Arytenoid Fixation 

Updated: Jul 27, 2021
Author: Paul C Bryson, MD; Chief Editor: Arlen D Meyers, MD, MBA 

Overview

Practice Essentials

Function of the cricoarytenoid (CA) joint depends on the complex interaction of several cartilaginous, muscular, and ligamentous structures. Any process affecting the normal neuromuscular inputs, supporting connective structures, or joint space may result in altered function and immobility. As a broad entity, CA (vocal-fold) immobility has dissonant etiologies, including central nervous system (CNS) pathology, neuromuscular disease, malignancy, local trauma, and psychogenic causes. Among these, cricoarytenoid (CA) joint fixation is a recognized, albeit relatively uncommon, entity. The terms cricoarytenoid (CA) immobility and cricoarytenoid (CA) fixation are often used inexactly and interchangeably; such use blurs their distinctions. See the image below.

Cartilages of the larynx, posterior view. Cartilages of the larynx, posterior view.

This discussion is limited to cricoarytenoid (CA) fixation resulting from altered function of the cricoarytenoid (CA) joint, which must be distinguished from other causes of vocal fold immobility to allow for timely diagnosis and effective treatment.

Workup in cricoarytenoid fixation

Operative direct laryngoscopy is the criterion standard for clinical evaluation of cricoarytenoid (CA) joint mobility.

Electromyography of the thyroarytenoid, cricothyroid, and posterior cricoarytenoid (CA) muscles help to clarify the status of laryngeal innervation, while videostroboscopy, electromyography, and computed tomography (CT) scanning may help to distinguish a fixed cricoarytenoid (CA) joint from an immobile vocal fold resulting from another cause.

Management of cricoarytenoid fixation

In general, acute cricoarytenoid (CA) rheumatoid arthritis is treated medically with anti-inflammatory and analgesic medications (with or without systemic steroid therapy).

Surgical procedures addressing arytenoid fixation can be organized into two categories. Techniques in the first group attempt to mobilize the cricoarytenoid (CA) joint in a manner analogous to joint mobilizations in the limbs. Techniques in the second group are based on the concession that the joint is irreparably fixed; they focus on improving the airway by alternative means.

Problem

Cricoarytenoid (CA) fixation, in contrast to other forms of vocal fold immobility, is a direct result of restricted joint motion without regard for the neuromuscular integrity of the larynx. This discussion is limited to processes affecting the joint space and resulting in loss of mobility.

Etiology

After cricoarytenoid (CA) joint fixation is diagnosed, determining the etiology is of paramount importance for therapeutic decision making. Following are the 3 general categories of causes of cricoarytenoid (CA) fixation:

  1. Arthritides, primarily rheumatoid arthritis, account for many clinical diagnoses of cricoarytenoid (CA) fixation. Other known causes of joint arthritis include gout, Reiter syndrome, and ankylosing spondylitis. Anecdotal evidence suggests a mumps-associated laryngeal arthritis. This category also may include fixation secondary to radiation therapy.

  2. Direct bacterial involvement of the joint space with infectious agents, such as streptococcal species, with resultant ankylosis is recognized.

  3. Direct or external laryngeal trauma may result in joint injury. Mechanisms of intubation-related joint injury are suggested. These include posterior or anterior arytenoid displacement secondary to the distal tip of the endotracheal tube engaging the arytenoid during intubation. Some have noted the possibility of posterior dislocation resulting from extubation with a partially inflated endotracheal tube cuff. Another potential cause is arytenoid chondritis secondary to prolonged endotracheal intubation, which ultimately results in fibrosis. Zhong et al reported on a patient who experienced arytenoid dislocation following anterior cervical corpectomy and fusion.[1]

Previous authors have speculated that long-term paralysis with resultant cricoarytenoid (CA) immobility may lead to joint fixation, as observed in other diarthrodial joints in the body. However, histologic studies have failed to demonstrate this association.

A study by Tanaka et al reported that in transoral videolaryngoscopic surgery for hypopharyngeal and supraglottic cancer, resection of the medial and lateral pyriform sinus can lead to postoperative voice impairment; consequent to the operation, scar contracture around the cricoarytenoid joint can fix the arytenoid cartilage toward the lateral position and patients can experience insufficient glottic closure.[2]

Pathophysiology

Laryngeal manifestations of arthritis, specifically rheumatoid arthritis, have been recognized for more than a century. The pathologic features of laryngeal rheumatoid arthritis are identical to those of other involved joints in the body.

