Abstract：
OBJECTIVE: Vocal cord paralysis has been reported as a common complication of button battery (BB) ingestion, and there is a need to confirm the mechanism of vocal cord paralysis for the development of a standardized treatment.
METHODS: A new CR2032 BB and artificial saliva were placed in a fresh pig esophagus with the recurrent laryngeal nerve (RLN); the negative electrode faced the nerve in the experimental group, while the positive electrode faced the nerve in the control group. The pH values of the intra- and extraesophageal walls were measured simultaneously. Pathological examination was performed after the esophagus and nerves were damaged.
RESULTS: After BB ingestion, the pH near the intraesophageal negative electrode increased rapidly, reaching 11.5 at 30 min and over 14 at 6 h, while the extraesophageal pH did not change at 1 h and began to accelerate after 2 h, reaching 10 at 6 h. After 6 h of exposure, the pathological section showed that the structure of the mucosa, submucosa, and muscle layer were destroyed; chromatin in the nucleus faded, and part of the nerve bundle in the adventitia had liquefaction necrosis.
CONCLUSIONS: The basic mechanism of vocal cord paralysis caused by BB ingestion is that the OH- generated by the electrolytic reaction of the negative electrode penetrates the esophageal wall and corrodes the RLN, which may be the cause of vocal cord paralysis caused by BB ingestion without esophageal perforation.
METHODS: A new CR2032 BB and artificial saliva were placed in a fresh pig esophagus with the recurrent laryngeal nerve (RLN); the negative electrode faced the nerve in the experimental group, while the positive electrode faced the nerve in the control group. The pH values of the intra- and extraesophageal walls were measured simultaneously. Pathological examination was performed after the esophagus and nerves were damaged.
RESULTS: After BB ingestion, the pH near the intraesophageal negative electrode increased rapidly, reaching 11.5 at 30 min and over 14 at 6 h, while the extraesophageal pH did not change at 1 h and began to accelerate after 2 h, reaching 10 at 6 h. After 6 h of exposure, the pathological section showed that the structure of the mucosa, submucosa, and muscle layer were destroyed; chromatin in the nucleus faded, and part of the nerve bundle in the adventitia had liquefaction necrosis.
CONCLUSIONS: The basic mechanism of vocal cord paralysis caused by BB ingestion is that the OH- generated by the electrolytic reaction of the negative electrode penetrates the esophageal wall and corrodes the RLN, which may be the cause of vocal cord paralysis caused by BB ingestion without esophageal perforation.
摘要：
目的：据报道，声带麻痹是纽扣电池（BB）摄入的常见并发症，并且有必要确认声带麻痹的机制，以开发标准化的治疗方法。
方法：将新的CR2032BB和人工唾液置于带有喉返神经（RLN）的新鲜猪食管中；实验组的负电极面对神经，而对照组的正极面向神经。同时测量食管内外壁的pH值。食管和神经受损后进行病理检查。
结果：摄入BB后，食管内负电极附近的pH值迅速增加，30分钟达到11.5，6小时超过14，而食管外pH在1小时时没有变化，2小时后开始加速，在6小时时达到10。暴露6小时后，病理切片显示粘膜结构，粘膜下层,肌肉层被破坏；细胞核中的染色质褪色，外膜部分神经束有液化坏死。
结论：摄入BB引起声带麻痹的基本机制是负极的电解反应产生的OH-穿透食管壁并腐蚀RLN，这可能是由于摄入BB而没有食管穿孔引起的声带麻痹的原因。
方法：将新的CR2032BB和人工唾液置于带有喉返神经（RLN）的新鲜猪食管中；实验组的负电极面对神经，而对照组的正极面向神经。同时测量食管内外壁的pH值。食管和神经受损后进行病理检查。
结果：摄入BB后，食管内负电极附近的pH值迅速增加，30分钟达到11.5，6小时超过14，而食管外pH在1小时时没有变化，2小时后开始加速，在6小时时达到10。暴露6小时后，病理切片显示粘膜结构，粘膜下层,肌肉层被破坏；细胞核中的染色质褪色，外膜部分神经束有液化坏死。
结论：摄入BB引起声带麻痹的基本机制是负极的电解反应产生的OH-穿透食管壁并腐蚀RLN，这可能是由于摄入BB而没有食管穿孔引起的声带麻痹的原因。
