Rln injury

Rln injury DEFAULT

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.

 

References
1. Hebl JR, Rose SH, Narr BJ, Rorie DK. Postoperative left vocal cord dysfunction caused by Ortner’s cardiovocal syndrome. Anesth Analg. 2001;92(4):1071-1072.

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.

Sours: https://www.todaysgeriatricmedicine.com/archive/MJ19p20.shtml

Recovery of laryngeal function after intraoperative injury to the recurrent laryngeal nerve

Review Article

Per Mattsson, Jonas Hydman, Mikael Svensson


Abstract: Loss of function in the recurrent laryngeal nerve (RLN) during thyroid/parathyroid surgery, despite a macroscopically intact nerve, is a challenge which highlights the sensitivity and complexity of laryngeal innervation. Furthermore, the uncertain prognosis stresses a lack of capability to diagnose the reason behind the impaired function. There is a great deal of literature considering risk factors, surgical technique and mechanisms outside the nerve affecting the incidence of RLN paresis during surgery. To be able to prognosticate recovery in cases of laryngeal dysfunction and voice changes after thyroid surgery, the surgeon would first need to define the presence, location, and type of laryngeal nerve injury. There is little data describing the events within the nerve and the neurobiological reasons for the impaired function related to potential recovery and prognosis. In addition, very little data has been presented in order to clarify any differences between the transient and permanent injury of the RLN. This review aims, from an anatomical and neurobiological perspective, to provide an update on the current understandings of surgically-induced injury to the laryngeal nerves.

Keywords: Regeneration; thyroid surgery; nerve injury; vocal fold paresis; laryngeal EMG


Submitted Dec 11, 2014. Accepted for publication Jan 26, 2015.

doi: 10.3978/j.issn.2227-684X.2015.01.10


Recurrent laryngeal nerve (RLN) injury and voice alteration after thyroid surgery

Thyroid and parathyroid surgery is associated with a risk of traumatic injury to the superior and inferior RLN. Injury to the RLN results in acute paralysis of the vocal fold on the affected side, which leads to dysphonia, dysphagia, and aspiration problems. The clinical signs may vary, however, depending on the position of the paralyzed vocal fold relative to the midline and the degree of glottic insufficiency. A significant number of patients may even present as asymptomatic, and vocal fold mobility needs to be examined before and after surgery to detect an iatrogenic injury to the RLN (1-4). The reported risk for RLN injury after thyroid/parathyroid surgery varies from center to center. In the literature, injury rates of up to 38% can be found (5). It is difficult to compare these numbers, since the rate of detected RLN injury is dependent on how close to surgery the laryngoscopic examination is performed. In a large, retrospective study of patients that underwent total thyroidectomy due to malignant disease, the risk of postoperative vocal fold paresis was found to be 9.5% (6), of which 22% became permanent with resulting demand for secondary surgical intervention of the paralyzed vocal fold.

Subjective voice deficits are common after thyroid surgery (7). Subjective and objective voice alterations (8,9) are common after total thyroidectomy and most of them are independent of injury to the RLN or the superior laryngeal nerve (SLN) (10-12). These voice changes are believed to be caused by temporary disturbances in the laryngeal mechanical framework or extralaryngeal scarring, and they usually resolve to subclinical levels within weeks or months after the operation (9,13,14). Dividing the sternothyroid muscle has been shown not to affect voice outcome in a significant way (15). Even though the RLN is the most important provider of laryngeal motor innervation, injury to the external branch of the SLN is also believed to cause significant voice changes, such as reduction in the fundamental frequency range, reduction in the highest obtainable fundamental frequency and vibratory phase asymmetry in the vocal folds (16-19). The external branch of the SLN has therefore gained increased attention among thyroid surgeons, and it is recommended that it should be preserved as well as the RLN during thyroid surgery (20).

In most cases of postoperative vocal fold paresis, the RLN is macroscopically intact and the injury is located within the peripheral nerve. To be able to prognosticate recovery, the surgeon would need to define the presence, location, and type of the nerve injury. However, very little data has been presented aimed at clarifying the differences between the transient and permanent injury of the RLN. This review aims to provide, from an anatomical and neurobiological perspective, an update on the current understanding of surgically-induced injury to the laryngeal nerves.


The laryngeal nerves

The larynx is innervated by two branches of the vagus nerve, the RLN, and the SLN. Both nerves carry motor, sensory, and autonomic (parasympathetic) fibers to the larynx (21). The lower motor neurons of the special efferent system controlling the intrinsic laryngeal muscles are located in the nucleus ambiguus in the lower brainstem, in a fairly well-studied somatotopical arrangement (22-30). The sensory neurons are located in the nodose ganglion and the parasympathetic cell bodies are located in the dorsal motor nucleus of the vagus in the brainstem. The mechanically complex laryngeal functions (airway protection reflexes, phonation, swallowing) require a rich and detailed neural control, projected through the RLN and SLN.

The RLN can be regarded as the most important motor nerve supply to the larynx, as it innervates 4 out of 5 intrinsic laryngeal muscles. It also has projections to the esophagus and trachea (23). The RLN divides into an anterior and posterior branch. The branching point is located either inside the larynx, or, as in roughly one third of cases, before the nerve entering point (31). The posterior branch projects superiorly to form the anastomosis of Galen with the internal branch of the SLN—this branch is probably sensory in nature (32). The anterior branch carries motor fibers (33,34) to the posterior thyroarytenoid muscle, lateral cricoarytenoid muscle and, finally, to the thyroarytenoid muscle (35-37). Within the larynx, the RLN and SLN break up into a plexus-like branching system (38), with several connections between the RLN and SLN (37). The exact functions of these small nerve branches are not fully known, but it has been demonstrated in animal experimental models that the intrinsic laryngeal muscles receive dual innervation from both the RLN and SLN (39,40).

The SLN originates from the inferior vagal ganglion at the C2 level in the neck (41). It divides into a larger, internal branch which enters the larynx through the thyrohyoid membrane (carrying sensory fibers down to the level of the glottis) and a smaller, external, branch which passes deep to the superior thyroid artery to innervate the cricothyroid muscle responsible for vocal fold lengthening and tension, important for high voice pitch (42). The external branch of the SLN continues through the cricothyroid muscle to reach the anterior glottis and the thyroarytenoid muscle. This branch, called “the human communicating nerve” (43), or “the cricothyroid connection branch” (44) thus represents an additional motor supply to the intrinsic laryngeal muscles other than the RLN, which may be important following RLN injury and reinnervation. This anatomy enables intraoperative monitoring of the external branch of the SLN through routine surface electrodes in the intubation tube (45), although the exact laryngological function of this nerve branch is not known (17).


Neurapraxia versus axonotmesis

From a clinical perspective, it is important to make the distinction between nerve conduction block, “neurapraxia”, and the more severe “axonotmesis”, which means presence of axonal injury (Figure 1). These classifications were first made by Seddon in 1942 (46) and later modified by Sunderland in 1951 (47). Surgically-induced nerve injuries seldom include complete transection of the nerve, but rather intraneural damage inside a macroscopically intact nerve due to pressure, crush or heating from adjacent use of cautery. Neurapraxia is the mildest form of injury, affecting the surrounding Schwann cells, but respecting the integrity of the axon (Figure 1A). The result is a conduction block lasting typically about 6-8 weeks followed by a complete return of function, when the Schwann cells have been repaired (48). This seems to be the case also for RLN injury (49). Following axonotmesis, there is a varying degree of axonal injury (Figure 1B), which could lead to neuronal death or dysfunctional reinnervation of the target cells. Axonotmesis, therefore, is associated with a poorer and more unpredictable outcome for functional restitution.

Figure 1 Schematic drawing of the RLN with intralaryngeal branches to IA, LCA and TA. The axon is surrounded by Schwann cells responsible for electrical propagation. Neurapraxia (A) with intact axonal integrity, facing spontaneous recovery. Axonotmesis (B) with disruption of axon and ongoing regeneration. RLN, recurrent laryngeal nerve; IA, interarytenoid muscle; LCA, lateral cricoarytenoid muscle; TA, thyroarytenoid muscle; LB, ligament of Berry; GA, anastomosis of Galen.


Neurobiology behind impaired function

The motor neuron terminates at the neuromuscular junction, the motor end plate. The neuron is the secondary neuron and is part of the peripheral nervous system (PNS), as opposed to the primary motor neuron [central nervous system (CNS)], which runs from the cortex to terminate on the secondary neurons. The myelin around the axons in the CNS comes from oligodendrocytes. The CNS myelin contains several factors which are inhibitory to axonal growth and regeneration, which is one of the major problems after CNS injury, such as stroke or spinal cord injury (50). In the PNS, on the other hand, the myelin around the axons is derived from the Schwann cell. This milieu is attractive for axonal growth, which is why the peripheral nerve injury is usually associated with regeneration after axonal disruption (51-55). Following a peripheral nerve injury, which involves peripheral axon disruption, the distal part (which is disconnected from the neuron) will be neurophysiologically active until it degenerates (56) [Wallerian degeneration (57)] which, under normal conditions, will take approximately one week. Thus, a complete injury to the RLN which separates the nerve into two different parts, will give a negative signal using intraoperative nerve monitoring (IONM) and the distal part a positive signal in the thyroarytenoid muscle for several days. Re-exploring the distal end of the RLN at our institution for nerve re-construction confirms the positive signal for up to five days after complete injury after thyroid surgery (unpublished observation). After axonal injury within the macroscopically intact RLN, the distal axon also degenerates and, to achieve any functional recovery, the axon has to regenerate. In the literature, there has been considerable speculation concerning the reasons for the poor (or absent) functional recovery seen after injury to the RLN despite the fact that the nerve looks macroscopically intact during surgery. One factor associated with the insufficient recovery is a potential misguidance of RLN axons during regeneration, leading to non-functional reinnervation of laryngeal muscles. There are, however, studies that show that the degree of accurate innervation is very high after crush injury to the peripheral nerve (90%) (58) since the axon is guided by intact mechanical factors of the intact endoneural tubes (59). This may reduce the impact of the misguidance as a negative factor in the injured intact RLN.

