Vocal cord (VC) palsy refers to the absence of VC motion due to injury to the vagus nerve or its branches, the superior laryngeal nerve (SLN) and/or the recurrent laryngeal nerve (RLN).
The SLN innervates the cricothyroid muscle (VC tensor)
The RLN innervates the posterior cricoarytenoid muscle (VC abductor) and the rest of the intrinsic laryngeal muscles (VC adductors).
Immobility of the VC refers to the absence of VC motion from any cause including disorders of the laryngeal joints.
Palsy of the VC may compromise important physiologic functions of the larynx: Breathing, swallowing, airway protection, and speech. Injury may:
Be unilateral or bilateral
Involve partial or complete transection
Result as a complication after head and neck surgery and has a potential for airway obstruction after extubation.
Require anesthesia care for phonosurgery
Epidemiology
Incidence
Post-thyroidectomy 1.62.9%; left VC affected twice as often as the right VC
Post-cardiovascular surgery: 2.3%
Prevalence
Increased with age >50 yrs, hypertension, diabetes mellitus (DM), and prolonged intubation
Morbidity
Dyspnea, dysphagia, ineffective cough, and recurrent aspiration
Psychological distress and professional issues related to voice impairment
Mortality
Rare, but can result from:
Complete airway obstruction secondary to unsuspected partial bilateral recurrent nerve injury after extubation from head and neck surgery
Pulmonary aspiration and recurrent aspiration pneumonias in bilateral VC palsy
Etiology/Risk Factors
Surgical trauma (44%)
Bilateral VC injury can occur after surgery involving thyroid, parathyroids, esophagus, and trachea
Left VC palsy can occur after mediastinal or cardiac surgery since the left RLN loops under the aortic arch before traversing up to the neck
Cancers (17%) include laryngeal tumors, chondromas/chondrosarcomas, and squamous cell carcinomas
Traumatic intubation or prolonged intubation (15%) leading to posterior subglottic stenosis
Neurologic causes (12%) include DM, amyotrophic lateral sclerosis, and myasthenia gravis
Inflammatory causes include Wegener's granulomatosis, amyloidosis, sarcoidosis, polychondritis, and gastroesophageal reflux diseases (GERD)
Idiopathic (12%)
Physiology/Pathophysiology
VC palsy can result from injury at three levels:
Centrally at the main trunks of the vagus nerve
Peripherally at its branches
Directly at the VCs themselves
Injury to SLN: The cricothyroid muscle is unable to tense the VCs, giving a weak and husky voice.
Injury to RLN: Abductors are more vulnerable to injury. Therefore, partial nerve damage may result in a selective abductor paralysis while a complete transection paralyzes both adductors and abductors.
Unilateral complete transection: Results in a paralyzed VC that lies midway between adduction and abduction, just lateral to the midline. Speech is not seriously affected because the normal VC compensates by moving toward the paralyzed VC
Unilateral partial transection: If the abductors are more severely paralyzed than the adductors, the affected VC lies in the midline, adducted position and can decreases the glottic opening
Bilateral complete transection: VCs are positioned midway between abduction and adduction. It is often erroneously believed to cause both vocal cords to meet at the midline and create complete airway obstruction: however, complete transection paralyzes both abductors and adductors. Breathing is still possible, however, the glottic opening is smaller than normal. This scenario is akin to administering succinylcholine; there is still an opening that allows for intubation
Bilateral partial transection: If the abductors are paralyzed but the adductors are spared, the adductors will bring the vocal cords to the midline and cause complete airway obstruction
Prevantative Measures
Avoid traumatic and prolonged intubation
Prevent RLN injuries during surgery, especially during thyroidectomy by identifying and preserving the nerve at its point of entry into the larynx, classically 0.51 cm below the inferior cornu of the thyroid cartilage
Use of the nerve-stimulator endotracheal tube (Xomed-Treace, Jacksonville, FL) can help detect the location of the RLN, especially in high risk situations:
Large distorting tumors
Re-excision thyroidectomy
Severe post-radiotherapy fibrosis of the neck
Pre-existing VC paralysis in patients undergoing bilateral paratracheal node dissection
Diagnosis⬆⬇
Diagnosis of potential VC palsy after head and neck surgery:
Ensure complete reversal of neuromuscular blockade to allow spontaneous ventilation at the conclusion of surgery
Extubate the patient while under deep inhalational anesthesia, followed by immediate insertion of a laryngeal mask airway
Use a fiberoptic bronchoscope to assess VC motion
If adequate VC motion is present during regular breathing, deep breathing, coughing, and phonation as the patient emerges, the patient can be extubated
If severe VC palsy is present, reintubate the patient for airway control and protection; administer IV steroids to decrease edema; consider a trial extubation after surgical edema has resolved; if repeated attempts at extubation fail, a tracheostomy should be performed
Diagnosis of pre-existing VC palsy as a co-morbid condition: By history, physical examination, and diagnostic procedures
