Recurrent Laryngeal Nerve Damage — Clinical Implications Following Cardiac Surgery
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
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
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
Potential Treatment Options
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;
Clinical Implications: Swallowing
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;
Signs and Symptoms
Potential Treatment Options
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.
2. Romagnoli E, Nasso G, Angeloni G, et al. Cardiovocal syndrome after transradial cardiac catheterization: an unusual complication. Int J Cardiol. 2008;124(3):e39-e41.
3. Weisberg NK, Spengler DM, Netterville JL. Stretch-induced nerve injury as a cause of paralysis secondary to the anterior cervical approach. Otolaryngol Head Neck Surg. 1997;116(3):317-326.
4. Wank M, Neuhuber WL. Local differences in vagal afferent innervation of the rat esophagus are reflected by neurochemical differences at the level of the sensory ganglia and by different brainstem projections. J Comp Neurol. 2001;435(1):41-59.
5. Lang IM, Medda BK, Babaei A, Shaker R. Role of peripheral reflexes in initiation of the esophageal phase of swallowing. Am J Physiol Gastrointest Liver Physiol. 2014;306(8):G728-G737.
6. Özbal Koç AE, Türkoğlu SB, Erol O, Erbek S. Vocal cord paralysis: what matters between idiopathic and non-idiopathic cases? Kulak Burun Bogaz Ihtis Derg. 2016;26(4):228-233.
7. Shafei H, el-Kholy A, Azmy S, Ebrahim M, al-Ebrahim K. Vocal cord dysfunction after cardiac surgery: an overlooked complication. Eur J Cardiothorac Surg. 1997;11(3):564-566.
8. Ishimoto S-I, Ito K, Toyama M, et al. Vocal cord paralysis after surgery for thoracic aortic aneurysm. Chest. 2002;121(6):1911-1915.
9. Konturek A, Barczyński M. The evolution and progress of mechanism and prevention of recurrent laryngeal nerve injury. Ann Thyroid. 2018;3:32.
10. Amer K. Anatomy of the thoracic recurrent laryngeal nerves from a surgeon’s perspective. Anat Physiol. 2017;7(4):272.
11. Hamdan AL, Moukarbel RV, Farhat F, Obeid M. Vocal cord paralysis after open-heart surgery. Eur J Cardiothorac Surg. 2002;21(4):671-674.
12. Joo D, Duarte VM, Ghadiali MT, Chhetri DK. Recovery of vocal fold paralysis after cardiovascular surgery. Laryngoscope. 2009;119(7):1435-1438.
13. Dimarakis I, Protopapas AD. Vocal cord palsy as a complication of adult cardiac surgery: surgical correlations and analysis. Eur J Cardiothorac Surg. 2004;26(4):773-775.
14. Itagaki T, Kikura M, Sato S. Incidence and risk factors of postoperative vocal cord paralysis in 987 patients after cardiovascular surgery. Ann Thorac Surg. 2007;83(6):2147-2152.
15. Rosenthal LH, Benninger MS, Deeb RH. Vocal fold immobility: a longitudinal analysis of etiology over 20 years. Laryngoscope. 2007;117(10):1864-1870.
16. Taenaka H, Shibata SC, Okitsu K, et al. Perioperative factors related to the severity of vocal cord paralysis after thoracic cardiovascular surgery: a retrospective review. Eur J Anaesthesiol. 2017;34(7):425-431.
17. Gavazzi A, de Rino F, Boveri MC, Picozzi A, Franceschi M. Prevalence of peripheral nervous system complications after major heart surgery. Neurol Sci. 2016;37(2):205-209.
18. Raut MS, Maheshwari A, Joshi R, et al. Vocal cord paralysis after cardiac surgery and interventions: a review of possible etiologies. J Cardiothorac Vasc Anesth. 2016;30(6):1661-1667.
19. Francis DO, McKiever ME, Garrett CG, Jacobson B, Penson DF. Assessment of patient experience with unilateral vocal fold immobility: a preliminary study. J Voice. 2014;28(5):636-643.
20. Chandran S. Surgical management of vocal fold paralysis and cricopharyngeal dysfunction as a cause of aspiration. Dysphagia. 2014;23(3):106-115.
21. Rohde SL, Wright CT, Muckala JC, Wiggleton J, Rousseau B, Netterville JL. Voice quality after recurrent laryngeal nerve resection and immediate reconstruction. Otolaryngol Head Neck Surg. 2012;147(4):733-736.
22. Siu J, Tam S, Fung K. A comparison of outcomes in interventions for unilateral vocal fold paralysis: a systematic review. Laryngoscope. 2016;126(7):1616-1624.
23. Teramoto S, Yoshida K, Hizawa N. Update on the pathogenesis and management of pneumonia in the elderly — roles of aspiration pneumonia. Respir Investig. 2015;53(5):178-184.
24. Maarel-Wierink CD, Vanobbergen JN, Bronkhorst EM, Schols JM, de Baat C. Meta-analysis of dysphagia and aspiration pneumonia in frail elders. J Dent Res. 2011;90(12):1398-1404.
25. Gould FD, Ohlemacher J, Lammers AR, et al. Central nervous system integration of sensorimotor signals in oral and pharyngeal structures: oropharyngeal kinematics response to recurrent laryngeal nerve lesion. J Appl Physiol (1985). 2016;120(5):495-502.
26. Nguyen S, Zhu A, Toppen, W, et al. Dysphagia after cardiac operations is associated with increased length of stay and costs. Am Surg. 2016;82(10):890-893.
27. Zhou XD, Dong WH, Zhao CH, et al. Risk scores for predicting dysphagia in critically ill patients after cardiac surgery. BMC Anesthesiol. 2019;19(1):7.
28. Miyata E, Tanaka A, Emori H, Taruya A, Miyai S, Sakagoshi N. Incidence and risk factors for aspiration pneumonia after cardiovascular surgery in elderly patients. Gen Thorac Cardiovasc Surg. 2017;65(2):96-101.
29. Heitmiller RF, Tseng E, Jones B. Prevalence of aspiration and laryngeal penetration in patients with unilateral vocal fold motion impairment. Dysphagia. 2000;15(4):184-187.
30. Leder SB, Suiter DM, Duffey D, Judson BL. Vocal fold immobility and aspiration status: a direct replication study. Dysphagia. 2012;27(2):265-270.
31. Hales P, Mossey-Gaston C. Surgery for lung cancer and the consequences for the swallow. Perspect ASHA Spec Interest Groups. 2016;1(13):162-168.
32. Jain S, Self WH, Wunderink RG, et al. Community-acquired pneumonia requiring hospitalization among U.S. adults. N Engl J Med. 2015;373(5):415-427.