scholarly journals THE ROLE OF POLYSOMNOGRAPHY (HOME SLEEP STUDY LEVEL III DEVICE) IN EVALUATION OF LEVELS OF UPPER AIRWAY OBSTRUCTION IN CASES OF OBSTRUCTIVE SLEEP APNOEA HYPOPNOEA SYNDROME: A STUDY

2016 ◽  
Vol 5 (74) ◽  
pp. 5501-5506
Author(s):  
Sreenivasulu G ◽  
Sushma N ◽  
Sudhindra G
Keyword(s):  
Airway Obstruction ◽  
Obstructive Sleep Apnoea ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Upper Airway Obstruction ◽  
Sleep Study ◽  
Obstructive Sleep ◽  
Home Sleep Study

scholarly journals 1244 A Curious Case of ASV Failure

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A474-A474
Author(s):  
Nishant Chaudhary ◽  
Mirna Ayache ◽  
John Carter
Keyword(s):  
Sleep Apnea ◽  
Airway Obstruction ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Upper Airway Obstruction ◽  
Neck Extension ◽  
Sleep Study ◽  
Obstructive Sleep

Abstract Introduction Positive airway pressure-induced upper airway obstruction has been reported with the treatment of obstructive sleep apnea (OSA) using continuous positive airway pressure (CPAP) along with an oronasal interface. Here we describe a case of persistent treatment emergent central sleep apnea (TECSA) inadequately treated with adaptive servo ventilation (ASV), with an airflow pattern suggestive of ASV-induced upper airway obstruction. Report of Case A 32-year-old male, with severe OSA (apnea hypopnea index: 52.4) and no other significant past medical history, was treated with CPAP and required higher pressures during titration sleep studies to alleviate obstructive events, despite a Mallampati Class II airway and a normal body mass index. Drug-Induced Sleep Endoscopy (DISE) showed a complete velopharynx and oropharynx anterior posterior (AP) collapse, long soft palate, which improved with neck extension. CPAP therapy, however, did not result in any symptomatic benefit and compliance reports revealed high residual AHI and persistent TECSA. He underwent an ASV titration sleep study up to a final setting of expiratory positive airway pressure 9 cm H2O, pressure support 6-15 cm H2O (auto-rate), with a full-face mask due to high oral leak associated with the nasal interface. The ASV device detected central apneas and provided mandatory breaths, but did not capture the thorax or abdomen, despite normal mask pressure tracings. Several such apneas occurred, with significant oxyhemoglobin desaturation. Conclusion We postulate that the ASV failure to correct central sleep apnea as evidenced by the absence of thoracoabdominal inspiratory effort, occurred due to ASV-induced upper airway obstruction. Further treatment options for this ASV phenomenon are to pursue an ASV-assisted DISE and determine the effectiveness of adjunctive therapy including neck extension, nasal mask with a mouth closing device and a mandibular assist device.

Upper airway obstruction in the critically ill

2016 ◽  
Author(s):  
Edmond Cohen
Keyword(s):  
Airway Obstruction ◽  
Pulmonary Function Tests ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Upper Airway Obstruction ◽  
Breath Sounds ◽  
Obstructive Sleep ◽  
Increased Risk ◽  
Facial Swelling ◽  
Conscious Patient

Upper airway obstruction (UAO) from any cause should be considered a life-threatening emergency. In a conscious patient, UAO may present as respiratory distress, stridor, dyspnoea, altered voice, cyanosis, cough, decreased or absent breath sounds, wheezing, the hand-to-the-throat choking sign in the case of a foreign body, facial swelling, and distended neck veins. The cause of UAO should be identified and airway management devices must be immediately available prior to any airway manipulation CT scan, flexible bronchoscopy, and pulmonary function tests should be performed to evaluate the cause and the extent of the obstruction. Obstructive sleep apnoea (OSA) patients are at increased risk of developing UAO. Endotracheal intubation, insertion of a supraglottic device, laser therapy, and endotracheal stents maybe life-saving

scholarly journals ERS statement on obstructive sleep disordered breathing in 1- to 23-month-old children

2017 ◽  
Vol 50 (6) ◽  
pp. 1700985 ◽  
Author(s):  
Athanasios G. Kaditis ◽  
Maria Luz Alonso Alvarez ◽  
An Boudewyns ◽  
Francois Abel ◽  
Emmanouel I. Alexopoulos ◽  
...  
Keyword(s):  
Airway Obstruction ◽  
Sleep Disordered Breathing ◽  
Objective Assessment ◽  
Upper Airway ◽  
Upper Airway Obstruction ◽  
Sleep Study ◽  
Mandibular Hypoplasia ◽  
Obstructive Sleep ◽  
Obstructive Sleep Disordered Breathing ◽  
Disordered Breathing

