Arytenoid Subluxation

Arytenoid dislocation and arytenoid subluxation (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.

Arytenoid subluxation (AS) 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.

Frequency

Arytenoid subluxation (AS) is considered to be a rare injury. A literature review by Brodsky et al reported that AS accounted for 0.1% of laryngeal injuries found after endotracheal intubation for surgery. ^[4]

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.

Intubation trauma is the most common etiologic factor for arytenoid subluxation (AS) cited in the world literature. A literature review by Frosolini et al suggested that arytenoid subluxation/dislocation (AS/AD) happens in 0.01% or more of patients who undergo endotracheal intubation. ^[5]

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.

Many 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 arytenoid subluxation (AS). Another theory suggests that traumatic extubation with a partially inflated cuff displaces the arytenoid posteriorly.

A retrospective study by Tsuru et al suggested that the risk of arytenoid dislocation/subluxation following tracheal intubation is greater in patients undergoing major cardiovascular surgery (odds ratio 9.9). The study also indicated that the risk is greater in cases of difficult intubation, in which intubation with direct laryngoscopy has been unsuccessful and must instead be carried out through other means, such as flexible fiberoptic laryngoscopy (odds ratio 12.1). ^[6]

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. ^[7] 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.

Upon presentation, patients with arytenoid subluxation (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.

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). ^[8]

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.

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.