ABSTRACT
OBJECTIVE: To investigate the effectiveness of intraoperative nerve monitoring at decreasing vocal fold movement impairment in children undergoing at-risk procedures. BACKGROUND: Children undergoing aerodigestive or cardiovascular procedures are at risk for recurrent laryngeal nerve injury, leading to vocal fold movement impairment. Although intraoperative nerve monitoring has been shown to decrease recurrent laryngeal nerve injury in adults, there is paucity of data in children. METHODS: This was a retrospective, single-center cohort study of children who underwent airway, esophageal, or great vessel surgery between 2018 and 2023. Vocal fold movement impairment was evaluated with pre- and postoperative awake flexible fiberoptic laryngoscopy. Vocal fold movement impairment rates and associated characteristics were compared between those with and without intraoperative nerve monitoring. RESULTS: Among 387 children undergoing 426 at-risk procedures, intraoperative nerve monitoring was used in 72.1% (n = 307) of procedures. Intraoperative nerve monitoring significantly reduced postoperative vocal fold movement impairment compared with those without (11.4% vs 20.2%, P = .019, 43.6% relative risk reduction, number needed to treat: 12). In children with a pre-existing vocal fold movement impairment (n = 79, 18.5%), intraoperative nerve monitoring provided enhanced protection (vocal fold movement impairment 7.8% with intraoperative nerve monitoring compared with 25% without, P = .046, 68.6% relative risk reduction, number needed to treat: 3). Bilateral vocal fold movement impairment was 14 times more likely without intraoperative nerve monitoring (1.8% overall, 0.3% with intraoperative nerve monitoring, 5.6% without; 95% confidence interval 1.6-123.2; P = .006). Increasing intraoperative nerve monitoring use correlated with decreasing vocal fold movement impairment rates year over year (P = .046). Multivariable logistic regression demonstrated intraoperative nerve monitoring to remain significantly associated with reduced risk of vocal fold movement impairment (odds ratio, 0.48; 95% confidence interval, 0.26-0.85; P = .013). CONCLUSION: Intraoperative nerve monitoring in children seems effective at decreasing recurrent laryngeal nerve injury and consequently vocal fold movement impairment. Intraoperative nerve monitoring should be considered in children undergoing cervicothoracic or cardiothoracic procedures, especially in those with preoperative vocal fold movement impairment.
ABSTRACT
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. CONCLUSION: 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. LEVEL OF EVIDENCE: Level III. TYPE OF STUDY: Retrospective, Two-center, Cohort study.
ABSTRACT
Historically, children afflicted with long gap esophageal atresia (LGEA) had few options, either esophageal replacement or a life of gastrostomy feeds. In 1997, John Foker from Minnesota revolutionized the treatment of LGEA. His new procedure focused on "traction-induced growth" when the proximal and distal esophageal segments were too far apart for primary repair. Foker's approach involved placement of pledgeted sutures on both esophageal pouches connected to an externalized traction system which could be serially tightened, allowing for tension-induced esophageal growth and a delayed primary repair. Despite its potential, the Foker process was received with criticism and disbelief, and to this day, controversy remains regarding its mechanism of action - esophageal growth versus stretch. Nonetheless, early adopters such as Rusty Jennings of Boston embraced Foker's central principle that "one's own esophagus is best" and was instrumental to the implementation and rise in popularity of the Foker process. The downstream effects of this emphasis on esophageal preservation would uncover the need for a focused yet multidisciplinary approach to the many challenges that EA children face beyond "just the esophagus", leading to the first Esophageal and Airway Treatment Center for children. Consequently, the development of new techniques for the multidimensional care of the LGEA child evolved such as the posterior tracheopexy for associated tracheomalacia, the supercharged jejunal interposition, as well as minimally invasive internalized esophageal traction systems. We recognize the work of Foker and Jennings as key catalysts of an era of esophageal preservation and multidisciplinary care of children with EA.