Laryngeal Nerve Injury
Related narrative: Laryngeal Nerve Injury
The larynx has two key functions, as a sphincter regulating the passage of air and as the origin of vocal sounds. The intrinsic muscles of the larynx which effect these functions are innervated by the superior and recurrent laryngeal branches of the vagus nerves. The superior laryngeal nerves innervate the cricothyroid muscles, which rotate the cricoid cartilage on the pivots of the inferior cornua of the thyroid cartilage. This action stretches and puts tension on the vocal cords, giving strength and endurance to the voice, particularly in the higher registers. The recurrent laryngeal nerves innervate all the other intrinsic muscles that allow ad- and abduction of the vocal cords, affecting frequency (pitch) of sounds and the sphincter function of the rima glottis. The latter function closes the glottis during swallowing, cough and valsalva, and opens the airway maximally during forceful respiration.
Compromise of the nerves of the larynx may be due to disease or external trauma, but is more commonly iatrogenic. The left recurrent laryngeal nerve is at risk of damage in the chest by involvement with bronchial and esophageal carcinoma, and with metastatic mediastinal lymphadenopathy. Both recurrent nerves are at risk with malignant cervical adenopathy. There is approximately a 1% recurrent nerve injury rate from thyroidectomy, and a similar, though less easily recognized incidence of superior laryngeal nerve injury. There is about a 3% incidence of recurrent nerve dysfunction or injury with anterior spine surgery, and a significantly higher incidence with reoperative carotid endarterectomy and reoperative thyroid/parathyroid surgery.
Nerve injury is seldom recognized at the time of surgery. If it is recognized, primary end-to-end repair is done if possible. A cable graft of greater auricular nerve may be used to bridge a gap. More commonly, dysfunction is recognized by subtle voice changes postoperatively and occasionally by dramatic airway obstruction immediately on extubation. Complicating the picture are the common, non-neurological voice changes after thyroid surgery. One study (Stojadinovic) found early subjective voice changes in 30% of 50 patients and 14% late symptoms. Eighty four percent of these patients had objective change in at least one voice parameter, without evidence of laryngeal nerve dysfunction.
Superior laryngeal nerve injury has its most profound impact on professional singers, and yet the notorious case of operatic soprano Amelita Galli-Curci is still evincing debate (Crookes). Unilateral recurrent nerve injury may not be detected in the early post-operative period, because the affected cord rests near the midline and allows adequate vocal and sphincter function, especially with compensatory hyper-adduction of the opposite cord. Manifestations of such injuries may be hoarseness and inadequate air intake during exertion. For some reason, partial injury results in greater adduction of the affected cord. Bilateral injury may result in fixed closure of the rima glottis at extubation and acute airway obstruction, requiring emergency reintubation and subsequent tracheostomy.
Strategies for avoiding injuries include careful surgical technique and intraoperative neurophysiologic monitoring. In 20% of individuals the superior laryngeal nerve remains close to the superior thyroid artery throughout its course and is at high risk during division of that vessel. Careful adherence to the superior pole of the thyroid is the prime operative strategy. Awareness of the variations in the location of the terminal recurrent laryngeal nerves is critically important. While the majority of nerves lie posterior to the inferior thyroid artery in the tracheoesophageal groove, a percentage lie anterior to the artery or farther posterior (see thyroid anatomy, frame 8). Some recurrent laryngeal nerves or their branches may be embedded in the suspensory ligament (of Berry) of the thyroid, and injured when that structure is divided. Rarely (1%) a nerve may be non-recurrent (see thyroid anatomy, frame 7).
Avoidance vs. exposure has been an ongoing debate for the past century. Visualization provides reassurance that the nerve is intact, and may prevent injury, especially with a large thyroid. However, there is an incidence of late neuropraxia that may be due to damage to the delicate vasa nervorum during exposure. Subtotal thyroidectomy for benign thyroid disease has been a historical method of avoiding damage to parathyroids and nerve. Intraoperative parathormone assay has the potential to reduce the extent of surgery in reoperative parathyroid surgery. Other factors in late dysfunction may be hematoma and edema.
Treatment of recurrent nerve dysfunction requires determination of whether the injury is temporary of permanent. Steroids have been advocated by some to reduce edema and speed recovery. In the past, it has been necessary to wait for up to nine months to assess whether recovery is possible, especially when the surgeon feels that he had visual confirmation of intact nerves. Now laryngeal electromyography (LEMG) may provide an earlier indication of the potential for recovery. If recovery is not likely, injection of newer synthetic materials into the vocal folds may be beneficial. If surgical laryngoplastic options are considered, the otolaryngologist is faced with the problem of balancing medialization of the cords for vocalization and airway protection against leaving an adequate glottic opening for air movement. Reinnervation with the ansa hypoglossi or omohyoid neuromuscular transfer to the posterior cricoarytenoid have yielded unpredictable results. Clinical trials are underway with pacing of the posterior cricoarytenoid.
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