Keywords

1 Applied Anatomy of the Laryngeal Nerves

The proper vagus nerve (VN) emerges from the cranial vault through the jugular foramen. It descends following the carotid axis, initially located medial to the internal jugular vein (IJV) and then in the posterior position between IJV and the internal carotid artery (ICA).

The cervical branches of the VN consist of the superior laryngeal nerve (SLN) and the inferior laryngeal nerve, also known as recurrent laryngeal nerve (RLN). The SLN arises from the center of the nodose ganglion, 3–4 cm below the jugular foramen. It descends medially to the ICA and, after 1.5–2 cm, to the external carotid artery. The SLN includes two branches: the internal branch, which supplies sensory fibers to the pharynx, and the external branch, which innervates the cricothyroid muscle [1]. The external branch is essential in the contraction of the true vocal fold, providing timbre to the voice. Moreover, it plays a role in the glottic closure reflex, which prevents aspiration during deglutition. The anatomy of the SNL is extremely variable. Cernea et al. [2] proposed a classification of the SNL anatomic variables: type 1 nerve, as the most common nerve variation, crossing the superior thyroid vessels >1 cm above the superior thyroid pole; types 2A and 2B, where the nerve crosses <1 cm above the superior pole or below its upper border, respectively.

The RLNs originate from the VN anterior to the aortic arches. Since the heart and great vessels migrate caudally and the neck elongates cranially during the embryological development, the RLNs are pulled down by the aortic arches. The right RLN loops around the subclavian artery and travels superiorly and medially toward the tracheal-esophageal groove. It runs for about 5–6 cm along the tracheal-esophageal groove with a more oblique angle on the sagittal plane compared to the left RLN [3]. Then, the nerve runs superiorly, it courses between the trachea and the thyroid gland before entering into the larynx. The left RLN passes anteriorly to the aortic arch before looping around the arch and traveling superiorly and medially toward the tracheal-esophageal groove.

The terminal part of the RLNs enters the larynx, underneath the thyroid gland, deep to the inferior border of the inferior pharyngeal constrictor muscle, posterior to the cricothyroid muscle (Fig. 16.1a,b). The nerve usually runs posterior to the middle thyroid vein and the cricothyroid joint. The relationships between the RLNs and the inferior thyroid artery (ITA), which represent one of the most important landmarks, is much more variable. On the left side, the nerve trunk lays posteriorly and anteriorly to the ITA in 52.1% and 13.7% of cases, respectively, while it may pass between the artery’s branches in 25.4% of cases. On the right side, the nerve trunk lays posteriorly and anteriorly to the ITA in 23% and 25.5% of cases, and between its branches in 36.5% of cases [3]. The presence of an aberrant right subclavian artery, also known as arteria lusoria, originating from the aortic arch, is associated with the presence of a right non-recurrent inferior laryngeal nerve (NR-ILN) (Fig. 16.1c). The incidence of this rare anatomic variant is reported to be between 0.3% and 0.8% of cases. On the left side, the NR-ILN may exceptionally occur in 0.004% of cases and it is typically associated with a right aortic arch with situs inversus. The presence of a NR-ILN can be preoperatively anticipated by preoperative bedside ultrasound scan, indicating the presence of an aberrant right subclavian artery (arteria lusoria) [4].

Fig. 16.1
Three intraoperative views of recurrent laryngeal nerves are labeled A to C. Surgical instruments part the skin, R L N prepared and the right inferior laryngeal nerve is revealed.

(a, b) Intraoperative view of recurrent laryngeal nerves (a right RLN, b left RLN) prepared along their entire cervical course, up to their entrance into the larynx. (c) Non-recurrent right inferior laryngeal nerve arising from the vagus nerve at cervical level

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Fibers that originate from the superior cervical sympathetic ganglion are connected with the RLN and develop the sympathetic-inferior laryngeal anastomotic branch (SILAB). They are usually thin, but sometimes have the same diameter as the RLN and are misinterpreted as a NR-ILN (Fig. 16.2a), which explains the reported coexistence of RLN and NR-ILN in the same patients [5]. A large SILAB, with the same diameter as the RLN, was found on the right side in 1.5% of right RLN in clinical studies and in 17% of cases in anatomical studies [6]. NR-ILNs may be connected with the sympathetic chain via large a SILAB mimicking a normal RLN (Fig. 16.2b).

Fig. 16.2
Two close-ups of the superior cervical sympathetic ganglion connected with the R L N and a large S I L A B connecting an N R-I L N with the sympathetic chain are labeled a and b, respectively.

