You are in: eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > LARYNGOLOGY Arytenoid DislocationArticle Last Updated: Jan 29, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 10
  Author: Joshua S Schindler, MD, Assistant Professor, Department of Otolaryngology, Oregon Health and Science University Joshua S Schindler is a member of the following medical societies: Alpha Omega Alpha and American Academy of Otolaryngology-Head and Neck Surgery Coauthor(s): Yvette V Leslie, MD, Instructor, Department of Otolaryngology, Vanderbilt University Medical Center Editors: John Schweinfurth, MD, Associate Professor, Department of Otolaryngology, University of Mississippi Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Dominique Dorion, MD, MSc, FRCSC, Program Director and Division Chair, Professor of Surgery, Division of Otolaryngology, University of Sherbrooke, Canada; 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: arytenoid dislocation, arytenoid subluxation, AS, fracture, disarticulation, laryngeal injury, larynx injury, upper aerodigestive tract instrumentation, cricoarytenoid joint disruption, cricoarytenoid joint dislocation, laryngeal trauma, larynx trauma, endotracheal intubation complications, upper airway instrumentation, vocal fold paralysis, intubation trauma INTRODUCTIONSection 2 of 10
  Arytenoid dislocation and arytenoid subluxation (AS) are rare laryngeal injuries that are usually thought to occur as complications of upper aerodigestive tract instrumentation. The terms arytenoid dislocation and AS have been used interchangeably to describe disruption of the cricoarytenoid joint. Arytenoid dislocation refers to complete separation of the arytenoid cartilage from the joint space. It usually results from severe laryngeal trauma. AS is likely a lesser injury and refers to the partial displacement of the arytenoid within the joint. Reports in the literature suggest that AS is a more common injury than arytenoid dislocation. AS is the focus of this article. History of the ProcedureArytenoid dislocation and AS have not been widely reported in the world literature. The conditions were first described in 1973 as rare and unusual complications of endotracheal intubation. By 1994, only about 31 cases had been reported. ProblemAS is usually a complication of upper airway instrumentation and endotracheal intubation. The normal articulation of the arytenoid cartilage is disrupted as it contacts the cricoid cartilage, resulting in reduced mobility of the true vocal fold and incomplete glottic closure that can mimic true vocal fold paralysis. FrequencyThe incidence of AS is unknown. It is considered a rare injury. Now, fewer than 80 cases have been reported in worldwide literature, and these are mostly case reports or small series. Only one case of AS was reported in a large series of 1000 intubated patients, in which 6.2% had laryngeal trauma. Because the clinical presentation of arytenoid malposition and dysphonia are common to AS/arytenoid dislocation and vocal fold paralysis, further studies are needed to establish the incidence of arytenoid trauma. EtiologyIntubation trauma is the most common etiologic factor for AS cited in the world literature. Blunt and penetrating neck trauma are less common causes. Other reported etiologies include, but are not limited to, direct laryngoscopy, whiplash injury, and idiopathic causes in rare cases. Associated anomalies (eg, laryngomalacia, acromegaly) have been identified as possible factors that can weaken the cricoarytenoid joint. Diabetes mellitus, chronic renal failure, history of rheumatic disease, and long-term corticosteroid use have also been implicated. However, no disease process or anatomic abnormality has been linked definitively with an increased risk of AS. No statistically significant sex or age predilections have been identified for AS. PathophysiologyMany mechanisms of injury to the cricoarytenoid joint have been postulated. Anterior and posterior arytenoid displacement secondary to intubation have been reported in the literature. Anterior displacement is thought to occur when the arytenoid is subluxed directly by the blade of a laryngoscope as it is inserted and lifted in an anterior direction. Another possibility is that the tip of the endotracheal tube or stylet can displace the arytenoid in the same fashion as in endotracheal tube insertion. Posterolateral force applied to the arytenoid by the convex curve of the endotracheal tube as it passes into the airway is one suggested mechanism for posterior AS. Another theory suggests that traumatic extubation with a partially inflated cuff displaces the arytenoid posteriorly. The proposed mechanisms of AS due to endotracheal manipulation are disputed. In an unfixed cadaveric larynx study