The axotomy induces a retrograde injury signal to the neuron in the brainstem which is attacked by microglia and also surrounded by a profound astroglial reaction (60-62). The neuron downregulates its production of transmitter substances and turns the gene transcription to regeneration and re-innervation. The neuron is exposed to stress and is dependent on a continuous inflow of growth factors from the periphery (54). Motor neurons are more likely to die in response to peripheral axotomy the closer the axotomy is to the neuronal soma in the brainstem or spinal cord. The more of the peripheral nerve which is in contact with the neuron soma, the more trophic support of growth factors is delivered to the neuron. The addition of growth factors radically improves the prognosis for the axotomized neuron (63-66). In addition, there are many experiments to support that distal peripheral nerve injury is associated with no or limited nerve cell death, including injury to the RLN (67).

The distal axotomy in the intact RLN also causes a synaptic displacement from the secondary motor neuron in the nucleus ambiguus, which then loses contact with higher cortical centers (68). These synapses from cortical neurons re-appear on the secondary motor neurons as the neurons manage to regenerate and re-establish contact with the target organ (muscle). The proceeding adaptation to the new neural circuits is referred to as plasticity of the nervous system. Thus, the macroscopically intact but injured RLN will recover spontaneously if there is only a conduction block caused by an impairment of electrical propagation due to Schwann cell affection. If there is a component of axonal injury within the nerve, the axon will not only have to re-innervate the laryngeal muscles, but the neuron in the brainstem will need a re-connection with cortical neurons by re-establishment of their synapses onto the secondary neuron in the brainstem.


Intraoperative nerve monitoring (IONM)

IONM of the RLN is performed by stimulating the peripheral nerve directly with an electrical current, with subsequent recording of muscle depolarization of the thyroarytenoid muscle. When a peripheral nerve is directly stimulated at supramaximal intensity, the result is depolarization of all axons and activation of all motor units projecting through the nerve, which leads to acetylcholine-mediated depolarization of muscle fibers. The intramuscular shift in electrical potential (voltage) can be recorded as a compound muscle action potential (CMAP), representing the sum of all motor unit activity. During IONM, the presence and the amplitude of the CMAP is utilized as an indirect measurement of motor nerve function during the surgery. Originally, RLN monitoring was made through needle electrodes inserted into the intrinsic laryngeal muscles. In modern clinical routine, thyroarytenoid depolarization is recorded through surface electrodes on the ventilation tube (69).

Manipulation of the surgical field may affect the RLN by traction, heating, entrapment or squeezing (crush injury), which leads to absence or reduced amplitude of the recorded CMAP following vagal stimulation. The neurobiological explanation for reduced CMAP amplitude is simply that a lower number of axons are transmitting the electrical signal, which means less depolarization of the monitored muscle. Provided that the vagal stimulation is performed in the same way [consistent with continuous monitoring (70)], the site of injury could be anywhere along the nerve, distal to the site of stimulation. When the signal is lost during surgery, it is not possible to use IONM to diagnose the type of nerve injury (axonotmesis or neurapraxia), it only tells us that there is a discontinuity of the electrical propagation within the nerve.

In order to categorize and group injuries to the RLN using IONM, one reported way is to define the injury to the RLN and loss of signal (LOS) from the vagal nerve as segmental (type 1) or global (type 2) (69,71). Looking at the basic neurobiology of the nerve, a LOS could originate from an injury anywhere from the stimulus (vagal nerve) to the neuromuscular endplate, including the muscle. The distal part of the nerve is excitable for several days after injury even after nerve transection injury (48), which makes it possible for the surgeon to pin-point the exact location of the nerve injury, by using the stimulation probe along the course of the peripheral nerve. A neurobiological explanation for the “global” (type 2) RLN injury could be that the location of the nerve injury is located distal to the nerve entry point under the inferior constrictor muscle, not affecting the whole neuron (i.e., a milder form of injury). From this perspective, type 1 and 2 injuries describe if the RLN conduction block is proximal or distal to the RLN/cricothyroid border (Figure 2).

Figure 2 The RLN and the NEP under the IC. NEP may serve as an anatomical landmark in the classification of loss of vagal signal during thyroid surgery, e.g., lesion proximal to NEP (when there is a defined injury segment) or lesion distal to NEP (silent nerve to the NEP). RLN, recurrent laryngeal nerve; NEP, nerve entry point; IC, inferior constrictor muscle; TG, thyroid gland; SLNi, superior laryngeal nerve internal branch; GA, anastomosis of Galen; LB, ligament of Berry.


Laryngeal EMG

Postoperative electrodiagnostic methods can be used to determine the presence and type of nerve injury, as well as to characterize the ongoing or completed reinnervation processes. Laryngeal electromyography (LEMG) was first introduced more than sixty years ago, and has evolved (72) into a valuable tool for laryngologists in diagnosing neurolaryngological disorders. It has been pointed out that LEMG is primarily a qualitative method (73) (presence of denervation potentials, degree of motor unit recruitment), which makes it a subjective test depending on the examiner and the technical settings. But LEMG has nevertheless been shown to have high positive predictive value in predicting the long-term outcome of patients with a poor prognosis (74-77) and it is used widely to predict recovery regardless of the etiology behind the vocal fold paresis. Patients with pathological electromyographic findings at least two months after the paresis are most likely to need laryngeal framework surgery (76). In the case of postoperative vocal fold paresis after thyroid/parathyroid surgery, the prognostic information obtained from LEMG can be helpful to identify those cases where future interventions are necessary, which could mean surgical or pharmacological reinnervation therapies, or vocal fold medialization procedures. For patients with only a conduction block (neurapraxia) of the RLN, vocal fold movement is most likely to return. When using LEMG to obtain this information after thyroid surgery, it is important to take into consideration the timing of the examination. Denervation activity (indicating axonotmesis and poor prognosis) typically appears at three weeks after the RLN injury (48), and lasts until reinnervation is complete. Reinnervation of the intrinsic laryngeal muscles can be expected to take place rather promptly, given the high regenerative capacity of the RLN (78), together with collateral reinnervation by adjacent, intact nerve fibers (40). The optimal time window for postoperative LEMG seems to be 2-4 weeks after the nerve injury (49). Interpretation and analysis of electrophysiological data requires the expertise of a trained neurologist or clinical neurophysiologist, while insertion of the needle electrodes into the appropriate intrinsic laryngeal muscles is best performed by an ENT specialist. LEMG thus requires the cooperation and coordination of different clinical resources. A consensus paper for LEMG guidelines in the areas of indications, technical considerations, implementations and data interpretation was published by Volk et al. (79) in 2012.


Regeneration promotion

A mixed injury of demyelination (neurapraxia) and axonotmesis within the macroscopically intact RLN has a worse prognosis than demyelination alone, because of the need for regeneration and reinnervation of the target. Reinnervation of the intrinsic laryngeal muscles following axonotmesis is considered problematic (80), due to misguided, unorderly regeneration and perhaps also collateral reinnervation originating from adjacent, intact nerve fibers (40). Pathological reinnervation leads to a change in the somatotopic map, not in line with normal vocal fold function. Theoretically, it would be beneficial for the functional restitution to pace up and enhance regeneration/reinnervation by the RLN.

In vitro, it has been shown that the pace of the regenerating axon is regulated at the tip (growth cone), the motion of which is highly dependent on a delicate regulation of calcium ions (81,82). It was demonstrated that altering the intracellular concentration of calcium ions had a strict correlation to the ability of the growth cone to sprout (82). The regulation of intracellular calcium is also closely linked to the actions of the voltage-gated calcium channels present in the cellular membrane (82). In vivo, it has been confirmed that the transient quick calcium currents across the membrane of the growth cone occur with a certain frequency. If the calcium transient calcium currents are to some extent inhibited the pace of axonal elongation increases, and vice versa (83-85). In fact, blocking of the rapid calcium flow current across the membrane would increase the total time for axonal elongation, a principle further evaluated in experimental models. Nimodipine, a voltage-gated calcium flow antagonist to the L-type channels has been evaluated in rodent models, and is a pharmacologically good choice because it penetrates the blood brain barrier better than most other calcium flow antagonists (86). After systemic administration of nimodipine, an improved regeneration and functional recovery has experimentally been achieved after injury to the sciatic (87), facial (88-90), hypoglossal (91) and RLNs (92). In the patient, nimodipine has been evaluated after recurrent laryngeal (49,93-95) and facial nerve injury (96-100), with promising functional outcomes. Taken together, there is substantial evidence that the administration of nimodipine after axonal injury to a peripheral nerve probably improves the functional outcome.

Even though there is emerging data that treatment with nimodipine may also be translated to the patient in some situations, the level of evidence for a using nimodipine for intraoperative RLN injury is still modest. Only a fraction of the patients with postoperative RLN paresis would benefit from a regeneration-promoting treatment (i.e., cases with axonotmesis). It is important, therefore, to search for further knowledge concerning diagnosis and prognosis after RLN injury after thyroid surgery.


Conclusions

Laryngeal dysfunction and voice problems are common after thyroid surgery, but only a fraction of these cases turn out to be chronic. Chronic laryngeal dysfunction is most commonly caused by axonal injury to the RLN or SLN. The clinical progress of symptoms and the eventual functional recovery of the target organ follow the general principles of peripheral nerve injury, even though the larynx can be regarded a special case in being functionally and neuroanatomically complex, with high demands for accurate neural supply. Today, it is possible for the clinician to utilize the information obtained from electrodiagnostic methods (IONM and postoperative LEMG), to characterize the nerve injury and predict the temporal course and functional result of the healing process. It is important to do so in order to be prepared for additional interventions, such as voice therapy, medialization surgery or regeneration/reinnervation therapies.


Acknowledgements

Disclosure: The authors declare no conflict of interest.


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Cite this article as: Mattsson P, Hydman J, Svensson M. Recovery of laryngeal function after intraoperative injury to the recurrent laryngeal nerve. Gland Surg 2015:4(1):27-35. doi: 10.3978/j.issn.2227-684X.2015.01.10

Sours: https://gs.amegroups.com/article/view/5617/6398
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Recurrent laryngeal nerve

Nerve in the human body

"Recurrent nerve" redirects here. For the supply to the thenar eminence, see recurrent branch of the median nerve.

The recurrent laryngeal nerve (RLN) is a branch of the vagus nerve (cranial nerve X) that supplies all the intrinsic muscles of the larynx, with the exception of the cricothyroid muscles. There are two recurrent laryngeal nerves, right and left. The right and left nerves are not symmetrical, with the left nerve looping under the aortic arch, and the right nerve looping under the right subclavian artery then traveling upwards. They both travel alongside the trachea. Additionally, the nerves are among the few nerves that follow a recurrent course, moving in the opposite direction to the nerve they branch from, a fact from which they gain their name.