The soft tissues surrounding the joint may have typical rheumatoid stigmata, including rheumatoid nodules.

Presentation

History

The typical history of a patient with cricoarytenoid (CA) fixation is identical to that for patients with other forms of joint immobility. Depending on the position of the immobilized vocal fold and the unilateral or bilateral nature of the dysfunction, symptoms may range from mild dysphonia to frank aspiration and even acute airway compromise. The diagnosis is contingent on the exclusion of the many other causes of immobility, and appropriate confirmatory examinations and studies are necessary.

Physical

In patients with an appropriate clinical history for cricoarytenoid (CA) fixation, physical examination should include complete head-and-neck examination, indirect laryngoscopy, and at least a cursory musculoskeletal survey. Operative direct laryngoscopy is the standard for clinical evaluation and definitive diagnosis of cricoarytenoid (CA) joint fixation (see Diagnostic Procedures).

In laryngeal rheumatoid arthritis, indirect laryngoscopy in the acute phase reveals erythema and swelling of the arytenoid mucosa. On clinical evaluation, 17-33% of patients with rheumatoid arthritis have identifiable laryngeal disease. Manipulation of the larynx is painful if the patient is awake. In the chronic stages of the disease, pain is unusual, and mucosal changes are somewhat less pronounced than before because they appear rough and thickened. Lateral bowing of the cords in inspiration, an uncommon finding in laryngeal paralysis, may be observed in both acute and chronic phases if both joints are involved.

Relevant Anatomy

The cricoarytenoid (CA) joint is a diarthrodial joint that includes a synovial lining and a fluid-filled bursa. The joint capsule and the ligamentous attachments, including the cricoarytenoid (CA) ligament, vocal ligament, and false vocal folds, limit normal motion of the joint. Motion of the arytenoid is characterized primarily as the arytenoid rocking over the long axis of the cricoid facet and gliding parallel to the long axis, as well as a small component of axial movement pivoting on the cricoarytenoid (CA) ligament. Three-dimensional analysis of cricoarytenoid mobility has demonstrated that the arytenoid has rotated superiorly, posteriorly, and laterally in full abduction.[3]

 

Workup

Imaging Studies

Although CT scanning may help in demonstrating arytenoid dislocation or cartilaginous fracture, the extent of ossification of the laryngeal cartilage and the plane and thickness of the sections limit the sensitivity of CT. In patients in whom the arytenoid is not ossified (ie, children, young adults), CT imaging is relatively unrevealing.

Plain radiography of the neck and larynx occasionally reveals evidence of cricoarytenoid (CA) joint pathology. Joint erosion and blurring may demonstrate active arthritis.

A retrospective study by Ravanelli et al reported that in patients with cT3 laryngeal squamous cell carcinoma (SCC), signal patterns from magnetic resonance imaging (MRI) with surface coils can indicate the etiology of arytenoid fixation. The investigators found that a normal signal pattern and one characterized by T2 hyperintensity, with no diffusion-weighted imaging (DWI) restriction, tend to be associated with arytenoid fixation stemming from mass effect and/or an inflammatory reaction. However, an intermediate T2 signal with DWI restriction strongly suggests arytenoid fixation resulting from neoplastic invasion.[4]

Diagnostic Procedures

Electromyography of the thyroarytenoid, cricothyroid, and posterior cricoarytenoid (CA) muscles help to clarify the status of laryngeal innervation. In general, a normal pattern of laryngeal-muscle activation and recruitment is expected in a patient with isolated cricoarytenoid (CA) fixation.

Videostroboscopy, electromyography, and CT scanning may help to distinguish a fixed cricoarytenoid (CA) joint from an immobile vocal fold of another cause. Of these examinations, videostroboscopy is the most readily available and useful to determine the exact position of the arytenoid, to assess subtle movements, and to determine the relative positions of the vocal folds, which may help to narrow the differential diagnoses.

With regard to electromyography, however, a retrospective study by Martínez-Martínez et al indicated that in patients with vocal fold immobility but normal laryngeal electromyography results, it is best not to assume that the immobility has resulted from cricoarytenoid (CA) fixation. The investigators found that immobility in such patients stemmed from a variety of causes, including idiopathic and iatrogenic etiologies, as well as central nervous system damage and external compression.[5]

Operative direct laryngoscopy is the criterion standard for clinical evaluation of cricoarytenoid (CA) joint mobility.