by Paulsen et al, the authors were unable to cause arytenoid dislocation or subluxation in 36 larynges via intubation, extubation, or manual manipulation. Although this study does not mimic the normal physiologic condition since all of the larynges were from cadavers and thus had no muscle tone, the study brings the diagnosis of arytenoid dislocation and AS into question. The study's authors propose that AS does not occur, but rather hemarthrosis of the cricoarytenoid joint leads to fibrosis and subsequent fixation. Other authors have proposed that what is thought clinically to be AS is actually a manifestation of paresis, either of the recurrent laryngeal or external branch of the superior laryngeal nerve. Arytenoid injury due to external neck trauma is often accompanied by other laryngeal injuries (eg, mucosal tears, thyroid or cricoid cartilage fractures, hematoma formation). Blunt neck trauma can cause anterior AS from inward pressure applied by a medially displaced thyroid ala. Posterior AS can also result from an anterior blow to the laryngeal framework that causes lateral splaying of the thyroid cartilages, thereby forcing the arytenoid posteriorly. Injury to the recurrent laryngeal nerves or external branch of the superior laryngeal nerve is also common to such injuries and may complicate both the diagnosis and treatment. ClinicalUpon presentation, patients with AS primarily report hoarseness. Breathy voice quality, vocal fatigue, and an inability to project the voice are also common symptoms. Dysphagia, odynophagia, sore throat, and cough are less common. Respiratory compromise that necessitates airway management is uncommon. A history of recent upper aerodigestive tract instrumentation or intubation should also prompt consideration of AS. A thorough laryngeal examination should be performed using a laryngeal mirror, flexible fiberoptic laryngoscope, or rigid telescope. Reduced vocal fold mobility and arytenoid edema with loss of arytenoid symmetry are physical signs that suggest acute AS. Poor glottic closure, posterior glottic chink, and malalignment of the true vocal folds are often noted. Importantly, note that recurrent laryngeal nerve paralysis can also manifest with the above symptoms and physical signs. Recurrent nerve paralysis can result from (1) pressure on the nerve from the endotracheal tube cuff in intubated patients or (2) external laryngeal trauma. Differentiation between recurrent laryngeal nerve paralysis and AS can be difficult if based only on history and physical examination findings. Further studies are frequently necessary to make the correct diagnosis. Making the distinction is important because early management of AS consists of endoscopic reduction, whereas early management of vocal fold paralysis frequently consists of observation with voice therapy. The opportunity for early endoscopic reduction may be lost if AS is misdiagnosed as vocal fold paralysis. Laryngeal electromyography (EMG) may be essential to make this distinction early following the injury. RELEVANT ANATOMYSection 3 of 10
The arytenoid cartilage is composed of hyaline and elastic cartilages. The cartilage is pyramid-shaped and consists of an apex, base, and 2 processes. The vocal process articulates with the vocal ligament, and the muscular process is the insertion point for the muscles that move the arytenoid. The base rests on the cricoid cartilage, and the apex articulates with the aryepiglottic fold and the corniculate cartilage (Santorini cartilage). Most cricoarytenoid motion is that of rocking and, to a lesser extent, gliding. The cricoarytenoid joint is a synovial joint enclosed by a joint capsule. The capsule receives posterior support from the posterior cricoarytenoid ligament, which usually prevents posterior subluxation. The cricoarytenoid joint controls adduction and abduction of the true vocal folds, which facilitates the main laryngeal functions of airway protection, respiration, and phonation. CONTRAINDICATIONSSection 4 of 10
Contraindications to surgical correction of arytenoid subluxation (AS) are based on the patient's comorbidities and his or her ability to tolerate surgery. Informed consent must be obtained prior to all surgical procedures. Laryngeal electromyography (EMG) findings of recurrent or superior laryngeal nerve paralysis represent at least a relative, if not strict, contraindication to surgical manipulation. Voice therapy is sometimes advocated for patients who refuse or do not require surgical intervention. WORKUPSection 5 of 10
Lab Studies
Imaging Studies
Other Tests
Diagnostic Procedures
TREATMENTSection 6 of 10