The present statement was produced by a European Respiratory Society Task Force to summarise the evidence and current practice on the diagnosis and management of obstructive sleep disordered breathing (SDB) in children aged 1–23 months. A systematic literature search was completed and 159 articles were summarised to answer clinically relevant questions. SDB is suspected when symptoms or abnormalities related to upper airway obstruction are identified. Morbidity (pulmonary hypertension, growth delay, behavioural problems) and coexisting conditions (feeding difficulties, recurrent otitis media) may be present. SDB severity is measured objectively, preferably by polysomnography, or alternatively polygraphy or nocturnal oximetry. Children with apparent upper airway obstruction during wakefulness, those with abnormal sleep study in combination with SDB symptoms (e.g.snoring) and/or conditions predisposing to SDB (e.g.mandibular hypoplasia) as well as children with SDB and complex conditions (e.g.Down syndrome, Prader–Willi syndrome) will benefit from treatment. Adenotonsillectomy and continuous positive airway pressure are the most frequently used treatment measures along with interventions targeting specific conditions (e.g.supraglottoplasty for laryngomalacia or nasopharyngeal airway for mandibular hypoplasia). Hence, obstructive SDB in children aged 1–23 months is a multifactorial disorder that requires objective assessment and treatment of all underlying abnormalities that contribute to upper airway obstruction during sleep.

Inspiratory flow limitation in obstructive sleep apnoea patients

2004 ◽  
Vol 106 (6) ◽  
pp. 563-565 ◽  
Author(s):  
Ramon FARRÉ
Keyword(s):  
Pilot Study ◽  
Airway Obstruction ◽  
Sleep Disorder ◽  
Obstructive Sleep Apnoea ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Obstructive Sleep Apnoea Syndrome ◽  
Bench Test ◽  
Flow Limitation ◽  
Obstructive Sleep

Patients suffering from the obstructive sleep apnoea syndrome (OSAS) experience nocturnal episodes of upper airway obstruction resulting in recurrent oxygen desaturations and arousals. Methods to quantify the nocturnal obstructive events are of interest for characterizing this prevalent sleep disorder. In a study published in this issue of Clinical Science, Bloch and co-workers propose the computation of a new index for objectively quantifying the degree of flow limitation in patients with OSAS. The results obtained in a bench test and in a pilot study in patients suggest that the flow limitation index proposed may help to better characterize the disturbed breathing events undergone by patients with OSAS.

scholarly journals The role of hyaluronic acid and hyaluronidase-1 in obstructive sleep apnoea

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Martina Meszaros ◽  
Adrian Kis ◽  
Laszlo Kunos ◽  
Adam Domonkos Tarnoki ◽  
David Laszlo Tarnoki ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Hyaluronic Acid ◽  
Obstructive Sleep Apnoea ◽  
Antioxidant Properties ◽  
Molecular Size ◽  
Sleep Apnoea ◽  
Low Molecular Weight ◽  
Sleep Study ◽  
Obstructive Sleep

Abstract Biological functions of hyaluronic acid (HA) depend on its molecular size. High-molecular weight HA (HMW-HA) is an important component of the endothelial wall and has anti-inflammatory and antioxidant properties. Under inflammation or hypoxia, HMW-HA is degraded by hyaluronidases, such as HYAL-1 resulting in pro-inflammatory low-molecular weight fragments. Obstructive sleep apnoea (OSA) is characterised by intermittent hypoxia and systemic inflammation. Our aim was to evaluate circulating HMW-HA and HYAL-1 in OSA. We recruited 68 patients with OSA and 40 control volunteers. After full-night sleep study blood samples were taken for HMW-HA and HYAL-1 measurements. HYAL-1 levels were significantly higher in patients with OSA compared to controls (0.59/0.31–0.88/ng/mL vs. 0.31/0.31–0.58/ng/mL; p = 0.005) after adjustment for gender, age, BMI and smoking. There was a trend for reduced HMW-HA concentrations in OSA (31.63/18.11–59.25/ng/mL vs. 46.83/25.41–89.95/ng/mL; p = 0.068). Significant correlation was detected between circulating HMW-HA and apnoea-hypopnoea-index (r = − 0.195, p = 0.043), HYAL-1 and apnoea-hypopnoea-index (r = 0.30, p < 0.01) as well as oxygen desaturation index (r = 0.26, p < 0.01). Our results suggest that chronic hypoxia is associated with increased plasma HYAL-1 concentration and accelerated HMW-HA degradation. Altered hyaluronan metabolism may be involved in the inflammatory cascade potentially leading to endothelial dysfunction in OSA.

scholarly journals Sleep disordered breathing following stroke

2004 ◽  
Vol 61 (3) ◽  
Author(s):  
P.M. Turkington ◽  
M.W. Elliott
Keyword(s):  
Blood Pressure ◽  
Airway Obstruction ◽  
Obstructive Sleep Apnoea ◽  
Sleep Disordered Breathing ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Obstructive Sleep ◽  
Ischaemic Penumbra ◽  
The Relationship ◽  
The Brain

In recent years there has been increasing interest in the relationship between obstructive sleep apnoea and stroke. It is clear that many patients who have had a stroke have marked obstructive sleep apnoea. This is seen during recovery but also during the acute phase when transient hypoxaemia and the blood pressure swings associated with upper airway obstruction, may worsen the ischaemic penumbra of the area of the brain which is compromised, leading to a worse outcome. There is some evidence to support this hypothesis. This article explores these issues.

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