The recurrent laryngeal nerves supply sensation to the larynx below the vocal cords, give cardiac branches to the deep cardiac plexus, and branch to the trachea, esophagus and the inferior constrictor muscles. The posterior cricoarytenoid muscles, the only muscles that can open the vocal folds, are innervated by this nerve.

The recurrent laryngeal nerves are the nerves of the sixth pharyngeal arch. The existence of the recurrent laryngeal nerve was first documented by the physician Galen.

Structure[edit]

The recurrent laryngeal nerves branch from the vagus nerve, relative to which they get their names; the term "recurrent" from Latin: re- (back) and currere (to run),[1] indicates they run in the opposite direction to the vagus nerves from which they branch.[2] The vagus nerves run down into the thorax, and the recurrent laryngeal nerves run up to the larynx.[3]: 930–931 

The vagus nerves, from which the recurrent laryngeal nerves branch, exit the skull at the jugular foramen and travel within the carotid sheath alongside the carotid arteries through the neck. The recurrent laryngeal nerves branch off the vagus, the left at the aortic arch, and the right at the right subclavian artery. The left RLN passes in front of the arch, and then wraps underneath and behind it. After branching, the nerves typically ascend in a groove at the junction of the trachea and esophagus.[4]: 1346–1347  They then pass behind the posterior, middle part of the outer lobes of the thyroid gland and enter the larynx underneath the inferior constrictor muscle,[3]: 918  passing into the larynx just posterior to the cricothyroid joint.[5] The terminal branch is called the inferior laryngeal nerve.[6]: 19 

Unlike the other nerves supplying the larynx, the right and left RLNs lack bilateral symmetry.[7] The left RLN is longer than the right, because it crosses under the arch of the aorta at the ligamentum arteriosum.[4]: 1346–1347 

Nucleus[edit]

The somatic motor fibers that innervate the laryngeal and pharyngeal muscles are located in the nucleus ambiguus and emerge from the medulla in the cranial root of the accessory nerve. Fibers cross over to and join the vagus nerve in the jugular foramen.[8]: 86–88  Sensory cell bodies are located in the inferior jugular ganglion,[9] and the fibers terminate in the solitary nucleus.[8]: 86–88 Parasympathetic fibers to segments of the trachea and esophagus in the neck originate in the dorsal nucleus of the vagus nerve.[9]

Development[edit]

During human and all vertebrate development, a series of pharyngeal arch pairs form in the developing embryo. These project forward from the back of the embryo towards the front of the face and neck. Each arch develops its own artery, nerve that controls a distinct muscle group, and skeletal tissue. The arches are numbered from 1 to 6, with 1 being the arch closest to the head of the embryo, and the fifth arch only existing transiently.[10]: 318–323 

Arches 4 and 6 produce the laryngeal cartilages. The nerve of the sixth arch becomes the recurrent laryngeal nerve. The nerve of the fourth arch gives rise to the superior laryngeal nerve. The arteries of the fourth arch, which project between the nerves of the fourth and sixth arches, become the left-sided arch of the aorta and the right subclavian artery. The arteries of the sixth arch persist as the ductus arteriosus on the left, and are obliterated on the right.[10]: 318–323 

After birth, the ductus arteriosus regresses to form the ligamentum arteriosum. During growth, these arteries descend into their ultimate positions in the chest, creating the elongated recurrent paths.[10]: 318–323 

Variation[edit]

In roughly 1 out of every 100–200 people, the right inferior laryngeal nerve is nonrecurrent, branching off the vagus nerve around the level of the cricoid cartilage. Typically, such a configuration is accompanied by variation in the arrangement of the major arteries in the chest; most commonly, the right subclavian artery arises from the left side of the aorta and crosses behind the esophagus. A left nonrecurrent inferior laryngeal nerve is even more uncommon, requiring the aortic arch be on the right side, accompanied by an arterial variant which prevents the nerve from being drawn into the chest by the left subclavian.[11]: 10, 48 

In about four people out of five, there is a connecting branch between the inferior laryngeal nerve, a branch of the RLN, and the internal laryngeal nerve, a branch of the superior laryngeal nerve. This is commonly called the anastomosis of Galen (Latin: ansa galeni), even though anastomosis usually refers to a blood vessel,[12][13]: 35  and is one of several documented anastomoses between the two nerves.[14]

As the recurrent nerve hooks around the subclavian artery or aorta, it gives off several branches. There is suspected variability in the configuration of these branches to the cardiac plexus, trachea, esophagus and inferior pharyngeal constrictor muscle.[15]

Function[edit]

The recurrent laryngeal nerves control all intrinsic muscles of the larynx except for the cricothyroid muscle.[15][a] These muscles act to open, close, and adjust the tension of the vocal cords, and include the posterior cricoarytenoid muscles, the only muscle to open the vocal cords.[16]: 10–11  The nerves supply muscles on the same side of the body, with the exception of the interarytenoid muscle, which is innervated from both sides.[15]

The nerves also carry sensory information from the mucous membranes of the larynx below the lower surface of the vocal fold,[17]: 847–9  as well as sensory, secretory and motor fibres to the cervical segments of the esophagus and the trachea.[8]: 142–144 

Clinical significance[edit]

Injury[edit]

An image of a surgical procedure in which the recurrent laryngeal nerve is visible
Recurrent laryngeal nerve visible during resection of a goitre

The recurrent laryngeal nerves may be injured as a result of trauma, during surgery, as a result of tumour spread, or due to other means.[16]: 12  Injury to the recurrent laryngeal nerves can result in a weakened voice (hoarseness) or loss of voice (aphonia) and cause problems in the respiratory tract.[16]: 11–12  Injury to the nerve may paralyze the posterior cricoarytenoid muscle on the same side. This is the sole muscle responsible for opening the vocal cords, and paralysis may cause difficulty breathing (dyspnea) during physical activity.[18] Injury to both the right and left nerve may result in more serious damage, such as the inability to speak. Additional problems may emerge during healing, as nerve fibres that re-anastamose may result in vocal cord motion impairment, uncoordinated movements of the vocal cord.[16]: 12–13 

Surgery[edit]

The nerve receives close attention from surgeons because the nerve is at risk for injury during neck surgery, especially thyroid and parathyroid surgery; as well as esophagectomy.[19][4] Nerve damage can be assessed by laryngoscopy, during which a stroboscopic light confirms the absence of movement in the affected side of the vocal cords. The right recurrent laryngeal nerve is more susceptible to damage during thyroid surgery because it is close to the bifurcation of the right inferior thyroid artery, variably passing in front of, behind, or between the branches.[17]: 820–1  The nerve is permanently damaged in 0.3–3% of thyroid surgeries, and transient paralysis occurs in 3–8% of surgeries; accordingly, recurrent laryngeal nerve damage is one of the leading causes of medicolegal issues for surgeons.[20]

Tumors[edit]

The RLN may be compressed by tumors. Studies have shown that 2–18% of lung cancer patients develop hoarseness because of recurrent laryngeal nerve compression, usually left-sided.[21] This is associated with worse outcomes, and when found as a presenting symptom, often indicates inoperable tumors. The nerve may be severed intentionally during lung cancer surgery in order to fully remove a tumor.[22]: 330  The RLN may also be damaged by tumors in the neck, especially with malignant lymph nodes with extra-capsular extension of tumor beyond the capsule of the nodes, which may invade the area that carries the ascending nerve on the right or left.

Other disease[edit]

In Ortner's syndrome or cardiovocal syndrome, a rare cause of left recurrent laryngeal nerve palsy, expansion of structures within the heart or major blood vessels impinges upon the nerve, causing symptoms of unilateral nerve injury.[23]

Other animals[edit]

Horses are subject to equine recurrent laryngeal neuropathy, a disease of the axons of the recurrent laryngeal nerves. The cause is not known, although a genetic predisposition is suspected. The length of the nerve is a factor since it is more common in larger horses, and the left side is affected almost exclusively. As the nerve cells die, there is a progressive paralysis of the larynx, causing the airway to collapse. The common presentation is a sound, ranging from a musical whistle to a harsh roar or heaving gasping noise (stertorous), accompanied by worsening performance. The condition is incurable, but surgery can keep the airway open. Experiments with nerve grafts have been tried.[24]: 421–426 

Although uncommon in dogs, bilateral recurrent laryngeal nerve disease may be the cause of wheezing (stridor) when middle-aged dogs inhale.[25]: 771 

In sauropod dinosaurs, the vertebrates with the longest necks, the total length of the vagus nerve and recurrent laryngeal nerve would have been up to 28 metres (92 ft) long in Supersaurus, but these would not be the longest neurons that ever existed: the neurons reaching the tip of the tail would have exceeded 30 metres (98 ft).[26]

Evidence of evolution[edit]

The extreme detour of the recurrent laryngeal nerves, about 4.6 metres (15 ft) in the case of giraffes,[27]: 74–75  is cited as evidence of evolution, as opposed to Intelligent Design. The nerve's route would have been direct in the fish-like ancestors of modern tetrapods, traveling from the brain, past the heart, to the gills (as it does in modern fish). Over the course of evolution, as the neck extended and the heart became lower in the body, the laryngeal nerve was caught on the wrong side of the heart. Natural selection gradually lengthened the nerve by tiny increments to accommodate, resulting in the circuitous route now observed.[28]: 360–362 

History[edit]

Ancient Greek physician Galen demonstrated the nerve course and the clinical syndrome of recurrent laryngeal nerve paralysis, noting that pigs with the nerve severed were unable to squeal. Galen named the nerve the recurrent nerve, and described the same effect in two human infants who had undergone surgery for goiter.[16]: 7–8 [29] In 1838, five years before he would introduce the concept of homology to biology, anatomist Richard Owen reported upon the dissection of three giraffes, including a description of the full course of the left recurrent laryngeal nerve.[30][31] Anatomists Andreas Vesalius and Thomas Willis described the nerve in what is now regarded as an anatomically standard description, and doctor Frank Lahey documented a way for its interoperative identification during thyroid operations.[32]

Notes[edit]

References[edit]

