May/June 2019

Recurrent Laryngeal Nerve Damage — Clinical Implications Following Cardiac Surgery
By Jennifer M. Pusins, CScD, CCC-SLP, BCS-S, IBCLC; Randi Melton; and Lily Darmon
Today’s Geriatric Medicine
Vol. 12 No. 3 P. 20

Injury to the recurrent laryngeal nerve (RLN) leading to vocal fold paralysis (VFP) following cardiac surgery has emerged in the literature as an independent risk factor for a number of serious adverse outcomes. Damage to the RLN can cause life-threatening complications, including pulmonary aspiration and obstruction of the airway. Postoperative dysphagia due to VFP is a known complication associated with cardiac surgery, and dysphagia is associated with increased rates of mortality and postsurgical morbidity. Injury to the RLN can also result in dysphonia, an alteration in acoustic qualities of the voice, which is not life threatening but can affect quality of life significantly. It’s imperative that speech-language pathologists working with patients who have undergone cardiac surgery are aware of the potential for postoperative laryngeal complications to promote early diagnosis and management, ensuring the highest quality of care is delivered.

The larynx is a complex, mucosa-covered collection of intricately organized cartilages, ligaments, and muscles. It’s composed of three large, unpaired cartilages (cricoid, thyroid, epiglottis), three pairs of smaller cartilages (arytenoids, corniculate, cuneiform), and multiple intrinsic muscles. It’s a dynamic, flexible, midline structure that connects the pharynx to the trachea and is involved in swallowing, breathing, and voice production.

The vagus nerve is very long, originating in the brain stem and extending down through the neck and into the chest and abdomen. Its functions contribute to the autonomic nervous system and supply innervation to the heart, major blood vessels, airways, lungs, esophagus, stomach, and intestines. The larynx is innervated by sympathetic fibers, the superior laryngeal nerve (SLN), and the RLN. The SLN branches off the vagus nerve and has an internal and external branch. The internal branch of the SLN provides sensory and autonomic innervation to the mucosa superior to the glottis, including sensory innervation to the superior portion of the laryngeal cavity, incorporating the epiglottis and superior surface of the vocal folds. The external branch of the SLN supplies motor innervation and visceral efferent to the cricothyroid muscle.

The RLN is also a branch of the vagus nerve. The left vagus nerve enters the thoracic cavity and turns into the left RLN branch, which winds around the aorta posterior to the ligamentum arteriosum. The left RLN is longer than the right and has a more complex route, making it more prone to compressive injury between the left pulmonary artery and the aorta.1,2

The right vagus nerve crosses the subclavian artery anteriorly and gives off the right RLN, which loops around the subclavian artery to reach the tracheoesophageal groove. The nerves then pass posterior to the cricothyroid joint as they enter the larynx at this level through fibers of the inferior constrictor muscles of the pharynx and ultimately become the inferior laryngeal nerve. The right RLN is shorter and reenters the neck and travels upwards to the groove between the trachea and esophagus, reaching the groove at the level of the thyroid cartilage. The course of the right RLN around the subclavian artery makes it vulnerable to stretch-related injury with neurapraxic damage.2,3

The RLN also carries general visceral sensory fibers from the region inferior to the glottis and sends branches to the inferior constrictor and cricopharyngeus muscles prior to entering the larynx. Additionally, the RLN carries afferent fibers from the muscles of the cervical esophagus, which have been shown to be crucial in initiation of the esophageal phase of swallowing.4,5 The RLN supplies sensory innervation to the laryngeal cavity below the level of the vocal folds and motor innervation to all laryngeal muscles except the cricothyroid. The inferior branch of the RLN innervates all intrinsic muscles of the larynx excluding the cricothyroid muscle, which is innervated by the SLN. These intrinsic muscles function in phonation; are paired bilaterally, with the exception of the transverse arytenoid muscle; and include the oblique arytenoid, transverse arytenoid, aryepiglottic, thyroepiglottic, posterior cricoarytenoid, lateral cricoarytenoid, thyroarytenoid, vocalis, and cricothyroid muscles. The vocal folds comprise the thyroarytenoid muscle wrapped in a thin layer of mucosa that functions with all other intrinsic muscles to control voice production. The posterior cricoarytenoid muscles abduct, or open, the vocal folds, and the lateral cricoarytenoid muscles adduct, or close, the vocal folds.

