利用超音波影像評估小兒阻塞性睡眠呼吸中止症患者的上呼吸道結構

Abstract

背景 阻塞性睡眠呼吸中止症是兒童常見的睡眠呼吸障礙之一，最常引起這疾病的原因為扁桃腺與腺樣體的過度增生，在睡眠中引起上呼吸道的塌陷，導致發生阻塞性的睡眠呼吸中止症。 近年許多研究顯示，上呼吸道相關的咽喉肌肉結構、脂肪堆積分布、扁桃腺等淋巴組織分布、舌根塌陷程度、側咽壁的厚度等等，在成人阻塞性睡眠呼吸中止症的患者與正常人比較，也有顯著增厚導致上呼吸道的塌陷以及內徑的縮小，但是，在小兒阻塞性睡眠呼吸中止症的相關研究並不多，也沒有明確的結論。 本試驗的目的為以耳鼻喉超音波檢查進行兒童之上呼吸道結構之測量，並尋找與小兒阻塞性睡眠呼吸中止症之嚴重度相關之上呼吸道結構之超音波影像參數，以及其之可能預測因子。 方法 這是一個前瞻性非侵入式的研究，患有睡眠障礙的兒童於接受手術前，接受耳鼻喉頭頸超音波檢查，針對上呼吸道軟組織結構做一測量，並以所獲得之超音波參數與睡眠生理檢查做一分析。 結果 從2016年一月至2017年二月，共有82位兒童（包含20位單純打鼾與62位睡眠呼吸中止症）接受超音波測量。兩組受試者間的年齡、性別、BMI、頸圍、扁桃腺與腺樣體之大小均無顯著差異。研究顯示，扁桃腺相關之超音波參數，包含大小與體積，在兩組間無差別。然而罹患阻塞性睡眠呼吸中止症的兒童，其在超音波所測得之靜止下與Müller法下所測得之側咽壁厚度，均比僅患單純打鼾之兒童來的厚，並達到顯著差異。（24.9±4.4 vs. 21.3±2.6 mm, p=0.001與29.9±5.5 vs. 24.1±2.9 mm, p<0.001）我們也發現，在靜止下與Müller法下所測得之側咽壁的厚度，均與AHI呈現相關，並達到顯著差異。在以邏輯式迴歸分析校正年齡、性別、BMI、扁桃腺與腺樣體大小後，我們發現無論是在靜止狀態或Müller法下所測得之側咽壁的厚度，均為兒童阻塞性睡眠呼吸中止症之危險因子。（OR 1.47, 1.09~1.96, p=0.011; OR 1.63, 1.14~2.34, p=0.007） 結論 超音波影像可以用來診斷兒童之上呼吸道週微軟組織結構，而扁桃腺的大小與體積，與兒童阻塞性睡眠呼吸中止症無顯著相關，然而，比起無阻塞性睡眠呼吸中止症之兒童，罹患阻塞性睡眠呼吸中止症之兒童呈現側咽壁較厚的情形，同時側咽壁也是兒童阻塞性呼吸中止症之一項危險因子。

Introduction: Obstructive sleep apnea (OSA) in children includes a spectrum of respiratory disorders characterized by upper airway collapse during sleep. The pathophysiology is mainly due to adenotonsillar hypertrophy, neuromuscular disorder, craniofacial anomaly and genetic defect. Several studies had revealed that the dynamic anatomy in upper airway, including superior constriction sphincter, fat pad deposition, lymphoid tissue and muscle tone of pharyngeal wall were all related to the collapsibility of upper airway during sleep in adults. Especially, the thicknesses of lateral pharyngeal wall (LPW) in OSA subjects are significantly different from non-OSA ones. However, there is still limited study addressed the dynamic upper airway structures in children with OSA by ultrasonography. The aims of this study are to measure the upper airway structures by ENT head and neck ultrasonography in children with OSA, and to elucidate the association between the ultrasonographic and polysomnographic parameters in these children. Methods: In this prospective cohort study, children with symptoms of sleep-disordered breathing received overnight sleep study (polysomnography, PSG) were invited to join this research after written informed consents obtained from each child or their parents. ENT head and neck ultrasonography were performed before surgery on the first date of admission. All the ultrasonographic and PSG parameters were compared and analyzed. Results: From January 2016 to February 2017, eighty-two children, including twenty primary snorer and sixty-two OSA subjects, received the ultrasound measurement pre-operatively. There were no significant differences in age, gender, BMI, neck circumference, tonsillar and adenoid grades between these two groups. Among the ultrasonographic parameters of upper airway structures, there were no differences in tonsil-related dimensions and volumes. However, the total LPW thickness was significantly higher in OSA children than primary snorers in both resting position (24.9±4.4 vs. 21.3±2.6 mm, p=0.001) and under Müller’s maneuver (29.9±5.5 vs. 24.1±2.9 mm, p<0.001). There was also significant correlation between the thickness of LPW and AHI in both resting and under Müller’s status. The total LPW thickness in resting and Müller’s status were independent factors of OSA severity in children by logistic regression analysis after adjusted with age, gender, BMI percentile, tongue position, tonsillar grade, and adenoidal size (OR 1.47, 1.09~1.96, p=0.011; OR 1.63, 1.14~2.34, p=0.007). Conclusions: Ultrasonography is a useful diagnostic tool to evaluate the dynamic upper airway structures in children with sleep-disordered breathing. By ultrasonography, the tonsil-related parameters dose not significantly relate to childhood OSA. However, LPW is significantly thicker in OSA children than non-OSA ones, and the thickness of LPW is significantly increasing under Müller’s maneuver in OSA children when comparing to non-OSA ones.