(a) A large sympathetic inferior laryngeal nerve anastomotic branch (SILAB) mimicking a non-recurrent inferior laryngeal nerve (NR-ILN). Following it along its entire course makes it possible to determine that it does not originate from the vagus nerve. (b) A large SILAB connecting a NR-ILN with the sympathetic chain (stellate ganglion) can be misinterpreted as a normally recurrent inferior laryngeal nerve if not followed up to its origin

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Accurate knowledge of the aforementioned anatomical variants is crucial for the correct identification of structures during surgical dissection and the prevention of laryngeal nerve injury.

2 Etiology, Prevalence and Risk Factors

Postoperative inferior laryngeal nerve injury can be transient or permanent, the latter defined by the lack of recovery of vocal cord function at 6–12 months after surgery. The prevalence of the post-thyroidectomy inferior laryngeal nerve injuries is widely variable, being influenced by the definition, based on routine or selective (in case of symptoms) laryngoscopic assessment, patient selection and surgical experience. The reported prevalence varies from 1.4% to 13.1% for transient palsy and from 0.4% to 3.5% for permanent lesions [7].

SLN damage may occur during the surgical dissection of the thyroid upper poles. To date, the incidence of lesions of the superior laryngeal branch is still unknown. Indeed, such surgical damage turns out to be extremely variable also based on the diagnostic techniques used to identify it. Whether laryngoscopy and phoniatric clinical evaluation are used, palsy rates range from 0% to 6%. When more accurate examinations, such as laryngeal electroneuromyography, are included in the analysis, higher rates are reported (up to 58% of cases) [8].

Disease- and patient-related factors (i.e., revisional surgery, large intrathoracic goiters, chronic thyroiditis or Grave’s disease, malignancy with extrathyroidal extension and paratracheal lymph node dissection, old age, smoking habit, diabetes, small size RLN) and inadequate surgical experience represent risk factors for RLN injury.

The neural damage to the laryngeal nerves may differ, leading to different recovery times. The physical mechanisms that may lead to nerve damage are stretching, crushing, diathermal injury and transection. Neurapraxia is defined as a temporary block of nerve conduction, and it usually heals spontaneously and completely within a few weeks. Axonotmesis is a myelin sheath lesion, with macroscopically intact nerve. Since axonal regrowth is spontaneous, the resulting muscular contraction, as well as the voice, may be of poor quality. Neurotmesis is defined as an interruption of the endoneurial, perineurial and/or epineurial sheaths. In this case, the nerve regrowth has low quality and muscular contractions are poor or even absent. Despite the operative finding of a macroscopically intact nerve, axonal regrowth is a slow process and is considered definitive after a 12-month period. If the neural sheath is interrupted or the nerve is frankly divided, axonal regrowth is uncertain and often of poor quality. Of note, limited arytenoid movement and impaired vocal fold movement are reported in 11% of patients after arytenoid dislocation due to endotracheal intubation [9].

3 Clinical Manifestations and Diagnosis

The external branch of the SLN innervates the cricothyroid muscle, which contributes to lengthening of the vocal fold and (along with cricoarytenoid muscle) regulation of the vocal fundamental frequency; its injury is clinically mild and its identification is often difficult. The spoken voice tends to be only slightly affected, while the singing voice is more influenced. In particular, the voice is weak, breathy, monotonous and characterized by inability to achieve high tones with weakness and increased effort to speak [10].

Clinical manifestations of a unilateral RLN nerve palsy are weak and breathy voice with a loss of vocal projection and phonation time, hoarseness, and dysphonia. Aspiration with dysphagia (in particular for liquids) may sometimes occur but is only rarely associated with aspiration pneumonia. The patient may also notice an inability to perform a Valsalva maneuver. Laryngospasm may occur because of a sudden, forceful, opposition of the glottic and supraglottic structures, and usually appears several weeks after surgery.

Bilateral RLN paralysis causes adduction of the vocal cords during inspiration, leading to obstruction of the airway with acute life-threatening dyspnea and aphonia and requiring emergent tracheotomy or re-intubation.

Laryngeal paralysis can also impair other functions that require tight glottal closure, such as coughing and stabilization of the thorax for heavy lifting. Symptoms frequently change over time because of the recovery of motion on the paralyzed side, the development of contralateral compensatory function or the shifting of vocal fold position toward the midline.

