Anatomical Basis of Obstructive Sleep Apnoea: A Review of Randomized Controlled Trials

医学 阻塞性睡眠呼吸暂停 气道 软腭 气道阻塞 颏舌 随机对照试验 腺样体肥大 呼吸暂停 麻醉 内科学 外科 腺样体切除术 扁桃体切除术
作者
Shrikrishna B.H.,G Deepa,Anupama Sawal,Trupti Balwir
出处
期刊:Cureus [Cureus, Inc.]
被引量:2
标识
DOI:10.7759/cureus.44525
摘要

Repeated obstruction and closure of the upper airway, sporadic hypoxic episodes, and sympathetic activity are symptoms of obstructive sleep apnea (OSA). Obstructive sleep apnoea is due to a combination of altered upper airway structure and muscular function, a low arousal threshold and increased loop gain. Although recurrent upper airway (UA) collapse during sleep is the most frequent clinical hallmark of OSA, the exact cause of this collapse is unknown. Furthermore, while continuous positive airway pressure aids in the management of OSA, many patients find it intolerable. As a result, a better knowledge of the causes of OSA may result in more effective treatments. We did a review of randomized controlled trials that were done in this regard in the last 10 years and whose full-text version is available on the PubMed database. A total of 20 articles were finalized for review after applying our criteria. The articles have proposed different theories regarding the anatomical basis responsible for obstructive sleep apnoea. The theories proposed by different studies in the last decade include reduced genioglossus and hypoglossal nerve activity, the pharyngeal muscles' failure to keep the airway open or tighten it, tonsils and adenoid hypertrophy, an oversensitive ventilatory control system and low respiratory arousal threshold, mandibular position, pharyngeal muscles' high sympathetic drive, cephalometric alterations such as mandibular and hyoid bone position and the length of the soft palate, obesity, and neck fat and fluid re-distribution in the body, from the lower to the upper parts while reclining. Given the diverse etiological characteristics of OSA patients and to increase our knowledge of the condition, additional study into this group is required. Filling any knowledge gaps that may exist in the anatomical basis of the onset of OSA is the main objective of this review paper.

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