Medical therapyVoice therapy is an important adjunctive treatment for all patients with arytenoid subluxation (AS). Proper voice use and vocal hygiene are important in the rehabilitation of cricoarytenoid joint integrity. Whenever possible, have the patient begin therapy with a trained speech and language pathologist with a background in voice disorders prior to surgery. Voice therapy is also advocated in patients who refuse or do not require surgical intervention. Patients can be taught compensation techniques for breathiness and hoarseness. In addition, patients can be trained to protect their airway from aspiration. Frequently, patients with AS or vocal fold paralysis develop muscle tension dysphonia that produces a strained voice quality, vocal fatigue, frequent neck pain, and a sore throat. These symptoms reflect lack of compensation for incomplete glottic closure in both processes. Voice therapy may help prevent and correct dysphonia by redirecting the patient into better compensatory techniques. Surgical therapySurgical therapy is the treatment of choice for AS. Several treatment options are available. Generally, the earlier the intervention, the better the outcome for voice quality. Treatment of AS can be divided into early and late interventions. Early treatment Early treatment of AS includes direct laryngoscopy and closed reduction of the displaced arytenoid. Injection of steroid preparations (eg, triamcinolone) into the cricoarytenoid joint space at the time of reduction is preferred by some practitioners. Tracheotomy may be required in the acute period of laryngeal edema and airway compromise. Other reports in the literature advocate arytenoidectomy via an endoscopic approach or externally via laryngofissure. Arytenoidectomy has not been widely accepted and could pose a greater risk of aspiration and poor airway protection. Usually, arytenoidectomy is reserved for when the arytenoid obstructs the airway or when all other interventions have failed. Late treatment Vocal fold medialization, via a type 1 thyroplasty with silastic implantation as described by Isshiki, is the treatment of choice for late AS. Other options for medialization include Gelfoam injection, autologous fat injection, and Teflon injection into the true focal fold. Teflon has largely fallen out of favor because of the possibility of granuloma formation. Gelfoam and fat are resorbed over time and are therefore considered temporary treatments. Gelfoam and fat are considered in patients who are likely to regain vocal fold mobility and closure. Direct laryngoscopy with attempted reduction of the displaced arytenoid, as in early AS, is another treatment option for late AS. The likelihood of successful reduction is greatly reduced in delayed diagnoses of AS because of fibrous ankylosis of the cricoarytenoid joint. Canine studies have shown that even minor injury to the joint capsule can affect arytenoid mobility. Arytenoid mobility can be significantly impaired, even with successful reduction. Although one large series demonstrated phonatory improvement with reductions as late as 1 year following injury, late endoscopic reduction has not been widely accepted as the first line of treatment for late AS. Preoperative detailsObtain informed consent prior to all surgical procedures. Include a careful discussion with the patient regarding risks of airway compromise and the possible need for tracheotomy. If extensive supraglottic edema is coexistent, treatment with oral steroids or antireflux agents may be considered prior to surgical therapy. Intraoperative detailsEndoscopic procedures are performed with the patient under general anesthesia or under local anesthesia with intravenous sedation. Various instrumentation techniques have been used to reduce the subluxated cartilage. Sataloff et al recommend the Holinger laryngoscope for anterior dislocations. The tip of the scope is contacted with the joint interface; the displaced arytenoid is then lifted and reduced posterolaterally. Other authors report success with the laryngeal spatula during endoscopy. For posterior subluxations, the Miller-3 straight intubating laryngoscope is favored for its unique curved tip. Sataloff et al describe placement of the laryngoscope in the pyriform sinus with the lip of the Miller blade in the subluxated joint. The cartilage is lifted and repositioned anteromedially. Smaller microlaryngeal instruments (ie, cups forceps) are less likely to be effective and may lacerate the mucosa. Intraoperative steroids have also been advocated by some authors. A preparation of triamcinolone acetate (Kenalog) at 40 mg/mL, in varying amounts, can be injected into the cricoarytenoid joint using a 25-gauge butterfly needle. This has been proposed to prevent joint ankylosis and reduce edema in persons with acute injuries. However, to date, intraoperative steroid injection has not been definitively shown to improve the