  1. ^"Recur". Free Dictionary. Merriam-Webster. Retrieved March 1, 2013.
  2. ^"Recurrent". Medical definition and more. Merriam-Webster. Retrieved March 1, 2013.
  3. ^ abDrake, Richard L.; Vogl, Wayne; Tibbitts, Adam W.M. Mitchell; illustrations by Richard; Richardson, Paul (2005). Gray's anatomy for students. Philadelphia: Elsevier/Churchill Livingstone. ISBN .
  4. ^ abcF. Charles Brunicardi; F. Brunicardi; Dana Andersen; E. Pollock Raphael; Timothy Billiar; David Dunn; John Hunter; Jeffrey Matthews; Raphael E. Pollock (September 11, 2009). Schwartz's Principles of Surgery (9th ed.). McGraw Hill Professional. ISBN .
  5. ^Agur, A. M. R.; Dalley, Arthur F. (2009). Grant's Atlas of Anatomy. Lippincott Williams & Wilkins. p. 770. ISBN .
  6. ^Ross, Lawrence M.; Lamperti, Edward D. (2006). Thieme Atlas of Anatomy: Neck and Internal Organs. Thieme. ISBN .
  7. ^Aronson, Arnold Elvin (2009). Clinical Voice Disorders. Thieme. p. 74. ISBN .
  8. ^ abcSchulte, Erik; Schumacher, Udo; Rude, Jürgen (2007). Thieme Atlas of Anatomy: Head and Neuroanatomy. Thieme. ISBN .
  9. ^ abAlberstone, Cary D. (2009). Anatomic Basis of Neurologic Diagnosis. Thieme. pp. 260–261. ISBN .
  10. ^ abcLarsen, William J. (1993). Human embryology. Churchill Livingstone. ISBN . Retrieved February 26, 2013.
  11. ^Quan-Yang Duh; Orlo H. Clark; Electron Kebebew (October 14, 2009). Atlas of Endocrine Surgical Techniques. Elsevier Health Sciences. ISBN . Retrieved March 6, 2013.
  12. ^Naidu, L.; Ramsaroop, L.; Partab, P.; Satyapal, K. S. (2012). "Galen's "Anastomosis" revisited". Clinical Anatomy. 25 (6): 722–728. doi:10.1002/ca.22011. PMID 22162120. S2CID 23512491.
  13. ^Langmore, Susan E. (January 2001). Endoscopic Evaluation and Treatment of Swallowing Disorders. Thieme. ISBN .
  14. ^Sañudo, Jose-Ramón; Maranillo, Eva; León, Xavier; Mirapeix, Rosa-María; Orús, Cesar; Quer, Miquel (June 1999). "An anatomical study of anastomoses between the laryngeal nerves". The Laryngoscope. 109 (6): 983–987. doi:10.1097/00005537-199906000-00026. PMID 10369294. S2CID 26161510.
  15. ^ abcYau, Amy Y.; Verma, Sunil P. (February 20, 2013). Meyers, Arlen D. (ed.). Laryngeal Nerve Anatomy. Medscape Reference. Retrieved January 5, 2014.
  16. ^ abcdeHydman, Jonas (2008). Recurrent laryngeal nerve injury. Stockholm. ISBN .
  17. ^ abMoore, Keith L (1992). Clinically Oriented Anatomy (3rd ed.). ISBN .
  18. ^Hartl, D. M.; Travagli, Jean-Paul; Leboulleux, Sophie; Baudin, Eric; Brasnu, Daniel F.; Schlumberger, Martin (2005). "Current Concepts in the Management of Unilateral Recurrent Laryngeal Nerve Paralysis after Thyroid Surgery". Journal of Clinical Endocrinology & Metabolism. 90 (5): 3084–3088. doi:10.1210/jc.2004-2533. ISSN 0021-972X. PMID 15728196.
  19. ^Yamamoto, Natsuhiro, Yamaguchi, Yoshikazu, Nomura, Takeshi, et al. Successful Assessment of Vocal Cord Palsy Before Tracheal Extubation by Laryngeal Ultrasonography in a Patient After Esophageal Surgery: A Case Report. A&A Case Reports. 2017;9(11):308-310. doi:10.1213/XAA.0000000000000601.
  20. ^Hayward, Nathan James; Grodski, Simon; Yeung, Meei; Johnson, William R.; Serpell, Jonathan (January 2013). "Recurrent laryngeal nerve injury in thyroid surgery: a review". ANZ Journal of Surgery. 83 (1–2): 15–21. doi:10.1111/j.1445-2197.2012.06247.x. PMID 22989215. S2CID 8581189.
  21. ^Spiro, Stephen G. (2007). "Initial Evaluation of the Patient With Lung Cancer: Symptoms, Signs, Laboratory Tests, and Paraneoplastic Syndromes: ACCP Evidenced-Based Clinical Practice Guidelines (2nd Edition)". Chest. 132 (3_suppl): 149S–160S. doi:10.1378/chest.07-1358. ISSN 0012-3692. PMID 17873166.
  22. ^David P. Carbone; Harvey I. Pass; David H. Johnson; John D. Minna (2010). Principles and Practice of Lung Cancer: The Official Reference Text of the IASLC. Lippincott Williams & Wilkins. ISBN . Retrieved August 12, 2013.
  23. ^Heikkinen, Jaakko; Milger, Katrin; Alejandre-Lafont, Enrique; Woitzik, Christian; Litzlbauer, Detlef; Vogt, Julia-Franziska; Klußmann, Jens Peter; Ghofrani, Ardeschir; Krombach, Gabriele A.; Tiede, Henning (2012). "Cardiovocal Syndrome (Ortner's Syndrome) Associated with Chronic Thromboembolic Pulmonary Hypertension and Giant Pulmonary Artery Aneurysm: Case Report and Review of the Literature". Case Reports in Medicine. 2012: 1–5. doi:10.1155/2012/230736. ISSN 1687-9627. PMC 3477763. PMID 23424588.
  24. ^Munroe, Graham; Weese, Scott (March 15, 2011). Equine Clinical Medicine, Surgery and Reproduction. Manson Publishing. ISBN . Retrieved March 2, 2013.
  25. ^Slatter, Douglas H. (2003). Textbook of Small Animal Surgery. Elsevier Health Sciences. ISBN . Retrieved March 2, 2013.
  26. ^Wedel, Mathew J. (June 2012). "A Monument of Inefficiency: The Presumed Course of the Recurrent Laryngeal Nerve in Sauropod Dinosaurs". Acta Palaeontologica Polonica. 57 (2): 251–256. doi:10.4202/app.2011.0019.
  27. ^Mammal Anatomy: An Illustrated Guide. Marshall Cavendish Corporation. 2010. ISBN .
  28. ^Dawkins, Richard (2009). "11. History Written All Over Us". The Greatest Show on Earth. New York: Free Press. ISBN . Retrieved November 21, 2009.
  29. ^Gross, Charles G. (May 1998). "Galen and the Squealing Pig". Neuroscientist. 4 (3): 216–221. doi:10.1177/107385849800400317. ISSN 1073-8584. S2CID 72125962.
  30. ^Owen, Richard (1841). "Notes on the dissection of the Nubian giraffe". Transactions of the Zoological Society of London. Zoological Society of London. pp. 217–248. Retrieved February 27, 2013.
  31. ^Robert James Berry; Anthony Hallam (1986). The Collins Encyclopedia of Animal Evolution. HarperCollins Publishers Limited. pp. 82–83. ISBN . Retrieved February 27, 2013.
  32. ^Ardito, Guglielmo; Revelli, Luca; D'Alatri, Lucia; Lerro, Valentina; Guidi, Maria Lavinia; Ardito, Francesco (February 2004). "Revisited anatomy of the recurrent laryngeal nerves". The American Journal of Surgery. 187 (2): 249–253. doi:10.1016/j.amjsurg.2003.11.001. PMID 14769313.

External links[edit]

Sours: https://en.wikipedia.org/wiki/Recurrent_laryngeal_nerve
The Recurrent Laryngeal Nerves and the Thoracic Surgeon

Optimal Management of Acute Recurrent Laryngeal Nerve Injury During Thyroidectomy

Abstract

Recurrent laryngeal nerve (RLN) injury is commonly encountered by thyroid surgeons and may carry with it great morbidity. Whether the injury is accidental or due to deliberate resection for oncologic soundness, the surgeon must be prepared to offer the best available treatment to patients, either at the time of injury or early in the recovery process. We review advances in treatment that allow optimal management of an acute RLN injury: ansa cervicalis–RLN reinnervation, in-office unsedated vocal fold injection augmentation, and electromyographic prognostication. The benefits and advantages of each procedure as well as relevant anatomy and techniques are delineated.

Introduction

Recurrent laryngeal nerve (RLN) injury is a severe consequence of head and neck surgery. It causes dysphonia, dysphagia, and occasionally significant aspiration. In addition to patient morbidity, injury also results in medicolegal challenges and significant loss of worker productivity at a high cost to both patients and society [1]. Those who operate in the region of the RLN are obligated to strive to protect the nerve and minimize patient morbidity by optimizing management when injury occurs.

This is especially true for thyroid surgeons, where intraoperative preservation of the RLN is a priority. Testament to this is the shear number of publications produced over many years on the topic [2••]. Consequently, at significant cost, new technology with indeterminate benefit has been developed and used to aid in localization and preservation of the RLN [3, 4]. Despite this, RLN injury is still common. During thyroidectomy, the incidence of permanent postoperative RLN paralysis is 0.3–3 % and is as high as 2–30 % in revision thyroid surgery [2••].

Owing to the increasing rate of surgery for thyroid cancer, it is likely the incidence of iatrogenic RLN injury will be even higher in the coming years. The incidence of thyroid cancer in the USA has been rising since the mid-1990s, and has increased by 5.5 % per year in males and 6.6 % in females since 2004. This growth continues because of both improved detection methods and higher incidence rates in an expanding US population [5]. Approximately 60,220 new cases of thyroid cancer are expected to be diagnosed in the USA in 2013, with 3 in 4 cases occuring in women [6].

One of the areas of highest preoperative concern for thyroidectomy patients is experiencing a postoperative voice change [7]. Poor vocal outcome from an RLN injury is of real concern to physicians and a focal point of medicolegal action. Approximately 46 % of thyroidectomy malpractice cases are related to RLN injury [8]. Over a 24-year period, an estimated $95 million was paid out in indemnity payments because of thyroidectomy-related malpractice claims. The average payment was $437,852 adjusted for inflation [9].