RLN Injury Following Cardiac Surgery
Unilateral VFP occurs when one vocal fold is paralyzed in the paramedian or lateral position with significantly limited movement. Surgical procedures are one of the most common cause of VFP, with surgical injury being responsible for approximately 40% of unilateral VFP and 50% of bilateral VFP.6 The reported incidence of VFP is 2% to 32% following cardiac surgical procedures.7,8 The RLN can be affected in various situations due to its anatomical relationship with several important structures. Injury to the RLN would result in paralysis in all intrinsic muscles of the larynx, with the exception of the cricothyroid muscle, resulting in VFP. The RLN has the ability to regenerate and reinnervate muscles after transection injury, although the functional recovery is typically poor.

The most common mechanisms of RLN injury include unintentional maneuvers leading to excessive traction and stretching of the nerve; mechanical damage resulting from compression, contusion, or external pressure; effect of high temperatures in the vicinity of the nerve producing thermal damage; and ischemia, clamping, or transection.9

RLN palsy ranks among the leading reasons for medicolegal litigation of surgeons due to the significant impact on quality of life. Cardiac operations are common causes of RLN palsy, especially aortic aneurysms and ductus arteriosus surgery.10

Clinical Implications: Voice
Voice control is a sophisticated physiology controlled by the vagus nerve and RLN, which both arise directly from the brain rather than segmentally from the spinal cord. RLN injury resulting in unilateral VFP is a well-documented complication of cardiac surgery, with an incidence raging from 0.67% to 23% for all types of thoracic cardiovascular procedures.11-15

Several mechanisms of RLN injury have been suggested, including the following11:

• central venous catheterization by direct trauma from the puncture site or secondary to thrombosis, fibrosis, or hematoma formation;

• traction on the esophagus due to unnatural position of head and neck during surgery;

• direct vocal fold damage from traumatic endotracheal intubation;

• trauma by compression of the RLN or its anterior branch at the tracheoesophageal groove by an inappropriately sized endotracheal tube cuff;

• faulty insertion of a nasogastric tube and/or ulceration and infection of the postcricoid areas with resultant vocal fold abduction dysfunction;

• median sternotomy and/or sternal traction pulling laterally on both subclavian arteries;

• direct manipulation and retraction of the heart during open-heart procedures; and

• hypothermic injury with ice/slush collecting the pleural cavity in close proximity to the left RLN.

Associated risk factors include the following11,16:

• Implantable ventricular assist device (VAD) surgery has been reported to be a significant independent risk factor for VFP.

• Direct manipulation and retraction of the heart during VAD insertion may also cause RLN injuries.

• Cardiovascular instability during the perioperative period may result in low perfusion and ischemia in laryngeal membrane producing edema and inflammation.

• Endotracheal tube cuff overinflation can cause physical trauma to the laryngeal membrane.

• VFP is associated with aortic surgery with a higher incidence with para-aortic procedures and aortic procedures extending to the distal arch.

• There is a significantly higher risk of VFP following thoracic aortic surgery with brachiocephalic artery reconstruction.

• Prolonged intubation period is associated with undesirable outcomes.

• Type 2 diabetes mellitus can be a factor.

Signs and Symptoms
Injury to the SLN after cardiac surgery can lead to vocal fold and soft palate paralysis.17 Phonatory deficits are characterized by dysphonia, hoarseness, breathy vocal quality, shortness of breath, inefficient throat clearing/cough, stridor, vocal fatigue, loss of range, reduced intensity, respiratory insufficiency, and airway obstruction.16 Hoarseness with vocal fold dysfunction after cardiovascular intervention has a reported incidence of 10.15%, commonly associated with stridor (49.45%) and left RLN palsy, which occurs more frequently than does right (70% vs 30%).18 Voice deficits following injury to the RLN can affect the patient’s quality of life, resulting in reduced social interaction, decreased self-perception, increased anxiety, and worsened depression, and can adversely affect employment.19

Potential Treatment Options
There are two categories of treatment options for patients with RLN damage: voice therapy and surgery. Voice therapy treatment options include strengthening the intrinsic muscles of the larynx, including phonating while pushing-pulling, hard glottal attacks, and vocal function exercises. It’s important to note that these exercises must be done with caution and under supervision, as they may have adverse medical implications for certain populations.

The aim of laryngeal surgery for VFP is to close the glottic gap and restore the laryngeal valve. Vocal fold medialization techniques, such as injection medialization and thyroplasty, aim to restore the laryngo-protective mechanism by closing the glottic gap.20 The morbidity risks associated with VFP support the surgical treatment of unilateral VFP.20,21 It’s important, however, to incorporate voice therapy treatments due to the compensatory nature of the healthy vocal fold.1 Surgical treatment options include the following21:

• medialization thyroplasty;
• injection laryngoplasty;
• arytenoid adduction; and
• laryngeal reinnervation.

