a Reported as number of operations/nerves at risk b Initial evaluation at postoperative day 2
combined with additional deficits following stroke, another known complication, place the patient undergoing carotid endarterectomy at unusual risk for aspiration.
Vocal fold paralysis follows 1.0-7.7% of carotid endarterectomies. Once again, as in the case of cervical spine surgery, prompt systematic evaluation of the larynx 2 days following surgery has revealed a much higher incidence (27%) than in other reports . This declines over the following months to a figure consistent with those reported elsewhere. Most cranial nerve injuries following carotid endarterectomy resolve or compensate; which is not entirely certain from available material.
A special concern in carotid surgery has to do with the frequent need for contralateral surgery. Should the first side be paralyzed, injury of the opposite side may result in an airway emergency, completely unexpected if the initial injury is undiagnosed. It is prudent to evaluate the larynx between operations. If the vocal fold is paralyzed, experience indicates that a delay of a few months is likely to restore mobility, and contralateral surgery will be safer.
Implantation of a vagal nerve stimulator for control of seizure disorders requires the placement of a coil-like electrode around the main trunk of the vagus in the neck, so it should be no surprise that vocal fold dysfunction is not rare in this population. Both the exact incidence and prognosis of vocal fold paralysis following placement of the vagal nerve stimulator remains to be established, but the most commonly reported side effect is hoarseness, occurring in as many as 35% of patients . Shaffer et al.  found that 2 of 10 patients recruited from among those who had undergone the procedure had immobile vocal folds, and 6 of 10 had electromyographic changes suggestive of denervation and/or recovery. In the experience of the author, 6 of 8 patients with vocal fold immobility following stimulator placement recovered spontaneously within 4 months of surgery. It is noteworthy that not all dysphonia in vagal nerve stimulator patients is related to surgical injury, as the electrical activity of the stimula tor itself causes vocal fold hypomobility and/or involuntary adduction during stimulation [29, 30]. As of this writing, the vagal nerve stimulator is undergoing federal review for treatment of drug-resistant depression. If approved, it could become a more significant source of vocal fold paralysis.
The recurrent nerve maybe injured during cri-copharyngeal myotomy near the cricothyroid joint as it enters the larynx. Newer endoscopic approaches to Zenker's diverticulum were initially thought to obviate this potential complication entirely, but this has not proved to be the case .
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