Considering the above facts, RLN injury will continue to occur with increasing frequency. In contrast to the extensive literature considering the prevention of RLN injury, few studies are devoted to the optimal the management of an acutely injured RLN. To best serve patients and minimize their morbidity, surgeons must be prepared to treat an acutely injured RLN whether it is identified in the operating room or in the early postoperative period. Herein we discuss the optimal management of an acute RLN injury identified either intraoperatively or postoperatively, using ansa cervicalis (ANSA)–RLN reinnervation, in-office vocal fold injection augmentation, and laryngeal electromyography (EMG).

Intraoperative Recognition

Recurrent Laryngeal Nerve Reinnervation

The RLN may be injured inadvertently or purposefully resected to allow oncologic resection of thyroid cancer. When discontinuity of the RLN is recognized intraoperatively, options exist: do nothing and rely on a secondary surgical procedure in the future such as a laryngoplasty, reanastomose the RLN, reconnect the RLN with a nerve graft, or reinnervate the RLN with an alternative nerve source.

Although relying on future surgery for vocal rehabilitation is an option, it is far from optimal, as the patient will suffer the morbidity related to the injury as well as a secondary surgical procedure. In contrast, successful reinnervation of the RLN will obviate the need for a second surgical procedure and demonstrate expertise in cases of inadvertent nerve injury. To decide on the best reparative option, the pathophysiology of RLN reinnervation must be understood as well as the advantages and disadvantages of the different techniques available.

The RLN is a mixed nerve with random positioning of both adductor and abductor axons [10]. When the axons of the nerve are transected, they regenerate in random fashion with some adductor axons innervating abductor muscles and vice versa [11]. This results in synkinetic reinnervation. In 2000, Crumley [12] detailed the clinical characteristics of synkinesis, describing four types of synkinesis to explain various laryngeal phenomena after recovery: type I—an immobile or poorly mobile vocal fold with unaffected voice; type II—spasmodic or twitching vocal folds; type III—hyperadducted vocal folds; type IV—hyperabducted vocal folds with possible aspiration. Only type I was deemed “favorable.” Owing to unfavorable synkinetic reinnervation, RLN–RLN reanastamosis or free nerve grafts can result in dysfunctional vocal folds, resulting in morbidity requiring intervention to correct the detrimental effects of synkinetic reinnervation [13, 14]. Overall, however, RLN–RLN or free graft anastomosis appears to result in favorable synkinetic reinnervation approximately 70–75 % of the time, although the study series are small [14–17].

Considering this success rate, if both nerve endings are identified and a tension-free anastomosis can be performed, although suboptimal, RLN–RLN reanastomosis is a viable option. In the situation of an inadvertently transected RLN, this reanastomosis should be performed at minimum, as without it the patient will inevitably need further surgery for vocal rehabilitation [14]. If it appears the anastomosis will be under tension, a greater auricular nerve graft can be used. The results are the same as with RLN–RLN, but the graft is in a separate surgical field and results in anesthesia of the ear lobule and surrounding skin. Other options for reinnervation include the neuromuscular pedicle, nerve implantation, and ANSA, hypoglossal, or vagus nerve to RLN anastomosis. Neuromuscular pedicle and nerve implantation do not appear to be as successful as ANSA–RLN reinnervation, and harvesting all or part of the vagus or hypoglossal nerve may result in significant patient morbidity [18••, 19].

The ANSA is an ideal nerve for RLN reinnervation. There is no morbidity related to its sacrifice. During a thyroidectomy, it is close to the surgical field and is rarely injured unless an aggressive neck dissection is being performed. The ANSA is approximately 1 cm from the RLN, so the nerve length needed for this short transposition is minimal (Fig. 1). Because of this, a tension-free anastomosis is nearly always possible. The ANSA has a diameter similar to that of the RLN and can be used for both ipsilateral and contralateral anastamosis [12, 20, 21]. The ANSA also naturally fires during phonation, and there is increased recruitment with increasing vocal volume [22, 23]. Success of ANSA–RLN reinnervation is attributed to restoration of bulk and tone in glottic musculature resulting in medialization of the vocal fold and correction of arytenoid malposition and muscular atrophy. Owing to the innervation of the adductor and abductor muscles with one type of axon, synkinesis does not occur as with RLN–RLN anastomosis. Additionally, the anatomic structure of the larynx is preserved. This allows subsequent injection augmentation or type 1 laryngoplasty to be performed in the 1–2 % of cases in which failure occurs. One limitation to ANSA–RLN reinnervation is that in elderly patients, reinnervation is not as robust, and they may have increased risk of failure [24•, 25].

Left recurrent laryngeal nerve (solid arrow) and superior root of the ansa cervicalis (arrowhead) with loop (hollow arrow) and common branch (dashed arrow). Note the proximity of the nerves after mobilization prior to transection

Full size image

Although first described in 1924 by Frazier [26], ANSA–RLN reinnervation had been dormant until Crumley [27] published his original series in 1986. In 1991, he published an update of 20 cases, of which seven and five patients had “excellent” and “normal” voice outcomes, respectively [28]. The study included three patients with preoperative synkinesis, corrected following ANSA–RLN reinnervation. One patient required postoperative injection medialization to improve voice quality, and one patient with a history of multiple prior laryngeal surgical procedures and subglottic stenosis did not show any voice improvement. Vocal fold position, muscle mass, and tension were restored and no synkinesis was seen. A 95 % success rate was reported for ANSA–RLN reinnervation.

In 2008, Lorenz et al. [25] studied a series of 46 patients who underwent delayed ANSA–RLN anastomosis with a median time to repair of 12 months. Thirty-seven of 38 patients who were followed up for a minimum of 3 months showed evidence of reinnervation and did not need a secondary procedure, a 97 % success rate. All patients who underwent preoperative and postoperative Consensus Auditory–Perceptual Evaluation of Voice (CAPE-V) and laryngovideostroboscopy showed improvement in voice severity, roughness, breathiness, and strain as well as glottic closure, straightened vocal fold edge, and decreased supraglottic effort.

Wang et al. [18••] performed a case–control study looking at the long-term efficacy of delayed ANSA–RLN reinnervation following thyroid cancer surgery. In a large series, 237 Chinese patients underwent ANSA–RLN reinnervation 6–42 months after surgery. The patients were followed for a mean of 5 years and matched with 237 controls. On laryngovideostroboscopy, 92.4 % of the patients had straight vocal fold edges, median or near-median vocal fold position, and symmetric and regular vocal fold vibration, with complete glottic closure during phonation. Significant improvement was demonstrated using the GRBAS scale. Maximum phonation time, jitter, shimmer, and noise to harmonic ratio were equivalent to those of controls. Reinnervation was confirmed on laryngeal EMG by the presence of significantly increased recruitment of motor unit action potentials in the thyroarytenoid muscle with phonation. Only four of 237 patients failed to restore adequate phonation. Two failures were due to technical reasons; one anastomosis was performed under significant tension and the other was avulsed during evacuation of a hematoma. Only two failures were due to inadequate reinnervation. Essentially, 98–99 % of the ANSA–RLN reinnervations were successful.

Aynehchi et al. [21] systematically reviewed the outcomes from 14 case series of laryngeal reinnervation procedures for unilateral vocal fold paralysis between 1966 and 2009. Owing to the heterogeneity of the available literature and difficulty in analyzing techniques and outcomes, it is difficult to extrapolate direct data comparing different techniques. However, an improvement in acoustic, perceptive, EMG, and glottic gap analysis was seen with all reinnervation techniques. ANSA–RLN anastomosis was the commonest reinnervation technique, performed in 43.5 % of procedures following thyroidectomy. It resulted in statistically significant better glottal closure than the other techniques, with a mean postsurgical time to reinnervation of 4.5 months.

It is clear that ANSA–RLN reinnervation works well when performed in a delayed fashion, with results similar to those of a type 1 laryngoplasty [24•]. Either can be performed for treatment of a chronic injury, but only ANSA–RLN reinnervation is available during surgery at the time of an acute injury. It is in the acute injury scenario when ANSA–RLN reinnervation is most powerful, especially in the face of a preoperative vocal fold paralysis or after RLN resection for cancer. The success of acute reinnervation is as good as that of delayed anastomosis, and the presence of malignancy does not affect the outcome of reinnervation.

Sanuki et al. [29] reported a series of 12 patients with thyroid cancer who experienced either nerve sacrifice or injury intraoperatively. Six patients had preoperative vocal fold paralysis and six underwent intraoperative sacrifice. Reconstruction was performed immediately using direct anastamosis (n = 1), free nerve graft (n = 9), or ANSA–RLN reinnervation (n = 2). Postoperative vocal perceptual analysis scores, aerodynamic function, and laryngovideostroboscopy findings were improved in all groups compared with values obtained before surgery from patients with preoperative vocal fold paralysis.

More detailed and extensive work on acute RLN reinnervation has been performed in Japan by Miyauchi et al. [20]. They retrospectively reviewed a series of patients who had undergone immediate reconstruction of the RLN after thyroid cancer resection. Thirty-four patients underwent reinnervation procedures, of which 19 were ANSA–RLN reinnervation [direct anastamosis (n = 5), free nerve graft (n = 8), vagus–RLN anastomosis (n = 2), and ANSA–RLN reinnervation (n = 19)]. Recovery of voice began between 2 and 5 months postoperatively, with maximum improvement at 12 months. On laryngoscopy, patients had a minimal glottal gap, with good bulk and tension of the vocal folds. Maximum phonation time was not significantly different from that in the 34 normal controls. A most important insight from Miyauchi et al. was that once they began using ANSA–RLN reinnervation, it became their preferred method of reconstruction. This was due to consistent access to the nerve, the available length of the ANSA for a tension-free anastomosis, no morbidity related to the graft harvest, and the ease of the procedure performed primarily with surgical loupes. Once they had adopting ANSA-RLN reinnervation, they had a statistically significant increase in their anastomosis rate from 18 to 82 %, further proving the utility of this method.