Clinical Implications: Swallowing
Swallowing is an essential action for alimentation and protection of the upper respiratory tract. A main cause of death in the elderly population is aspiration pneumonia caused by impaired swallow function, which is called dysphagia.22,23 Damage to the RLN results in increased incidence of reduced airway protection during the swallow, leading to dysphagia and risk of aspiration pneumonia.24 Sensory feedback from the larynx, carried by the vagus nerve, is essential for the appropriate swallow motor pattern to be generated by the central pattern generator in the brainstem. Connections between the sensory fibers of the RLN, the motor neurons of the RLN, and the motor nuclei of the hypoglossal nerve are vital to the integrity of swallow physiology safety.25

Research has reported an incidence of postoperative dysphagia to be between 44% to 87%, with an incidence of aspiration pneumonia reported in 16% of patients following cardiac surgery.26 The development of pneumonia following cardiac surgery is the leading cause of mortality, with a reported incidence of 9.8% in elderly patients.27,28 It’s generally accepted that the risk of aspiration is increased in patients with VFP directly correlated with the degree of impaired airway protection and probability of aspiration.29

RLN damage has been found to lead to a significant, sustained increase in the number of swallows that result in aspiration. RLN lesions can lead to impairments in the esophageal stage of swallowing, and the degree of impairment is correlated with aspiration severity.25 The reported frequency of aspiration in patients with VFP ranges from 38% to 53% depending on etiology.29 An individual with a diagnosis of VFP has more than double the odds of aspirating as does someone without VFP.30

Several risk factors for postoperative dysphagia and/or aspiration pneumonia have been reported, including the following26,28,31:

• advanced age;
• prolonged intubation;
• pre- and postoperative cerebral vascular disorders;
• use of transesophageal echocardiography;
• reduced muscular reserve as a result of the age of the patient or the critical stage post surgery;
• lower body mass index;
• preoperative congestive heart failure;
• anemia; and
• longer operation time.

Signs and Symptoms
Patients with unilateral VFP typically exhibit ipsilateral VFP, supraglottic laryngeal and pharyngeal abnormalities with reduced laryngeal elevation, weak pharyngeal stripping wave, and pharyngeal retention, all of which increase the risk of aspiration.30 Patients with unilateral VFP and dysphagia may present with alteration of bolus transit through the upper esophageal sphincter and have limited adaptation in swallow timing related to increases in bolus volume.32 The presence of a weakened cough may contribute to an increased risk of aspiration pneumonia due to inability to clear aspirated material.

Potential Treatment Options
The primary goals of dysphagia intervention are to safely support adequate nutrition/hydration and help patients return to safe and efficient oral intake, determine the optimum methods/techniques to maximize swallow safety and efficiency, minimize the risk of pulmonary complications, reduce patient and caregiver burden, maximize the patient’s quality of life, and develop treatment plans to improve safety and efficiency of the swallow. Treatment options for dysphagia consist of medical, surgical, and behavioral interventions.

Medical interventions include pharmacological management and use of nonsurgical alternative means of nutrition (ie, tube feeding). Surgical interventions are available and may improve glottal closure, increase airway protection, and/or improve opening of pharyngoesophageal segment. Behavioral treatments can be rehabilitative in nature, aiming to restore normal swallow function using techniques such as exercises, which are designed to alter swallow biomechanics by improving underlying physiological function. The intent of these exercises is to improve function rather than compensate for an underlying deficit. Compensatory techniques alter swallow function when used but do not result in a lasting functional change or improvement in physiology when the technique is not used. Certain techniques may be used for both compensatory and rehabilitative purposes. Environmental strategies may include modifications to the texture of food to allow for safe, efficient oral intake. This may include changing the viscosity or thickness of liquids and/or modifying the texture/consistency of solid foods.

— Jennifer M. Pusins, CScD, CCC-SLP, BCS-S, IBCLC, is an assistant professor and clinical supervisor at Florida’s Nova Southeastern University. Pusins is a board-certified specialist in swallowing and swallowing disorders and her area of clinical expertise is in the assessment and management of dysphagia across the life span. She’s presented at the state, national, and international levels on various topics related to dysphagia.

— Randi Melton is a graduate student at Nova Southeastern University in the Master of Science in Speech-Language Pathology program. She has a specific interest in dysphagia and has worked with patients with dysphagia during her clinical practicums.

— Lily Darmon is a graduate student clinician pursuing a Master of Science in Speech-Language Pathology at Nova Southeastern University. She received her BA in Exceptional Student Education with an Endorsement in Teaching English as a Second Language at Florida Atlantic University. She has clinical experience working with dysphagia and strong desire to further her knowledge and clinical practice in this area.

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