背景:用于治疗长间隙食管闭锁(LGEA)的牵引诱导食管生长(Foker)过程依赖于对食管施加渐进张力以诱导生长。由于其抗纤维化和肌肉松弛特性,我们假设肉毒杆菌毒素A(BTX)可以促进牵引诱导的食管生长。
方法:对2021年至2023年接受BTX增强Foker程序进行LGEA修复的儿童进行了一项回顾性的两中心队列研究。BTX(10单位/毫升,2单位/kg,每个食管袋)在牵引开始时应用。牵引时间,并发症,从2014年到2021年,吻合结果与历史对照(Foker过程无BTX)进行了比较。
结果:20名婴儿(LGEAA型:12,B:4,C:4;35%再次手术;中位[IQR]年龄3[2-5]个月),接受BTX增强的Foker手术(开胸手术外牵引:9;微创[MIS]多阶段内牵引:11)。BTX增强的外部和外部牵引控制患者的平均间隙长度相似(平均值[SD],50.6毫米[12.6]vs.44.5毫米[11.9],p=0.21)。与对照组相比,BTX增强的外部牵引过程明显更快(平均值[SD],12.1[1.6]天vs.16.6[13.2]无BTX,p=0.04),尽管术前间隙长度相似。对于接受微创手术的患者,牵引时间没有差异。在两个队列中,并发症或吻合结果均无显著差异。
结论:肉毒杆菌毒素可能在促进LGEA修复的牵拉诱导的食管生长过程中发挥作用。最大限度地减少牵引时间可以减少外部牵引时的镇静和瘫痪负担。需要进一步的研究来阐明BTX对食道的影响。
方法:三级。
方法:回顾性,双中心,队列研究。
BACKGROUND: The
traction-induced esophageal growth (Foker) process for the treatment of long gap esophageal atresia (LGEA) relies on applying progressive tension to the esophagus to induce growth. Due to its anti-fibrotic and muscle-relaxing properties, we hypothesize that Botulinum Toxin A (BTX) can enhance traction-induced esophageal growth.
METHODS: A retrospective two-center cohort study was conducted on children who underwent a BTX-enhanced Foker process for LGEA repair from 2021 to 2023. BTX (10 units/ml, 2 units/kg, per esophageal pouch) was applied at the time of
traction initiation. Time on traction, complications, and anastomotic outcomes were compared against historical controls (Foker process without BTX) from 2014 to 2021.
RESULTS: Twenty infants (LGEA type A:12, B:4, C:4; 35% reoperative; median [IQR] age 3 [2-5] months), underwent BTX-enhanced Foker process (thoracotomy with external traction: 9; minimally invasive [MIS] multi-staged internal
traction: 11). Mean gap lengths were similar between BTX-enhanced external and external traction control patients (mean [SD], 50.6 mm [12.6] vs. 44.5 mm [11.9], p = 0.21). When compared to controls, the BTX-enhanced external traction process was significantly faster (mean [SD], 12.1 [1.6] days vs. 16.6 [13.2] without BTX, p = 0.04) despite similar preoperative gap lengths. There was no difference in time on
traction for those undergoing a minimally invasive process. There were no significant differences in complications or anastomotic outcomes in either cohort.
CONCLUSIONS: Botulinum toxin may play a role in accelerating the traction-induced esophageal growth process for LGEA repair. Minimizing time on
traction can decrease sedation and paralysis burden while on external
traction. Further studies are needed to elucidate the effects of BTX on the esophagus.
METHODS: Level III.
METHODS: Retrospective, Two-center, Cohort study.