In 2009, Miyauchi et al. [30] reviewed 88 cases of RLN reconstruction after nerve sacrifice during thyroid surgery. Sixty-five patients had reconstruction with ANSA–RLN anastomosis. Patients’ voices began to improve within 3–5 months. Laryngoscopy revealed midline vocal folds with good tension and tone as well as a minimal glottal gap. Recovery of phonatory function was assessed quantitatively with the phonation efficiency index (PEI), a ratio of maximum phonation time to vital capacity. Eighty-seven percent of patients had a PEI similar to that of normal subjects at 1 year. The validity of the PEI, which Miyauchi et al. constructed, is unclear. Of note, 47 % of anastomoses were performed intralaryngeally to the distal end of the RLN. This is critical because RLN injury or cancer invasion often occurs close to the cricothyroid joint. This leaves only a small section of exposed distal nerve, making performing an anastomosis technically difficult. In these cases, incision of the inferior constrictor with removal of the inferior horn of the thyroid cartilage exposes extra length of usually undisturbed RLN. This extra length of intralaryngeal nerve allows a tension-free anastomosis to be performed despite a distal nerve injury.

Operative Technique and Anatomy

Anatomy

To successfully perform an ANSA–RLN reinnervation, a surgeon must be mentally prepared, know the relevant anatomy, and understand the surgical technique. The ANSA is formed from two nerve roots that join inferiorly to form a loop. The superior root, or the descendens hypoglossi, receives branches of communication from C1 and C2 and comes off cranial nerve XII, whereas the inferior root arises from the junction of the cervical rami, usually C2–C4 [31]. The superior root leaves cranial nerve XII just inferior to the origin of the occipital artery and descends obliquely along the carotid artery. The inferior root passes posterolaterally to the internal jugular vein 57–81 % of the time, otherwise passing medially. The two branches join as a loop deep to the superior belly of the omohyoid, at the point where the muscle crosses the great vessels. The loop is in this location 64 % of the time, although it may rest anywhere between the occipital artery and 4 cm above the sternum. Following formation of the loop, the nerve branches innervate the sternohyoid and sternothyroid. The common ANSA branch is approximately 4.3 cm long and 0.9 mm wide, making it a good anatomic fit in length and diameter for anastamosis to the RLN [32]. In the past, the nerve branch to the sternothyroid or common branch was used with good surgical outcome [12]. However, the ascending fibers or descending fibers of the superior root are slightly easier to mobilize and are commonly used for ANSA–RLN reinnervation as well. An elegant study of the ANSA using Sudan black to stain the axons noted a greater number of motor axons traveling cranially versus caudally in the superior root of the ANSA [31]. Considering this, the best nerve to use for reinnervation may be the ascending aspect of the superior root.

ANSA–RLN Reinnervation Procedure

Variations of the procedure have been described; however, the most important factor is exposure of the relevant nerve endings and achieving a tension-free anastomosis. To identify the ANSA, the superior belly of the omohyoid can be found crossing beneath the sternocleidomastoid muscle. The omohyoid is then dissected from surrounding fascia and retracted superiorly where it overlies the internal jugular vein. The loop of the ANSA is generally just beneath the muscle. The common branch to the strap muscles is then identified and dissected distally. A branch similar in thickness to the ANSA should be chosen, transected, and mobilized toward the RLN. Alternatively, the superior root of the ANSA can be dissected cranially. The root is then transected far enough cranially so the ascending aspect of the ANSA can be mobilized and sutured to the RLN without tension. On occasion, the RLN is injured or sacrificed at the cricothyroid joint; as such, a distal stump is not readily available for anastamosis. In this case, the inferior constrictor muscle can be divided and the inferior horn of the thyroid cartilage removed to identify an additional 0.5–1 cm of intralaryngeal RLN [18••, 30]. When the ipsilateral ANSA has been resected or its viability is in question, a contralateral ANSA anastomosis can be performed by routing the nerves anterior to the thyroid cartilage [33••]. Nerve edges are trimmed sharply and epineurium is exposed and gently peeled back to allow separation and identification of fascicles. Three to four 9.0 nylon sutures are used to approximate the nerve ends. Care should be taken to suture only the epineurium and protect the fascicles from injury. The sutures should approximate the nerve endings so they are not strangulated or do not overlap. Performing the anastomosis with either surgical loupes or an operating microscope does not appear to affect vocal outcome [20].

Temporary Injection Augmentation

As it takes 3–5 months for the reinnervation to significantly improve the voice, a temporary bridging injection augmentation of the paralyzed vocal fold should to be performed [20]. This can be conducted in the operating room if the contralateral RLN was not placed at risk during the surgery and is known to be functioning normally. If the status of the contralateral nerve is unknown, the patient should be awoken and adequate motion of the corresponding vocal fold confirmed. The injection is then performed which the patient unsedated, under topical anesthesia at any time when that the patient is mentally and physically ready. Typically, the injection is performed 1–2 weeks following surgery, but can be performed as early as the first postoperative day (see later for injection details).

The combination of ANSA–RLN reinnervation and an early vocal fold injection results in a patient having only 1–2 weeks of morbidity from their vocal fold paralysis, as long as the reinnervation is successful, as is expected 97–99 % of the time. This algorithm for treatment relegates one of the most feared complications of thyroid surgery to a minimally morbid treatable circumstance.

Postoperative Recognition

Injection Augmentation

If a patient has symptomatic vocal fold paralysis recognized in the early postoperative period, the “watching and waiting” approach is no longer the preferred method of treatment. Injection augmentation of the vocal fold can be performed in the office soon after thyroid surgery, under topical anesthesia with minimal patient morbidity or discomfort and with a low complication rate [34, 35•]. As evidence of its utility, the rate of in-office injections has eclipsed that of those performed in the operating room [35•]. Additional benefit is realized by the decreased cost of an injection performed in the office compared with the operating room [36].

There are many options for temporary injectable materials [37•]. The choice is usually based on duration of the material’s persistence, as well as the surgeon’s familiarity and success with it. The authors prefer micronized AlloDerm as it causes minimal inflammation and is very forgiving. Its drawback is that it must be reconstituted prior to use. There are also multiple approaches to performing the injection: peroral, transcutaneous, or transnasal [38•]. The authors prefer the thyrohyoid approach as described by Achkar et al. [39•] and Amin [40] with a needle bending modification. The benefit of most injections lasts 3–4 months and allows the patient good phonatory function while reinnervation occurs. As the injected material resorbs, vocal fold bulk, position, and phonatory function will be maintained by the newly innervating axons, whether arising from a reinnervated RLN or an injured but intact RLN.

The benefits of early vocal fold injection go beyond that of just “positioning” the vocal fold while reinnervation occurs. It appears that early vocal fold injection decreases patients’ need for a secondary laryngoplasty. Friedman et al. [41•] retrospectively reviewed 35 patients with postsurgical or idiopathic vocal fold paralysis into whom hyaluronic acid gel has been injected within 1 year of injury. Twenty of thirty-two patients (62.5 %) with injection medialization performed less than 6 months following injury maintained adequate voice outcomes, whereas all three patients with injection later than 6 months after injury needed further reconstruction. Yung et al. [42••] retrospectively reviewed 54 patients with vocal fold paralysis and also found that patients who underwent temporary injection medialization were less likely to undergo permanent medialization laryngoplasty (26 %) as compared with patients who were conservatively managed (65 %).

The decreased need for intervention after early vocal fold injection is likely secondary to more rapid and robust reinnervation. Experiments involving reinnervation of the facial nerve demonstrate that periodic stimulation of an animal’s whiskers will increase the rate and function of facial nerve regeneration [43•, 44]. This concept can be applied to RLN reinnervation. If the vocal folds are brought into apposition with an injection augmentation, the paralyzed vocal fold will receive vibrotactile and afferent nerve stimulation during phonation that it otherwise would not have had if it were lateralized and injection augmentation had not been performed. This stimulation may parallel that of whisker stimulation, hence increasing the rate and robustness of RLN reinnervation. In this vein, voice therapy may be beneficial as an adjunctive treatment, providing patients exercise and mandated vocal fold stimulation be performed throughout the day.

Electromyographic Prognostication

Electromyographic prognostication is an important adjunct in the care of patients in whom RLN paralysis is recognized postoperatively. Two to 6 months after injury, EMG helps predict which patients may regain vocal fold function and which are unlikely to recover. Temporary augmentation should be offered to those awaiting recovery, whereas early laryngoplasty for permanent medialization would benefit those with minimal chance of return of vocal fold function. Thus, EMG can be used to guide treatment, limit unnecessary temporary procedures, and speed the time to full rehabilitation.

Munin et al. [45] have investigated the role of EMG in evaluating synkinesis and prognosticating recovery. In their original study performed in 2003, they retrospectively evaluated 31 patients with vocal fold paralysis for whom EMG was performed less than 6 months after injury. An excellent prognosis was predicted by EMG findings of normal motor unit recruitment and configuration with a full or slightly decreased interference pattern and no fibrillation potentials. A poor prognosis was determined by diminished motor unit recruitment, repetitive motor unit firing, and a decreased interference pattern with spontaneous activity. A fair prognosis showed moderately decreased motor unit recruitment, diminished interference pattern, and normal or polyphasic motor unit potentials. The positive predictive value for recovery of vocal fold motion was 66.7 %, as four of six patients prognosticated as excellent showed recovery. Only in five of 25 patients with a poor prognosis was there resolution, giving a negative predictive value of 80 %.

In 2010 the same group proposed an EMG protocol for determination of adductor synkinesis to combine with their previous criteria. Forty-six patents with vocal fold paralysis and available EMG data were retrospectively reviewed. Synkinesis was determined by the ratio between motor unit potentials in the thyroarytenoid muscle during adductor and abductor tasks. Synkinesis was defined as a ratio of 0.65 or greater. For patients with good motor unit recruitment who prognostically had potential for excellent recovery using their original EMG criteria, the presence of synkinesis downgraded them to a poor prognosis. This addition of synkinesis to the protocol improved the negative predictive value of EMG from 53 to 100 %, whereas the positive predictive value was 76 % [46•].

Smith et al. [47] further improved the positive predictive value of EMG by adding quantitative analysis of wave amplitude and turns. Adding this information to the previous criteria improved the positive predictive value to 100 %, whereas the negative predictive value dropped slightly to 89.5 %, with seven of eight correct predictions.

Conclusions

RLN injury after thyroid surgery can cause significant patient morbidity. Surgeons treating this injury should be aware of the optimal treatment following injury. If it is recognized intraoperatively, using the most current techniques of ANSA–RLN reinnervation and in-office vocal fold injection augmentation will restore the voice within 1–2 weeks of surgery. If RLN injury is recognized postoperatively, early vocal fold injection will decrease the length of disability and the need for a secondary operation, whereas EMG will shorten the waiting time to permanent rehabilitation and minimize the unnecessary use of further temporary procedures. Together, these management techniques decrease patient morbidity, demonstrate surgical and medical expertise, and decrease costs to society associated with lost worker productivity, extra surgical procedures, and medicolegal costs.