outcome of endoscopic reduction. Medialization thyroplasty is performed with the patient under local anesthesia with intravenous sedation, as needed. Ensure that the patient is awake in order to assess voice quality while positioning the vocal fold implant. The optimal voice quality for each patient is obtained using this method. Postoperative detailsMonitor all patients for airway compromise in the postsurgical period. Common signs include respiratory distress, tachypnea, and stridor. Also monitor oxygen saturation levels. If symptoms develop, prompt fiberoptic laryngoscopy is indicated, as is intravenous steroid therapy to reduce laryngeal edema. Racemic epinephrine has also been recommended to reduce airway edema. Supportive measures, including humidified oxygen, are also useful. Close observation in an intensive care unit may be warranted. Tracheotomy may be indicated if these measures are ineffective. The use of postoperative antibiotics, antireflux medications, and tapered oral steroid therapy for patients to complete at home are often advocated. Oral narcotic analgesics may be necessary. Follow-upMost patients who have endoscopic arytenoid reductions are scheduled for a follow-up visit within 2-4 weeks. A period of voice rest may be recommended to allow the cricoarytenoid joint to stabilize. Patients who undergo medialization thyroplasty are usually scheduled for a follow-up visit within 1-2 weeks. A period of voice rest, from 3 days to 1 week, may also be advocated. All patients require voice therapy for speaking; when applicable, voice therapy is required for singing. Whenever possible, have the patient begin speaking voice therapy prior to surgical intervention. COMPLICATIONSSection 7 of 10
Failure to reduce the arytenoid is the most common complication of endoscopic reduction of arytenoid subluxation (AS). Histologic studies have shown that fibrosis of the cricoarytenoid joint can occur as early as 24 hours following injury. Recurrence of subluxation after successful reduction is a related complication of the endoscopic approach. This complication is likely due to laxity of the ligamentous support of the cricoarytenoid joint following injury. Iatrogenic disruption of the laryngeal mucosa can occur during attempts to reduce the arytenoid, thereby increasing the risk of infection. Instrumentation of the airway can result in supraglottic edema, glottic edema, or both, thereby causing airway compromise. Possible complications of medialization thyroplasty include the following: bleeding, infection, or hematoma of the surgical site; malpositioning of the implant, causing airway compromise or poor voice quality; extrusion of the implant; and chondritis. OUTCOME AND PROGNOSISSection 8 of 10
Early diagnosis and intervention is the best hope for a favorable outcome in the treatment of arytenoid subluxation (AS). Some patients are able to compensate for the immobile vocal fold and return to near-normal voice quality without surgical intervention. However, most patients require either endoscopic reduction in the early period or medialization procedures in the late period to achieve subjective and objective improvement in voice quality. Outcomes for both procedures have been favorable, although not uniformly successful. FUTURE AND CONTROVERSIESSection 9 of 10
Arytenoid subluxation (AS) continues to be a rare, but challenging, problem for the laryngologist. Future management of AS will be directed toward developing more effective means of restoring cricoarytenoid joint structure and mobility, thereby improving phonatory outcomes for patients with this injury. Newer concepts that may add more treatment options for patients with AS are evolving. The use of botulinum toxin as an adjunct to endoscopic reduction for anteromedial AS has been reported in a recent study. The study proposes that reduction of the arytenoid alone often fails because the surgeon cannot control unbalanced forces placed on the arytenoid by the intrinsic laryngeal musculature. Injection of botulinum toxin into the laryngeal adductor muscles on the affected side weakens these forces and allows the arytenoid to remain in the reduced position. Ten patients were studied, and results were favorable. Some controversy exists in the literature over the timing of endoscopic reduction. One retrospective series reported favorable voice outcomes in patients who had endoscopic reduction as long as 1 year following injury. This finding challenges the dictum that medialization techniques are the best intervention for late treatment of AS. However, the overall consensus seems to be that, beyond 1 month following injury, the best voice outcomes will likely be obtained using medialization. REFERENCESSection 10 of 10
Article Last Updated: Jan 29, 2007 |