History: Previous surgeries, intubations, and other causes of VC palsy
Ask about symptoms: Onset of voice changes, dyspnea, dysphagia
Physical examination: Assess the patient's voice and listen for breathy voice, hoarseness. Assess the patient's breathing; respirations may be stridorous
Examine the larynx by indirect mirror examination, direct and fiberoptic nasopharyngolaryngoscopy: Evaluate mucosa for scarring, subglottic stenosis, arytenoid mobility, VC asymmetry and motion
Videostrobolaryngoscopy:
Provides additional information in cases of VC abnormalities when asymmetric mucosal wave patterns are present
Uses pulses of light to study successive phases of VC activity
Evaluates range and symmetry of motion of both VCs throughout their vibratory cycle
Laryngeal electromyography (EMG): Analyzes the electrical motor unit of the cricothyroid and thyroarytenoid muscles to test the SLN and RLN, respectively
Distinguishes neuromuscular pathology from intrinsic VC and laryngeal joint pathology
Performed at one month post-injury (baseline) and at two months post-injury (follow-up), this test helps to determine prognosis by evaluating VC recovery status
Pulmonary function tests and flow-volume loops: Findings are consistent with a variable extrathoracic airway obstruction (during spontaneous ventilation)
Flattening of inspiratory loop
Normal expiratory loop
CT scan from skull base to mediastinum: Helps to assess the entire trajectory of the vagus and recurrent laryngeal nerves to detect pathology
MRI can be used in lieu of CT in pregnant patients, children, or patients with neurologic pathology
Differential Diagnosis
Cricoarytenoid joint ankylosis: Diagnosed by direct visualization during laryngoscopy and palpation of the suspected joint to rule out ankylosis causing VC immobility. Laryngeal EMG is also useful.
Experimental procedures: Nervemuscle transfer to the posterior cricoarytenoid muscle, electrical pacing
Completely non-functional larynx with life-threatening recurrent aspiration pneumonias: Perform total laryngectomy as a last resort
Follow-Up⬆⬇
Spontaneous recovery occurs in 55% of patients with bilateral VC palsy; 50% of these patients recover within 1 year after initial diagnosis
Closed Claims Data
VC paralysis accounts for 0.6% of total claims (25 out of 4,183 claims) from The ASA Closed Claims Project 1998
References⬆⬇
DeckerJ, DeckertL.Vocal cord dysfunction. Am Fam Physician. 2010;81(2):156159.
DralleH, SekullaC, LorenzK, et al.Intraoperative monitoring of the recurrent laryngeal nerve in thyroid surgery. World J Surg. 2008;32:13581366.
HillelAD, BenningerM, BlitzerA, et al.Evaluation and management of bilateral vocal cord immobility. Otolaryngol Head Neck Surg. 1999;121:760765.
JeannonJP, OrabiAA, BruchGA, et al.Diagnosis of recurrent laryngeal nerve palsy after thyroidectomy: A systematic review. Int J Clin Pract. 2009;63:624629.
RubinAD, SataloffRT.Vocal cord paresis and paralysis. Otolaryngol Clin North Am. 2007;40(5):11091131.
478.30 Paralysis of vocal cords or larynx, unspecified
478.31 Unilateral paralysis of vocal cords or larynx, partial
478.32 Unilateral paralysis of vocal cords or larynx, complete
478.33 Bilateral paralysis of vocal cords or larynx, partial
478.34 Bilateral paralysis of vocal cords or larynx, complete
ICD10
J38.00 Paralysis of vocal cords and larynx, unspecified
J38.01 Paralysis of vocal cords and larynx, unilateral
J38.02 Paralysis of vocal cords and larynx, bilateral
Clinical Pearls⬆⬇
Special anesthetic considerations in patients with pre-existing VC paralysis presenting for general anesthesia:
Patients with known VC palsy are at risk for recurrent aspiration pneumonias; elective surgery should be undertaken only after resolution
These patients should be intubated as atraumatically as possible.
In patients with normal airways, direct laryngoscopy allows the benefit of direct vision during passage of the endotracheal tube through the glottis.
In patients with difficult airways, fiberoptic laryngoscopy facilitates visualization of the VCs and trachea.
Beware, however, that endotracheal tube passage over a bronchoscope through the VCs is done blindly and may cause further trauma.
Be vigilant of the risk of injury to the affected VC during extubation; may cause respiratory obstruction or aspiration during emergence.
Special anesthetic considerations in patients presenting for VC medialization with monitored anesthetic care (MAC):
Procedure involves:
Creation of a window in the thyroid ala cartilage
Insertion of an implant in that window to medialize the affected VC
Adjustment of VC medialization performed under fiberoptic visualization of affected VC motion with patient vocalization on command
Fixation of implant in the optimal position
Anesthesia objectives:
The patient should be comfortable during the creation of the cartilage window.
The patient should be able to cooperate and phonate during the insertion and fixation portion of the procedure to help achieve optimal VC approximation.
Pharmacologic agents used:
Prior airway nebulization with 4% lidocaine to decrease laryngeal reflexes
Anticholinergics such as scopolamine or glycopyrrolate to help dry airway secretions
Corticosteroids such as dexamethasone to decrease VC edema
Antitussives such as codeine to decrease coughing during the procedure