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Disclosure

Tova Fischer Isseroff and Michael Jay Pitman both declare no conflict of interest.

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Affiliations

  1. Department of Otolaryngology—Head and Neck Surgery, The New York Eye and Ear Infirmary, 310 East 14th St., 6th Floor, New York, NY, 10003, USA

    Tova Fischer Isseroff

  2. Department of Otolaryngology, The Voice and Swallowing Institute, The New York Eye and Ear Infirmary, 310 East 14th St., 6th Floor, New York, NY, 10003, USA

    Michael Jay Pitman

Corresponding author

Correspondence to Michael Jay Pitman.

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Isseroff, T.F., Pitman, M.J. Optimal Management of Acute Recurrent Laryngeal Nerve Injury During Thyroidectomy. Curr Otorhinolaryngol Rep1, 163–170 (2013). https://doi.org/10.1007/s40136-013-0020-y

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Keywords

  • Recurrent laryngeal nerve
  • Ansa cervicalis
  • Laryngeal reinnervation
  • Thyroidectomy
  • Vocal fold paralysis
  • Dysphonia
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Injury rln

Recurrent Laryngeal Nerve Injury

Continuing Education Activity

Recurrent laryngeal nerve injuries are a common cause of vocal cord paresis and resulting in voice changes or hoarseness. The etiology, history, and management of these injuries are complicated and requires an interprofessional approach to provide optimal medical care. This activity illustrates the evaluation and management of recurrent laryngeal nerve injuries and highlights the role of the interprofessional team in improving care for patients with this condition.

Objectives:

  • Identify the etiology of patients presenting with recurrent laryngeal nerve injuries.

  • Summarize the physical exam findings associated with recurrent laryngeal nerve injuries.

  • Explain the management considerations for patients with recurrent laryngeal nerve injuries.

Access free multiple choice questions on this topic.

Introduction

The recurrent laryngeal nerve (RLN) branches off the vagus nerve (cranial nerve X) and has an indirect course through the neck. It supplies innervation to all of the intrinsic muscles of the larynx, except for the cricothyroid muscles, as well as sensation to the larynx below the level of the vocal cords. The right RLN branches from CN X around the level of T1-T2 loops under the right subclavian artery traveling posteriorly, and moves back up through the neck. The left RLN arises anteriorly at the level of the arch of the aorta and loops posteriorly under the aortic arch and back up through the neck.[1][2] Overall, the anatomical course of the recurrent laryngeal nerve is important to understand as it shows the many areas that the nerve might be injured.

Etiology

Given the coursing nature of the recurrent laryngeal nerve, there are many injuries that can cause pathology, and damage to the nerve anywhere along its path that can cause impaired vocal function. One of the more commonly cited injuries is secondary to surgical intervention. One study reviewing over 800 patients showed that surgical intervention was the most important cause.[3] This can include any surgical interventions of the chest, neck, or skull base. However, the most frequently studied interventions are thyroidectomies and parathyroidectomies. One study showed that permanent, operation-related vocal cord palsies from injury to the recurrent laryngeal nerve had an incidence of approximately 1%. They also reported the incidence of RLN injuries after thyroid surgery and parathyroid surgery to be 14% and 7%, respectively.[4]

Another common cause of RLN injury is secondary to tumors. In fact, one study found that non-laryngeal malignancy accounted for 24.7% of all unilateral vocal cord paralysis, 80% of those being pulmonary or mediastinal.[5] Therefore, it is important to assess for malignancy before RLN injury is labeled as idiopathic.

Endotracheal intubation is also responsible for a significant number of RLN injuries. When RLN injury after intubation is suspected, it is necessary to also consider arytenoid dislocation as a possible cause.[6] Although masses, surgery, and idiopathic are among the most common causes, viral illness, diabetic neuropathy, and trauma have also been reported less frequently.

In an article reviewing multiple studies on unilateral RLN injury, surgery is cited as the most common cause with most studies putting it as the cause of 30 to 40% of all RLN injuries. Tumors are the second leading cause accounting for approximately 17% to 32% of injuries. Idiopathic causes are cited around 10% to 27% of all RLN injuries with endotracheal intubations last at around 7% to 11% of all causes.[7]

In another article reviewing 2,267 cases of unilateral vocal cord palsy, the top three causes were surgery, cancer, and idiopathic accounting for 36.9%, 29.7%, and 20.9% of cases, respectively.[8] Therefore recurrent laryngeal nerve injury and unilateral vocal cord palsy seem to have similar etiologies, as expected.

Epidemiology

It is important to note that there is poor epidemiological data on RLN injuries, and additional studies are needed to further elucidate this. This is likely secondary to the multiple causes of vocal cord palsy, with RLN injuries being only a portion of these as well as the relative difficulty in diagnosing RLN injuries. One study that followed a cohort of 325 patients found that males were twice as likely to present with laryngeal nerve palsy. They also found the mean age to be 55 years old.[9] Another study reported the incidence of vocal cord paralysis, a common presenting symptom of RLN injury, to be 0.42% of new patients seen. However, they reported that males were three times more likely to be affected than females. They also reported a similar age group stating that most patients were in their 5th and 6th decades of life.[10]

History and Physical

Injury to the recurrent laryngeal nerve has the potential to cause unilateral vocal cord paralysis. Patients with this typically complain of new-onset hoarseness, changes in vocal pitch, or noisy breathing. Bilateral vocal cord paralysis is much less common due to both left and right recurrent laryngeal nerves being affected but can present with more serious symptoms, including significant difficulties breathing and swallowing. Recent surgeries of the head/neck or recent intubation should prompt suspicion of possible injury to the recurrent laryngeal nerve. Signs of underlying malignancy should also be investigated, such as hemoptysis, severe coughing, unexplained weight loss, tobacco/alcohol use, or dysphagia. Less common causes, including recent viral illness or neck trauma, may also point towards an underlying RLN injury.

Physical examination of the head and neck may show lymphadenopathy secondary to underlying malignancy. Examination of the thyroid may also show thyroid nodules or irregularities, prompting further investigation for malignancy as a cause. Unilaterally decreased breath sounds in the lung apex may also point towards a tumor of the pulmonary apex, also known as a Pancoast tumor. In this case, clinical symptoms of Horner syndrome, thoracic outlet syndrome, or superior vena cava syndrome may also be seen on examination.

Evaluation

As usual, a thorough history and physical examination should be performed to guide clinical evaluation. Once recurrent laryngeal nerve injury is suspected, imaging can be considered. It is important to consider that the RLN travels from the base of the skull to the thorax, and imaging can involve any or all of these areas. For instance, a screening chest x-ray can be considered if a pulmonary cause is suspected. In general, evaluation with CT is the most common imaging modality and usually involves the entire length of the recurrent laryngeal nerves. Evaluation with a CT scan can also show signs of possible vocal cord paralysis.[11]

However, when patients present with vocal cord paralysis, direct laryngoscopy is usually considered before CT, and imaging is generally preferred as an adjunct study.[12] Flexible laryngoscopy has been shown to have excellent reliability when evaluating vocal fold motion.[13] Strobolaryngoscopy is an additional tool that can be utilized to evaluate vocal fold vibrations.[14]

Laryngeal ultrasonography is also a newer technique that can be considered when evaluating recurrent laryngeal nerve injury. One study evaluated 112 patients for vocal cord palsy using ultrasonography and compared this with laryngoscopy, the current gold standard. It showed that laryngeal ultrasonography was 83.3% sensitive and 97.2% specific for detecting vocal cord palsy and had a negative predictive value of 99%.[15]

Treatment / Management

The primary treatment options for recurrent laryngeal nerve injury include voice therapy or surgery. In general, early reinnervation techniques are based on the extent of nerve injury and the disease course. Less serious RLN injuries in which there is no definite transection of the nerve can usually be monitored for around six months with voice therapy as needed. If the recurrent laryngeal nerve becomes separated during surgical intervention, end-to-end anastomosis is performed to repair the nerve.[16]

After a period of conservative treatment, vocal fold medialization techniques can be implemented. This moves the affected vocal cord closer to the unaffected vocal cord, creating improved contact. Vocal fold medialization techniques can include medialization thyroplasties, injection laryngoplasty, arytenoid adduction, and laryngeal reinnervation.

Type 1 thyroplasty involves making an external incision to place an implant that permanently moves the affected vocal cord medially. Overall this is a safe procedure that has a low major complication rate, lower than outpatient thyroidectomy.[17]

Injection laryngoplasty is when the affected vocal cord is injected with a material, filling the vocal cord and moving it medially. These injectables can include carboxymethylcellulose, hyaluronic acid derivatives, collagen derivatives, calcium hydroxyapatite, or autologous fat/fascia. However, a Cochrane review has shown no definitive advantage or disadvantage for any specific material.[18]

Arytenoid adduction is a procedure that involves placing a permanent suture through the muscular portion of the arytenoid cartilage. This pulls the affected vocal cord medial to correct vocal cord paralysis secondary to RLN injury. The procedure is often utilized in conjunction with other corrective procedures.

Differential Diagnosis

The differential for recurrent laryngeal nerve injury with resulting vocal cord paralysis can include:

  • Iatrogenic – Endotracheal intubation or during surgical procedures of the skull base, neck, or chest

  • Malignancy – Especially of the skull base, neck, or chest

  • Trauma – Including the neck and chest in addition to the larynx

  • Neurological – Including stroke (specifically lateral medullary syndrome), bulbar palsies, and demyelinating diseases

  • Idiopathic – Diagnosis of exclusion

Prognosis

In general, recurrent laryngeal nerve injuries can be temporary or permanent, and prognosis can vary greatly based on a variety of factors including mechanism of injury and extent of the injury, to name a few. In addition, recovery can be complete or incomplete, highlighting the complexity of nerve injuries and prognosis.

Neuropraxia is the mildest injury. With this injury, the axon remains intact, and nerve function returns in 6-8 weeks. Axonotmesis involves damage to the axon and has varying degrees of severity and prognosis.[19] In one study that reviewed patients undergoing total thyroidectomy secondary to malignancy, 9.5% of patients had recurrent laryngeal nerve injuries resulting in vocal cord paresis with 22% of those becoming permanent, requiring additional interventions.[20] In general, patient prognosis is a complex topic that requires an individual approach for each patient.

