as the only indispensable therapeutic option becoming more rare. At present, the only indications are in very occasional conditions of life-threatening obstructive sleep apnoea syndromes and in patients on whom continuous positive airway pressure is not tolerated or is not effective (severe deoxygenation or hypercapnia, severe respiratory disorder index, severe obstructive sleep apnoea syndrome-related arrhythmias, severe excessive daytime sleepiness, heart diseases or ischaemic encephalopathy exacerbated by obstructive sleep apnoea syndromes, obstructive pneumopathy exacerbated by obstructive sleep apnoea syndromes, severe obstructive sleep apnoea syndromes with few chances of resolution with other surgical procedures or failure of the latter). Moreover, it is the only therapeutic solution in rare nocturnal laryngeal stridor due to multisystemic atrophy (in which obstructive sleep apnoea syndrome is due to nocturnal laryngospasm of neurologic origin). Therapeutic tracheotomy must be permanent (tracheostomy) and, therefore, preferably carried out with a specific technique (skin-lined tracheotomy), able to guarantee greater stability, less risk of granulation tissue, wider opening of the tracheostomy, sufficient reversibility. In our experience, very few patients (10 cases) withsleep disorder breathing have been submitted to skin-lined tracheotomy. Of these, the majority were submitted to surgery for severe apnoea due to nocturnal laryngospasm on account of multisystemic atrophy (n = 7), while only 3 cases of obstructive sleep apnoea syndromes were submitted to skin-lined tracheotomy, i.e., 0.7% of the 424 patients operated on for obstructive sleep apnoea syndrome and 1.7% of the 175 operated on for severe, or very severe, obstructive sleep apnoea syndromes (RDI > 40). Skin-lined tracheotomy was not followed by important complications and expected results were achieved with immediate disappearance of daytime symptoms and considerable improvement in nocturnal apnoea. Besides sleep-related disorders, numerous clinical situations with indications for a permanent tracheotomy may benefit from the skinlined technique, such as severe laryngeal or tracheal stenoses, laryngeal diplegias, miasthenia gravis, lateral amyotrophic sclerosis, intractable aspiration, severe emphysema.
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PMID:Role of skin-lined tracheotomy in obstructive sleep apnoea syndrome: personal experience. 1546 94

We present a case of laryngospasm in a 12-year-old male who experienced sudden, nocturnal episodes of breathing difficulties and agitation. Apart from laryngospasm, the main differential diagnoses included frontal seizures, sleep-related choking syndrome, sleep asthma, sleep apnoea and REM sleep behaviour disorder. The video and the EEG recordings supported the diagnosis of laryngospasm. The pH-metry confirmed the existence of reflux. Its treatment successfully controlled the episodes. This case illustrates, with a typical video recording, this infrequent type of paroxysmal event with an important differential diagnosis.[Published with video sequences].
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PMID:Sleep-related laryngospasm: a video-polysomnographic recording. 1656 30

There are many different types of sleep disorders. The majority of sleep-related breathing disorders can be attributed to sleep apnoea syndrome. Nocturnal choking sensation is a different symptom, for which we present two cases. Nocturnal choking sensation is a terrifying symptom for the patient and the diagnostic approach can be challenging. Aside from sleep choking syndrome, this symptom may appear with nocturnal laryngospasm, insular epilepsy and nocturnal gastro-oesophageal reflux. A thorough patient history and observation of the nocturnal event, sometimes supported by EEG findings, may provide the clue to the diagnosis. These kinds of nocturnal symptoms are best analyzed in a clinic specialized in both epilepsy and sleep disorders.
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PMID:[Nocturnal choking sensation]. 2402 Jun 23

Since its approval by US Food and Drug Administration in 1999 the clinical use of dexmedetomidine has been gaining in popularity. The indications and clinical applications of this drug have been expanded significantly. In this paper we reviewed its pharmacokinetics, pharmacodynamics, mechanisms of action and mainly focused on its clinical uses and outcomes. Common clinical uses of dexmedetomidine include pre-operative anxiolysis, heart rate control during intubation, treatment of bronchospasm, prevention of laryngospasm and avoiding opioid-induced post-operative respiratory depression and nausea and vomiting. Avoiding opioid induced respiratory depression has been especially beneficial in patients with sleep apnea syndrome. Other problems that can be prevented with dexmedetomidine are tachydysrhythmias, myocardial ischemia, delirium and acute kidney injury. Dexmedetomidine is an excellent sedative drug for intubated patients and it greatly facilitates neurological evaluation. It has been used successfully as a patient-controlled anesthesia drug and to prevent shivering. It is also used as an adjuvant to local anesthetics. It has been suggested that dexmedetomidine is a drug that has many beneficial effects and should be used more frequently by anesthesia care providers to prevent common problems in the peri-operative period. With judicious titration to effect during the intravenous administration of this drug the occurrence of side effects can be minimized. It is very likely that this drug will ascend to take a much more prominent role in future anesthesia practice.
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PMID:Is It Time for an Expanded Role of Dexmedetomidine in Contemporary Anesthesia Practice? - A Clinician's Perspective. 3159 18

Negative pressure pulmonary edema (NPPE) caused by airway obstruction was often life-threatening. Major cause of NPPE in adult patients was reported as post-operative laryngospasm. Therefore, NPPE was recognized widely among surgeons and anesthesiologist, but physicians also could face NPPE case in several clinical situation. NPPE in this case was caused by sleep apnea syndrome (SAS) as relatively rare cause. A 65-year-old female presented to emergency department due to disturbance of consciousness during sleep. This patient had desaturation requiring oxygen administration. Computed tomography showed pulmonary edema in bilateral lung fields. Comprehensive examination had no evident organic airway obstruction, and echocardiography showed normal cardiac function. This patient had been diagnosed with severe SAS with the apnea hypopnea index of 32 times/h. Therefore, we thought that the NPPE could be caused by severe SAS in this case. Continuous positive airway pressure therapy could improve this patient's symptoms promptly, and this patient could discharge without a complication. We should consider SAS as a cause of NPPE when examining NPPE patients especially with onset during sleep.
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PMID:Negative pressure pulmonary edema related with severe sleep apnea syndrome: A case report. 3268 65