Bilateral Vocal Cord Paralysis Following Endotracheal Intubation

Abstract

\s=b\Bilateral vocal cord paralysis following endotracheal intubation is an uncommon cause of respiratory obstruction. We report one case, adding to ten previously identified. We dissected eight human cadaver larynges and noted the path of the anterior ramus of the recurrent laryngeal nerve. It appeared to be particularly vulnerable to compression injury as it passed between the arytenoid cartilage and the thyroid lamina. This point was confirmed by histologic sections of intubated larynges. (Arch Otolaryngol Head Neck Surg 1986;112:877-882) Bilateral vocal cord paralysis (BVCP) is an unusual complica¬ tion following endotracheal intuba¬ tion. The patient presents with acute onset of respiratory distress following extubation associated with stridor and tachypnea. These symptoms are rapidly alleviated on reintubation. Endotracheal intubation as the sole cause of vocal cord paralysis was first described in the 1950s.12 Review of the literature identified ten cases of BVCP in adults following intubation. The development of upper-airway (Dr Brandwein). obstruction after a short course of intubation with or without spontane¬ ous recovery, in addition to the physi¬ cal findings at the time of direct lar¬ yngoscopy, are the clinical features that can differentiate BVCP following intubation from other clinical causes of obstruction. In contradistinction to this rare clinical entity, unilateral vocal cord paralysis following recurrent laryn¬ geal nerve (RLN) injury occurs more frequently (42 cases in one series3). It may present as only transient hoarse¬ ness following surgery. A number of theories have been suggested to explain the phenomenon of RLN injury. Positioning the patient's head for surgery so that it is hyperextended and rotated was postu¬ lated to stretch the RLN and cause torsional injury that is reversible.2 Yamashita et al" described vocal cord paralysis as a direct result of a com¬ pression injury caused by the endotra¬ cheal tube cuff.We present a case of BVCP in which respiratory obstruction followed extu¬ bation. The significance of findings from human adult cadaver RLN dis¬ section in the development of this syndrome is discussed. REPORT OF A CASEA 70-year-old woman with a chief com¬ plaint of epigastric pain and weight loss was admitted for treatment of a gastric outlet obstruction. Her medical history included peptic ulcer disease, which was treated with cimetidine. Physical examina¬ tion showed a mildly obese woman with epigastric tenderness. Although no formal laryngeal examination was performed, the patient was not hoarse and the vocal cords appeared normal at the time of initial intubation.During the operation, general anesthesia was achieved by rapid sequence induction with fentanyl citrate, isoflurane, and nitrous oxide. Intubation was performed easily with a No. 7.5 polyethylene endotra¬ cheal tube, and the cuff was inflated with 8 cm3 of air. An antrectomy and selective bilateral vagotomy were performed with a total operative time of three hours. The patient was extubated in the recovery ...

Postoperative Bilateral Palsy of Terminal Laryngeal and Pharyngeal Branches of the Vagal Nerve

“…Several cases of bilateral vocal cord paralysis following endotracheal intubation or the use of laryngeal mask airways are reported and discussed [5,6]. Brandwein examined human cadaver larynges and found that the recurrent laryngeal nerve seemed to be vulnerable to compression between the arytenoid cartilage and the thyroid lamina.…”

Vocal Cord Paralysis Secondary to Impacted Esophageal Foreign Bodies in Young Children

“…Even short-term nontraumatic intubations have been rarely reported to cause unilateral or even bilateral paralysis. 8,9 It is well-known that endotracheal intubation can cause vocal cord paralysis. The proposed mechanism for intubation-related cord paralysis is entrapment of the anterior (adductor) ramus of the recurrent nerve 6 to 10 mm below the level of the cords among the thyroid lamina, the superiorly located arytenoid, and the inflated cuff of the endotracheal tube.…”

“…The proposed mechanism for intubation-related cord paralysis is entrapment of the anterior (adductor) ramus of the recurrent nerve 6 to 10 mm below the level of the cords among the thyroid lamina, the superiorly located arytenoid, and the inflated cuff of the endotracheal tube. 9 The effect of nitrous oxide diffusion into the cuff raising its pressure is also considered to be important. No pediatric cases (intubations sans cuffs) have ever been reported.…”

“…The explanation for the abductor paralysis (the median position of the cords) is that either there is variable innervation (occasionally the anterior-adductor-ramus has been found to innervate all the intrinsic muscles of the larynx 10 ) or the uninhibited action of the intact cricothyroid innervation via the superior laryngeal nerves results in the bilateral adduction. 9 The point is made that when the cuff of the endotracheal tube is located in the cricoid region, the circumferential ring of cartilage confers protection from compression injury to the nerves from the tube/cuff. In contrast to the proposed mechanism for intubation-related paralysis (described above), the bilateral abductor paralysis in case 2 was attributable to an esophageal foreign body just below the cricopharyngeus.…”

Vocal cord paralysis associated with difficult gastric tube insertion

“…12 Brandwein et al, described the immediate onset of symptoms of bilateral vocal cord paralysis induced by endotracheal tubes after extubation in 50% and within a few hours in all except one patient. 24 In the case of gastric tubes, the onset of symptoms, which all included hoarseness, was longer; usually occurring more than four days and up to 12 days after operation. ~.2 The reason for this difference could be that in the case of endotracheal tubes, because the mechanism of paralysis is presumably direct compression of the anterior ramus of the recurrent laryngeal nerve or a temporary and local disturbance of blood flow to the nerve, the time needed for the onset of symptoms is relatively short, while in the case of gastric tubes, the mechanism is thought to be erosion or ulceration of the posterior cricoid plate due to compression by the tube located between the cricoid cartilage and the cervical spine, followed by a diffuse inflammatory process leading to perichondrifts, anterior cricoid infection, posterior subglottic stenosis and vocal cord immobility, so a longer time is needed for hoarseness to develop.…”