Complications

One of the most serious complications is respiratory distress occurring from bilateral recurrent laryngeal nerve injury. However, this is rare, as unilateral RLN injury is much more common. Aspiration with resulting aspiration pneumonia is a substantial complication to consider in susceptible patients. In addition, the resulting dysphagia or voice changes from unilateral injury can still pose substantial morbidity to patients and affect the overall quality of life. This is especially true for patients who have a career based on the use of their vocal cords, such as speakers or singers.

Deterrence and Patient Education

Patients with recurrent laryngeal nerve injuries should be educated based on the suspected etiology. If the nerve injury occurred after surgical intervention where no transection of the nerve was noted, patients could generally be assured that the resulting vocal cord palsy is likely temporary. However, if concerning symptoms of underlying malignancy is present, the patient should be educated about the importance of follow-up. In general, patients with no concerning signs of underlying malignancy or trauma can be reassured that one of the leading causes of injury is idiopathic and typically not permanent. Although, as previously stated, patients should undergo appropriate workup as this is a diagnosis of exclusion.

Enhancing Healthcare Team Outcomes

Recurrent laryngeal nerve injury with resulting vocal cord paralysis is a complicated condition that requires an interdisciplinary approach. Physicians and nurses in the primary care setting may be required to evaluate patients presenting with RLN injury from a variety of etiologies and will need to determine the clinical management of the patient. This requires input from additional specialists. Most notably, ENT evaluation with laryngoscopy is necessary as an initial assessment. Radiology is also helpful for any adjunct evaluation with CT imaging.

Once the etiology of the RLN injury is identified, clinical management can be decided by the team. Of note, a recent review article shows the improved reliability and accessibility of reinnervation techniques in the management of RLN injury.[21] Overall, recurrent laryngeal nerve injuries can be evaluated on a case-by-case basis and often require healthcare team input for proper evaluation and management. [Level 5]

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Laryngeal Nerve Injury — Clinically Oriented Anatomy Moore

Table of Contents

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Rekurrens

Image: “Strumaresection; N.laryngeus recurrens completely.” by THWZ – Own work. License: CC BY-SA 3.0


Anatomy and Function of the Recurrent Laryngeal Nerve

Drawing of the left recurrent laryngeal nerve

Image: “Drawing of the left recurrent laryngeal nerve.” by Jkwchui – Based on drawing by Truth-seeker2004. License: CC BY-SA 3.0

The recurrent laryngeal nerve (RLN) receives sensory innervation from the trachea, esophagus, and pyriform sinus before it enters the larynx deep into the inferior constrictor muscle and posterior to the cricothyroid articulation. The inferior thyroid artery and its branch, the inferior laryngeal artery, are responsible for blood supply to the RLN, which may pass anteriorly, posteriorly, or between the branches of the inferior thyroid artery.

Motor fibers of the RLN supply the lateral and posterior cricoarytenoid and thyroarytenoid muscles, as well as the oblique and transverse interarytenoid muscles. The posterior cricoarytenoid muscle is responsible for the abduction of vocal cords, while the thyroarytenoid, interarytenoid, and lateral cricoarytenoid muscles are responsible for the adduction of the vocal folds. The RLN supplies motor innervation to the inferior constrictor and cricopharyngeus muscles and provides sensory innervation to the subglottis and vocal-fold mucosa.

Anatomy of the vocal folds

There are two pairs of vocal folds; the true folds consist of muscles, ligaments, and lining mucosa. The false folds are present superior to the true folds. The laryngeal ventricle is a recess that separates true folds from the false. Vocal folds extend from the arytenoid cartilage posteriorly to the midline anteriorly. Both vocal folds approximate only during Valsalva and cough. True vocal folds divide the larynx into supraglottic, glottic, and subglottic compartments.

The laryngeal muscles can be subdivided into intrinsic and extrinsic muscles. The former is responsible for the mobility of vocal folds and phonation, and includes the posterior and lateral cricoarytenoid, interarytenoid, cricothyroid, and thyroarytenoid muscles. During inspiration, true vocal folds are abducted laterally, while during phonation, they move medially towards the midline.

All intrinsic muscles of the larynx are innervated by the RLN except the cricothyroid muscle, which is innervated by the external branch of the superior laryngeal nerve. The RLN is responsible for sensory innervation of laryngeal mucosa in the region inferior to the vocal folds.

Pathology of Recurrent Laryngeal Nerve Injury

Recurrent laryngeal nerve paralysis can involve the left, right, or both RLNs. The left RLN, being more superficial and longer running from the chest up through the neck, is more susceptible to injury than the right nerve. Injury can be due to surgery, trauma, bacterial or viral infections, neurotoxic drugs, or tumors.

Causes of Recurrent Laryngeal Nerve Injury

Right RLN injury arises due to the following:

  • Neck trauma
  • Benign or malignant thyroid disease
  • Carcinoma of the esophagus
  • Surgical trauma
  • Subclavian artery aneurysm
  • Idiopathic causes (mainly viral neuritis)
  • Cervical lymphadenopathy

Left RLN injury is likely to arise due to the following:

  • Trauma
  • Thyroid diseases
  • Thyroid and esophageal carcinomas
  • Cervical lymphadenopathy
  • Bronchogenic carcinoma
  • Aortic aneurysm
  • Enlarged left auricle
  • Intrathoracic surgery
  • Idiopathic

Bronchogenic carcinoma is an important cause that must always be ruled out in the case of left RLN injury. The most common cause is non-thyroid cervical surgery. Paralysis of the RLN can occur due to central causes affecting the nucleus ambiguus and its associated vagus nerve, and also result from conditions such as bulbar and pseudobulbar palsy, jugular foramen syndrome, and parotid tumors. Other lesions can be due to demyelinating diseases, skull base tumors, and cerebrovascular accidents.

RLN injury in the neck is due to thyroid tumors or surgery, cervical spine surgery, esophageal tumors, and deep penetrating wounds to the neck.

RLN injury in the chest may occur due to cardiac surgery, lung cancer, pulmonary tuberculosis, oesophageal cancer, mitral stenosis, and thoracic aortic aneurysm.

Bilateral RLN paralysis can be fatal. It is mostly caused during thyroid and cervical surgeries, trauma, endotracheal intubation, central brain disorders, diabetic neuropathy, organophosphorus poisoning, myasthenia gravis, and neurodegenerative disorders such as poliomyelitis and amyotrophic lateral sclerosis.

Clinical Manifestations of Recurrent Laryngeal Nerve Injury

The RLN is responsible for motor innervation of the laryngeal muscles. Injury to the nerve leads to the loss of adduction and abduction of vocal foldsand results in its subsequent dysfunction during phonation, breathing, and deglutition.

In unilateral nerve injury, the paralyzed vocal fold is situated in the paramedian or partially lateral position and does not affect the airway patency, although phonation and deglutition are affected. However, compensation by the contralateral vocal folds may help in phonation. Therefore, unilateral RLN injury leads to hoarseness of voice and dysphagia that may improve and lead to asymptomatic presentations.

The airway is patent (without obstruction) due to abduction of the vocal folds. During phonation, a weak voice results due to the escaping air from the partially closed glottis. Deglutition, especially that of fluids, is impaired in glottal incompetence. Additionally, central lesions of the vagus nerve may cause sensory loss.

In bilateral injury that is mostly sustained during surgery, serious manifestations may be witnessed as soon as the patient is extubated.

Bilateral paralysis of the vocal folds can lead to stridor, difficulty in breathing, and aspiration. Breathing can be mildly distressed or severely impaired with biphasic stridor. The positioning of the denervated vocal folds is close to the midline and the glottis shows a narrow opening. Phonation may still be preserved in bilateral paralysis, but with inadequate intensity. Preoperative assessment of vocal-fold function is mandatory for legal purposes. Postoperative assessment is required for early detection of a malfunction, even if the patient is asymptomatic.

Diagnosis of Recurrent Laryngeal Nerve Injury

Patient history may often exclude factors such as heavy-metal neurotoxicity caused by lead and mercury, neurodegenerative disorders, alcoholism, diabetes, and neurotoxic drugs including phenytoin and isoniazid. Therefore, accurate medical history is essential to evaluate the possible etiology. MRI/CT of the head, neck, and chest, and esophagoscopy may be helpful in diagnosing neoplastic lesions affecting the nerve.

Vocal folds can be examined using indirect or fiberoptic laryngoscopy. Rigid laryngoscopy is helpful in differentiating between neurogenic paralysis of the vocal folds and cricoarytenoid arthritis secondary to prolonged endotracheal intubation or rheumatoid arthritis.

Management of Recurrent Laryngeal Nerve Injury

Unilateral nerve injury can be managed conservatively for up to 6 months to allow for spontaneous healing in the case of neurapraxia. For total nerve transection during surgery, corrective surgery should be considered as early as possible. Surgical intervention includes augmentation, medicalization, and reinnervation to improve voice quality. Electromyography is considered to assess spontaneous recovery or determine the need for corrective surgery. Nimodipine has been suggested for the treatment of idiopathic and iatrogenic unilateral and bilateral vocal-fold paralysis without total transection, as it helps with neuronal regeneration and recovery.

Vocal fold augmentation (injection laryngoplasty) involves transoral or transcervical injection of collagen, hyaluronic acid, and autologous fat into the paralyzed cord. This results in bringing the paralyzed cord closer to the midline to prevent aspiration and cough, and improves phonation.

Medialization thyroplasty is performed by inserting an implant lateral to the paralyzed cord to shift it medially. Silicone or Gore-Tex sheets are implanted using a transcervical approach through the thyroid cartilage; these sheets are adjustable and allow for tuning of the voice.

Reinnervation of the vocal folds can be achieved using microsurgical techniques, but are met with limited success.

In the case of bilateral nerve injury, patients need breathing assistance and airway reconstruction. Permanent or temporary tracheostomy, endotracheal intubation, and reinnervation are emergency procedures that can be performed if required. Posterior establishment of the airway through the glottis using laser cordectomy is ideal to improve both breathing and quality of phonation. This is achieved via partial transection of the cords and arytenoid to establish an airway through the glottis. Some patients can benefit from lateralization of the vocal cords after arytenoidectomy; however, the outcome of this procedure on the quality of phonation is not satisfactory.

Sours: https://www.lecturio.com/magazine/recurrent-laryngeal-nerve-injury/

You will also be interested:

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