You are in: eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > LARYNGOLOGY Arytenoid FixationArticle Last Updated: May 17, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 9
  Author: Robert A Buckmire, MD, Associate Professor,Department of Otolaryngology-Head and Neck Surgery, University of North Carolina; Chief, Divison of Voice and Swallowing Disorders, Director, University of North Carolina Voice Center Robert A Buckmire is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, and National Medical Association Editors: John Schweinfurth, MD, Associate Professor, Department of Otolaryngology, University of Mississippi Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Stephen G Batuello, MD, Consulting Staff, Colorado ENT Specialists; Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders; Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine Author and Editor Disclosure Synonyms and related keywords: cricoarytenoid fixation, CA fixation, cricoarytenoid ankylosis, CA ankylosis, arytenoid ankylosis, cricoarytenoid joint fixation, CA joint fixation INTRODUCTIONSection 2 of 9
  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 CNS pathology, neuromuscular disease, malignancy, local trauma, and psychogenic causes. Among these, CA joint fixation is a recognized, albeit relatively uncommon, entity. The CA immobility and CA fixation are often used inexactly and interchangeably; such use blurs their distinctions. This discussion is limited to CA fixation resulting from altered function of the CA joint, which must be distinguished from other causes of vocal fold immobility to allow for timely diagnosis and effective treatment. ProblemCA 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. EtiologyAfter 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 CA fixation:
Previous authors have speculated that long-term paralysis with resultant CA immobility may lead to joint fixation, as observed in other diarthrodial joints in the body. However, recent histologic studies have failed to demonstrate this association. PathophysiologyLaryngeal 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. ClinicalHistory The typical history of a patient with 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 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 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 ANATOMYSection 3 of 9
The 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 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 CA ligament. WORKUPSection 4 of 9
Imaging Studies
Diagnostic Procedures
Histologic FindingsHistologic involvement of the 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. TREATMENTSection 5 of 9
Medical therapyIn rheumatoid arthritis involving the larynx, treatment options depend on the chronicity of the disease. In general, acute 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 therapySurgical procedures addressing arytenoid fixation can be organized into 2 categories. Techniques in the first group attempt to mobilize the 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 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. In 1986, Schaefer et al described a surgical procedure for mobilizing fixed CA joints. 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 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 CA joint and consequently the final functional outcome. 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. 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. 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. 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. 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 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. 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. COMPLICATIONSSection 6 of 9
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 PROGNOSISSection 7 of 9
The outcome and prognosis of 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 CONTROVERSIESSection 8 of 9
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 CA joint ankylosis, as it does in other diarthrodial joints. However, histologic studies have failed to demonstrate this phenomenon in the 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. REFERENCESSection 9 of 9
Article Last Updated: May 17, 2006 |