  • The recommended technique requires that the patient be under general anesthesia with deep paralysis.

  • In the ideal situation, the patient is in laryngeal suspension, and the examiner uses 1 hand to externally stabilize the larynx while attempting endoscopic manipulation of the arytenoid.

  • This technique is intended to avoid misinterpreting movement of the entire larynx as arytenoid mobility.

  • Surrounding tissues, as well as the arytenoid, should be palpated to determine the presence of scarring or associated lesions.

  • Lateral displacement of 1 arytenoid accompanied by passive medial movement of the other may indicate interarytenoid tethering.

  • Careful attention to the exact placement of the laryngoscope is also important.

  • Placement of the blade too deeply in the laryngeal inlet may artificially restrict motion.

  • Note any associated subglottic stenosis and/or tracheal stenosis at the time of endoscopy.

Histologic Findings

Histologic involvement of the cricoarytenoid (CA) joint was found in 47-78% of patients with rheumatoid arthritis examined on postmortem studies.

Early changes include thickened synovium and cellular hyperplasia with a plasma cell and/or lymphocytic infiltrate. Late changes include effusions originating from the hypertrophied lining leave fibrin deposits within the joint cavity. Progressive alterations lead to destruction of the articular surfaces. The ultimate loss of joint space is secondary to a reparative process laying down vascular, fibrous, and fatty tissue.

 

Treatment

Medical Therapy

In rheumatoid arthritis involving the larynx, treatment options depend on the chronicity of the disease. In general, acute cricoarytenoid (CA) rheumatoid arthritis is treated medically with anti-inflammatory and analgesic medications (with or without systemic steroid therapy). Adjunctive vocal rest, local heat, and humidification may prove helpful. Periarticular local steroid injections have helped in ameliorating acute joint dysfunction.

Treatment of infectious causes of joint fixation requires appropriate antimicrobial therapy for the infecting agent.

Surgical Therapy

Surgical procedures addressing arytenoid fixation can be organized into 2 categories. Techniques in the first group attempt to mobilize the cricoarytenoid (CA) joint in a manner analogous to joint mobilizations in the limbs. For example, in joint fixation resulting from traumatic fracture or dislocation of the cricoarytenoid (CA) joint, expedient relocation of the displaced arytenoid appears to be the procedure of choice, similar to the treatment choice for a dislocated knee or shoulder. Techniques in the second group are based on the concession that the joint is irreparably fixed; they focus on improving the airway by alternative means. This second category also applies to causes of glottic airway restriction other than joint ankylosis.[6]

In 1986, Schaefer et al described a surgical procedure for mobilizing fixed cricoarytenoid (CA) joints.[7] This procedure was performed through a midline thyrotomy in which a superiorly based mucosal flap was elevated from the arytenoid and posterior commissure mucosa. The medial aspect of the cricoarytenoid (CA) joint was then explored, and adhesions in the joint space were lysed until the arytenoid was thought to gain passive mobility. The posterior glottis was expanded by advancing the mucosal flap. Finally, a modified endotracheal tube (Portex stent; Smiths Medical, Kent, United Kingdom) was secured in the glottis to temporarily support the arytenoids in a lateralized position; it was removed approximately 2-3 weeks after surgery during a brief endoscopic procedure.

This procedure was performed in 4 patients, and the cannula was later removed in 3. The authors strongly believed that early postoperative speech therapy improved the range of motion of the cricoarytenoid (CA) joint and, consequently, the final functional outcome.

Closed reduction can be effectively used to treat arytenoid dislocation, according to a prospective study by Lee et al, with early surgical intervention improving outcomes of this procedure. The study involved 22 patients with arytenoid dislocation, including 16 with anterior dislocation and 6 with posterior dislocation. Patients were treated with closed reduction with or without adjunct therapy (injection laryngoplasty or botulinum toxin administration), with the exception of one patient who recovered spontaneously. Of the treated patients, 18 regained arytenoid motion, accompanied by voice improvement, with recovery sustained 6 months postsurgery. The investigators also found that patients who underwent closed reduction within 21 days after the presumed dislocation event tended to have better restoration of arytenoid motion.[8]

A study by Cao et al found that 26 out of 33 patients with an arytenoid dislocation were satisfied with the outcome following closed reduction performed under local anesthesia, with significant improvements found in grade, roughness, breathiness, asthenia, maximum phonation time, self-assessed Voice Handicap Index, jitter%, shimmer%, normalized noise energy, and noise-to-harmonic ratio.[9]

