Mistretta Antonina, Modica Domenico Michele, Pitruzzella Alessandro, Burgio Stefano, Lorusso Francesco, Billone Sebastiano, Valenti Carla, Vita Giulia, Poma Salvatore, Amata Marta, Vita Pietro, Gallina Salvatore
Otolaryngology Unit, Department of Biomedicine and Advanced Diagnostic, University of Palermo, Palermo, Italy.
Otorhinolaryngology Unit, Villa Sofia-Cervello Hospital, Palermo, Italy.
Iran J Otorhinolaryngol. 2022 May;34(122):145-153. doi: 10.22038/IJORL.2022.57642.2986.
One of the most important complications of OSAHS in children is growth delay. The aim of this study was to investigate changes in clinical body growth, and laboratory growth in children with OSAHS after adeno-tonsillar surgery.
In our study, among 102 children suffering from sleep-disordered breathing, 70 met the inclusion criteria because they were affected by OSAHS and adenotonsillar hypertrophy. In total, 96 children affected by adeno-tonsillar hypertrophy (55 males and 41 females) underwent nocturnal cardiorespiratory monitoring with Embletta MPR, monitoring for post-operative 24 hours. Patients underwent blood sampling to evaluate preoperative GH and IGF-1 serum levels, "placement" in Cacciari's growth charts and adenotonsillectomy and saturation monitoring for post-operative 24 hours. According to auxological parameters, 82.86% of the patients were below the fiftieth percentile of BMI Cacciari's growth charts and IGF-1 preoperative serum levels were below the normal range. All patients underwent adenotonsillectomy.
All 70 patients recovered from OSAHS according to the results of nocturnal cardiorespiratory monitoring after six months. IGF-1 serum levels significantly increased after three months and one year after. All the auxological parameters showed a significant increase after surgery. We calculated the average annual growth in height of the patients before and after adenotonsillectomy (AT): the growth rate was impaired by OSAHS (5.4±1.3 cm/year), while in the following year post-surgery we found a significant growth speed acceleration (9.9±1.7 cm/year, P=0.001).
In conclusion, growth delay in children can be caused by OSAHS, and when it is due to adenotonsillar hypertrophy, adenotonsillectomy is to be considered as the therapy of choice.
儿童阻塞性睡眠呼吸暂停低通气综合征(OSAHS)最重要的并发症之一是生长发育迟缓。本研究旨在调查腺样体扁桃体切除术后OSAHS患儿临床身体生长及实验室生长指标的变化。
在我们的研究中,102例患有睡眠呼吸障碍的儿童中,70例符合纳入标准,因为他们患有OSAHS和腺样体扁桃体肥大。共有96例腺样体扁桃体肥大患儿(55例男性,41例女性)使用Embletta MPR进行夜间心肺监测,并监测术后24小时。患者接受血液采样以评估术前生长激素(GH)和胰岛素样生长因子-1(IGF-1)血清水平,根据卡恰里生长图表进行“定位”,并接受腺样体扁桃体切除术及术后24小时的饱和度监测。根据体格测量参数,82.86%的患者BMI低于卡恰里生长图表的第五十百分位数,术前IGF-1血清水平低于正常范围。所有患者均接受了腺样体扁桃体切除术。
根据夜间心肺监测结果,所有70例患者在6个月后均从OSAHS中康复。IGF-1血清水平在术后3个月和1年后显著升高。所有体格测量参数在术后均显著增加。我们计算了腺样体扁桃体切除术前和术后患者的平均每年身高增长:OSAHS使生长速度受损(5.4±1.3厘米/年),而在术后次年我们发现生长速度显著加快(9.9±1.7厘米/年,P = 0.001)。
总之,儿童生长发育迟缓可能由OSAHS引起,当是由腺样体扁桃体肥大所致时,应考虑将腺样体扁桃体切除术作为首选治疗方法。