Abstract
The external branch of the superior laryngeal nerve (EBSLN) innervates the cricothyroid muscle (CTM) to promote lengthening and thinning of the vocal fold, thus increasing voice pitch. The close relation with the superior thyroid vessels (STV) puts the EBSLN in risk every time the superior pole of the thyroid is dissected. It travels downward to innervate the CTM, lateral to the thyroid cartilage and to the inferior pharyngeal constrictor muscle (IPCM), being eventually covered by this muscle fibers as it approaches its entry point. During its descending course, the EBSLN curves and crosses the STV posteriorly. The lower this crossing occurs in the neck, the higher the risk of surgical damage to the nerve by transection, traction, entrapment, thermal damage or disrupted blood supply. The chances of surgical trauma are also increased by size and weight of the specimen, shorter neck length and non-white ethnicity. Voice changes following thyroid surgery are common and multifactorial. The actual rate of vocal impairment due to EBSLN injury is unclear, since changes to the everyday speaking voice can be minimal and laryngeal findings are usually subtle and controversial. CTM electroneuromyography (EMG) is the most accurate tool to diagnose abnormal EBSLN conductivity, but it is technically difficult and barely applicable in routine practice. Recommended approaches to prevent injury include: (I) individual distal ligature of the STV by the thyroid capsule; (II) visual identification of the nerve and its trajectory and (III) electrostimulation with either observation of CTM twitch or intraoperative nerve monitoring (IONM) via dedicated endotracheal tube electrodes. There is accumulating evidence that a combination of visual and standardized electrophysiological EBSLN identification with meticulous division of the STV improves preservation rates. IONM bears the additional benefits of prognostication, quantification and documentation of neural function once it allows intraoperative laryngeal EMG.
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