Su et al reported that three patients with bilateral vocal fold immobility and mechanical fixation of the cricoarytenoid (CA) joint were successfully treated first with release of the joint via an external approach and then with exo-endolaryngeal suture lateralization. The joint-release procedure permitted the endolaryngeal mucous membrane to be preserved and allowed one patient to be decannulated and two individuals to experience dyspnea improvement.[10]

The second group of procedures is aimed at ameliorating static glottic airway insufficiency. Standard surgical approaches for treatment of adynamic glottic narrowing include transverse laser cordotomy, partial cordectomy, arytenoidectomy, lateralization procedures, and tracheotomy. Tracheotomy remains the criterion standard for maximizing the airway and preserving phonatory function.

In 1985, Ejnell et al reported their technique for mobilizing a fixed arytenoid with subsequent lateral fixation.[11] The object of this procedure, in contrast to the previously described method, is mobilization for the express purpose of arytenoid refixation in an advantageous position. The technique is performed by using jet ventilation or through a preexisting tracheostoma with the patient under general anesthesia. Coordinated endoscopy and external work are necessary to lateralize the true vocal fold. The arytenoid is initially positioned by passing a dilator through the glottis. Concurrent external lateral fixation is then affected by passing 2 needles through the thyroid lamina to create a suture loop around the vocal fold under direct vision of the endoscopist. The suture is then tied externally over the thyroid cartilage to maintain the position.

Cummings et al described a variation of this technique in 1999.[12] Their novel device and technique attempt to provide adjustable vocal-fold lateralization with a modified thyroplasty technique performed under flexible laryngoscopic visualization. Their design localizes the height of the true vocal fold by placing an external needle through a 1-cm, round window in the thyroid cartilage. A double helical cam device is then inserted medially to engage the soft tissue of the thyroarytenoid muscle lateral to the vocal process. The double-helix design allows the now-engaged tissue to be lateralized by independently backing out the outer cam and by drawing the inner helix and the vocal cord outward into the desired position. Subsequent adjustments after healing are theoretically feasible.

More recently, Rovo et al (2008) have described endoscopic arytenoid lateropexy for severe posterior glottic stenosis involving one or both cricoarytenoid joints.[13] This novel technique employs a specially designed, right-angled scythe for sharp division of the arytenoid and cricoid cartilage. Once scar lysis and cricoarytenoid (CA) joint mobility are achieved, a modified, steel sheath reinforced Lichtenberger endo-extralaryngeal needle carrier is used place a suture through the vocal process. The needle is then passed through the posterior aspect of the thyroid cartilage and secured through a small (about 0.5cm) transcervical incision.

When complete, the arytenoid is in a posterior, lateral, and superior position which is felt to be a more physiologic position for the abducted arytenoid than prior lateralization techniques. This procedure is temporary and is intended to keep the posterior commissure tissues apart following CO2 laser lysis. Sutures are removed once re-epithelialization is complete. The authors demonstrate improvements in peak inspiratory flow, breathing at rest, and voice (once sutures were removed) in a large majority of patients. Additionally, radiographic evidence of transient postoperative aspiration resolved completely a few weeks after surgery.

The transverse laser cordotomy, which Kashima (1991) popularized, is designed to enlarge the posterior glottic airway while maintaining close opposition of the anterior true vocal folds for phonation.[14] A radial incision is made in the membranous vocal fold immediately anterior to the vocal process of the arytenoid. The resulting wedge-shaped defect in the posterior glottis is due to the anterior retraction of the thyroarytenoid muscle. In cricoarytenoid (CA) fixation, the magnitude of posterior glottic enlargement with cordotomy is entirely independent of arytenoid position and mobility, unlike with the techniques designed to achieve vocal-fold lateralization. The technical ease and minimal tissue destruction in this procedure are additional advantages. Cutting techniques other than the CO2 laser were more recently proposed to affect the same posterior cordotomy surgical defect.

Medial (partial) arytenoidectomy has also gained popularity because of its ability to directly enlarge the posterior respiratory glottis while minimally affecting the anterior phonatory glottis and preserving more of the native laryngeal structure in comparison to the total arytenoidectomy procedure. A comparison of postsurgical airway and phonatory outcomes for transverse cordotomy and medial arytenoidectomy to treat bilateral vocal-fold immobility demonstrated that the procedures yielded satisfactory and fairly comparable outcomes.