An essential component of the examination for dysphonia is inspection of the larynx via either flexible or rigid video laryngoscopy to assess the positioning and motility of the vocal cords. Laryngoscopy can detect a gradual shift of the paralyzed vocal fold toward median and paramedian position. In general, vocal symptoms are directly related to the distance of the paralyzed vocal fold from the midline. The voice is weak when the glottis cannot close completely during phonation, and it becomes breathy or aphonic when the glottic gap is large.

Laryngeal electromyography for the diagnosis and management of laryngeal paresis/paralysis is useful for differentiating neural disruption from structural immobility, evaluating the electrical activity of the muscles within the larynx and predicting which patients will not recover vocal fold motion after a nerve injury [11].

4 Prevention and Management

In cases of previous cervical surgery or clinical examination that suggests vocal abnormality, preoperative laryngeal examination is mandatory in order to detect pre-existing laryngeal dysfunction. In the other cases, preoperative laryngeal examination is recommended. About 20% of patients show vocal and swallowing impairments without evidence of RLN nerve injury and age > 50 years is reported as an independent risk factor [12].

Routine identification and dissection of the RLN course during thyroidectomy is the gold standard to prevent injury. A meticulous dissection technique, avoidance of excessive traction, a judicious choice of hemostatic techniques and correct nerve exposure maneuvers prove to be essential in order to preserve the nerve.

The use of intraoperative intermittent or continuous nerve monitoring (IONM) has been widely investigated to assess RLN functional integrity during surgery. However, it should not replace an appropriate and meticulous surgical technique and knowledge of RLN anatomy and its variations [13]. The use of IONM is recommended in thyroid cancer surgery, in patients with locally advanced disease and/or massive central neck nodal involvement, in reoperations and in the case of previous documented vocal cord paralysis. However, despite routine IONM use is not recommended by all the guidelines, it is a valuable adjunct in all thyroid surgeries, since complex anatomy and difficult dissection cannot be anticipated in all cases. IONM can confirm the visual identification of the RLN and provide guidance for the surgeon, particularly in difficult situations. It helps to identify anatomic variations of the nerve, and in particular to distinguish motor and sensory fibers in the case of extra laryngeal branches. IONM findings are accurate in predicting postoperative vocal cords motility. In a review by Schneider et al. [14] the negative predictive value of loss of neuromonitoring signal (LOS) and early vocal fold paralysis (VFP) for intermittent and continuous IONM ranged from 97.3–99.8% to 99.8–100%, respectively, while the positive predictive value from 37.8–80.5% to 47.6–88.2%, respectively. LOS is commonly subdivided into segmental LOS type I, with a clear point of injury, or global LOS type II, where the level of injury cannot be defined. Although IONM quite accurately predicts transient VFP in the first postoperative days, the transition to a permanent (6–12 months postoperatively) paralysis is not clear in the absence of intraoperative evidence of inadvertent or planned transection.

It has been recently demonstrated that type II LOS with preserved arytenoid motility on postoperative day 15, evaluated at fibro laryngoscopy, is associated with recovery of vocal cord motility [15].

Postoperative laryngoscopic examination should be performed in every patient who underwent thyroid surgery (Fig. 16.3).

Fig. 16.3
A postoperative view of the right vocal fold palsy in paramedian position.

Right vocal fold palsy in paramedian position

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Patients with VFP and dysphonia are best treated by a team effort between the otolaryngologist and a speech-language therapist. They can implement potentially useful compensatory strategies while identifying and eliminating behaviors that might be counterproductive. Early voice therapy may enable significant improvement in vocal function [16]. In addition, treatment with corticosteroid [17] and vitamin B complex may be useful in the early phases.

Although VFP is by definition a hypofunctional disorder, patients may exhibit a compensatory hyperfunctional behavior, such as muscle tension dysphonia [18]. VFP results in glottic insufficiency, reduced subglottic pressures and less airway protection during swallowing. This may determine aspiration, which can be identified by history or development of an aspiration pneumonia. Such a condition may be evaluated with a fiberoptic endoscopic examination of swallowing function or an upper gastrointestinal contrast study. Swallow therapy often includes the clinical observation of patients during meals and the teaching of techniques to obtain a safer swallow. Such techniques may include head inclination, chin tuck, effortful swallow and the supraglottic swallow technique.