Endoscopic or open arytenoidectomy is another approach for enlarging the posterior glottic airway. The technique for endoscopic laser arytenoidectomy, as Ossoff et al elucidated in 1984, allows for the direct and relatively atraumatic ablation of the arytenoid cartilage without the morbidity of an external incision.[15] The addition of direct laser ablation to the armamentarium improved the relative ease of performance when compared to the endoscopic delivery and excision technique previously described by Thornell. Disadvantages of laser arytenoidectomy include the attendant airway risks of CO2 laser surgery, including airway fires and peripheral thermal damage.

As previously noted, tracheotomy remains the criterion standard for providing a safe adequate airway while maintaining native glottal tissue for phonatory function.

Complications

Potential complications of laser arytenoidectomy include the attendant airway risks of CO2 laser surgery, including airway fires and peripheral thermal damage. Postoperative aspiration is a potential complication of all airway-enlarging procedures, including tracheotomy. Furthermore, the extent of tissue alteration and/or destruction carries a proportional risk of degrading vocal quality. Therefore, the ideal surgical procedure is minimally destructive to the normal laryngeal anatomy and provides durable and reproducible airway and vocal function.

Outcome and Prognosis

The outcome and prognosis of cricoarytenoid (CA) fixation depends entirely on the etiology. However, given the relative infrequency of this diagnosis, it is not surprising that the literature contains no reports of clinical outcomes from large series of patients grouped by specific etiology and treatment strategies.

Future and Controversies

Given the infrequent reports of this entity, a routine workup of vocal-fold immobility is appropriate when it is encountered. Of no surprise, standard etiology-based treatment protocols for arytenoid fixation have yet to be established. Increased awareness of this diagnosis and careful attention to the natural history of patients ideally guide the physicians' therapeutic care plan.

The relationship of prolonged joint immobility to joint fixation is a disputed point. Intuition and reason suggest that prolonged immobility may result in cricoarytenoid (CA) joint ankylosis, as it does in other diarthrodial joints. However, histologic studies have failed to demonstrate this phenomenon in the cricoarytenoid (CA) joint. Possible reasons for this inconsistency may include the non–weight-bearing status of these joints and their potential for low-amplitude passive motion with respiratory airflow.

 

Questions & Answers

Overview

What is cricoarytenoid (CA) fixation?

How does cricoarytenoid (CA) fixation differ from other forms of vocal fold immobility?

What causes cricoarytenoid (CA) fixation?

What is the pathophysiology of cricoarytenoid (CA) fixation?

Which clinical history findings are characteristic of cricoarytenoid (CA) fixation?

Which physical findings are characteristic of cricoarytenoid (CA) fixation?

What is the anatomy relevant to cricoarytenoid (CA) fixation?

Workup

What is the role of imaging studies in the workup of cricoarytenoid (CA) fixation?

What is the role of EMG in the workup of cricoarytenoid (CA) fixation?

How is a cricoarytenoid (CA) fixation differentiated from other causes of an immobile vocal fold?

What is the role of laryngoscopy in the workup of cricoarytenoid (CA) fixation?

Which histologic findings are characteristic of cricoarytenoid (CA) joint fixation?

Treatment

How is cricoarytenoid (CA) fixation medically treated?

What is the role of surgery in the treatment of cricoarytenoid (CA) fixation?

Which mobilizing surgical procedures are performed in the treatment of cricoarytenoid (CA) fixation?

Which surgical procedures are used to ameliorate static glottic airway insufficiency in the treatment of cricoarytenoid (CA) fixation?

What is the role of surgical lateralization procedures in the treatment of cricoarytenoid (CA) fixation?

What is the role of endoscopic arytenoid lateropexy in the treatment of cricoarytenoid (CA) fixation?

What is the role of transverse laser cordotomy in the treatment of cricoarytenoid (CA) fixation?

What is the role of medial (partial) arytenoidectomy in the treatment of cricoarytenoid (CA) fixation?

What is the role of endoscopic or open arytenoidectomy in the treatment of cricoarytenoid (CA) fixation?

What is the role of tracheotomy in the treatment of cricoarytenoid (CA) fixation?

What are the possible complications of cricoarytenoid (CA) fixation treatment?

What is the outcome and prognosis of cricoarytenoid (CA) fixation?

What is the role of prolonged joint immobility in cricoarytenoid (CA) fixation?