When voice therapy does not provide a positive effect, in particular when the glottic gap is wide because the immobile vocal fold lies in abducted or intermediate position, injection laryngoplasty may be indicated. In this procedure, a bulking material is injected into the true vocal fold in an attempt to medialize the edge of the vocal fold. Some of the approved injection materials are hyaluronic acid, carboxymethylcellulose, and calcium hydroxyapatite. In addition, injection laryngoplasty can be performed using centrifuged autologous fat, which reduces the risk of allergic reactions and local granulomatosis possibly caused by synthetic materials [19] (Fig. 16.4).

Fig. 16.4
Two photographs of laryngoscopy evaluation after autologous fat injection. The evaluations are recorded after three and six months and are labeled a and b, respectively.

(a) Three-month laryngoscopy evaluation after autologous fat injection. (b) Six-month laryngoscopy evaluation after autologous fat injection

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Laryngeal reinnervation of a paralyzed vocal fold of a severed, avulsed or sacrificed RLN, with an intraoperative direct repair end-to-end anastomosis, does not restore normal motion but usually results in a vocal fold fixed in a favorable median or paramedian position. The reinnervated vocal folds are usually positioned toward the median position. This situation is better described as synkinesis, simultaneous contraction of adductors and abductors. In cases showing extreme misdirection in reinnervation, however, paradoxical motion of the vocal folds may occur. The most common indication for reinnervation is a unilateral neurogenic RLN injury with no expectation for recovery. Reinnervation could thus be applied intraoperatively in cases where nerve sacrifice is expected or unavoidable [20].

Also, the ansa cervicalis-to-recurrent laryngeal nerve anastomosis is an established technique for the reconstruction of RLN involved in cancer or scar processes. The presence of a distal RLN stump and ansa cervicalis is necessary to proceed with this type of anastomosis. The nerve should be released to permit a tension-free anastomosis and the neurorrhaphy has to be performed using 8–0 nylon sutures and placing two to four epineural sutures around the anastomosis. When this approach is chosen, a recovery time close to 6–12 months should be considered.

Bilateral vocal fold immobility (BVFI) is a different entity from unilateral dysfunction as it affects breathing more than voice. In cases of thyroidectomy, the underlying process will be neurogenic in the majority of cases, secondary to an injury to both RLNs. Bilateral RLN injury will result in flaccid paralysis of the bilateral vocal fold. In addition, a certain amount of laryngeal edema from the intubation and procedure is to be expected. This combination may create a restriction of airflow, especially if the vocal folds are fixed in a median or paramedian position. When BVFI occurs, especially if the vocal folds are in adducted position, the patient typically wakes up from surgery demonstrating acute, persistent and worsening inspiratory stridor, increased work of breathing and respiratory failure. These patients usually require urgent airway management, either intubation or surgical. After reintubation, treatment with high doses of corticosteroids for at least 24–48 hours may be useful with subsequent laryngoscopic reassessment [21].

In some cases, if presentation is mild, patients can be supported with positive pressure ventilation until they fully wake up and are able to better control their breathing. BVFI can be confirmed on-site using direct or indirect laryngoscopy. Other patients may be diagnosed later on as they present for routine postoperative follow-up or because they show signs of breathy dysphonia or dyspnea on exertion.

The treatment of BVFI is guided by the symptomatology of the patient and prognosis for recovery. Unless transected, the RLN holds potential for recovery over the next 6 to 12 months. Thus, in selected cases observation could be acceptable for patients with minimal symptoms. Tracheotomy can be an acceptable solution for patients with a permanent or transient palsy while waiting for nerve recovery. Vocal fold or arytenoid lateralization (or laterofixation) has also been described as a reversible approach to enlarge the airway in cases of temporary BVFI. More definitive surgical options include medial arytenoidectomy, described by Crumley [22], which attempts to improve airway size by creating a concavity along the glottic edge of the body of the arytenoid cartilage, leaving the vocal process and attachment of the vocal ligament intact. Transverse cordotomy, as described by Kashima [23], is performed by making a transverse cut through the vocal fold just anterior to the vocal process without exposing cartilage. Novel treatments exist, including adductor botulinum toxin injection, selective bilateral laryngeal reinnervation, and laryngeal pacing, but the evidence is still scarce, and the research is ongoing [24].

5 Conclusions

Laryngeal nerve palsy represents one of the most frequent complications of thyroid surgery. Thorough knowledge of anatomy, adequate surgical skills, meticulous dissection, possibly associated with IONM, are essential for its prevention. Nonetheless, if a laryngeal nerve palsy occurs proper patient information and adequate multidisciplinary management involving otolaryngologist and speech-language therapist are necessary.