Arytenoid subluxation is partial displacement of the arytenoid cartilage within the cricoarytenoid joint. It is a rare complication that typically occurs after a traumatic injury to the cricoarytenoid junction during laryngoscopy and intubation, upper airway instrumentation and external laryngeal trauma. The arytenoids are a pair of small pyramid-shaped cartilages which articulate with the cricoid cartilage at the cricoarytenoid joint. Both the arytenoids and cricoarytenoid joints are relatively fragile and very vulnerable to injury during laryngoscopy and intubation. Clinicians commonly visualize the bulge in the mucosal surface overlying the arytenoids during laryngoscopy. [Figure 1]
The arytenoids are composed of an apex, a base, and two processes (vocal and muscular). The vocal processes extend anteriorly and provide attachment to the vocal ligament, and are responsible for tension, relaxation, or approximation of vocal folds, while the muscular processes extend posterolaterally and provide a point of insertion for the lateral and posterior cricoarytenoid muscles. These muscles are responsible for opening and closing the glottis by creating lateral and medial movements of the attached vocal cords. The apex articulates with the aryepiglottic fold, and corniculate cartilages and the base articulates with the cricoid cartilage through several ligaments that form the capsule of the synovial cricoarytenoid joint. The cricoarytenoid joint controls the abduction and adduction of the true vocal cords, allowing respiration, phonation and airway protection.
One often sees the terms subluxation and dislocation used interchangeably. However, a dislocation refers to a complete separation of the arytenoid cartilage from the joint space whereas a subluxation is partial displacement of the arytenoid within the joint. Both can be considered the same disease with varying degree of severity, sharing the same pathophysiology. A subluxation can be classified as anterior when the displacement is anteromedial or posterior when the displacement is posterolateral.
Arytenoid subluxation is usually related to acute traumatic events to the cricoarytenoid junction. Protrusion of an endotracheal tube stylet, an unanticipated difficult airway leading to prolonged or traumatic intubations, the use of a gum elastic bougie, blind intubation techniques (e.g., utilization of a lighted stylet or light-wand) and insertion of bulky double lumen tubes, have all been implicated. The degree of experience of the laryngoscopist, dental malocclusion, retrognathia, and a large tongue may also play a role. There are also reports of severe cough and even spontaneous arytenoid dislocation.
Several systemic diseases as well as chronic steroid use, laryngomalacia and acromegaly may lead to the weakening of the cricoarytenoid joint capsule, thus exacerbating this complication. An elevated BMI might be an independent risk factor, and major cardiac surgery involving the use of transesophageal echocardiography (TEE) probe may also be a possible explanation for the increased incidence. Insertion of the TEE probe is the likely inciting event in these cases.
The incidence of arytenoid subluxation after endotracheal intubation has been reported to be between 0.01 and 0.1%. Although the reported incidence suggests that it is rare, the true incidence may be higher. Rudert et al. reported a much higher incidence of 30% in his case series of patients referred to him with prolonged hoarseness following instrumentation of the larynx; 80 to 90% of all cases were related to intubation trauma.
As the arytenoid is extremely mobile with a small oval articulating surface, it is vulnerable to displacement from its normal position during intubation. In fact, even slight pressure from the tip of the endotracheal tube directed toward the cricoarytenoid joint is enough to cause anteromedial displacement, dislocating the cartilage. Difficult (prolonged and traumatic) intubation is, therefore, a significant risk factor for arytenoid subluxation or dislocation. Traumatic extubation with a partially inflated cuff may also lead to posterolateral arytenoid displacement.
Subluxation results in hypomobility of the true vocal cords and incomplete closure of the glottis, mimicking vocal cord paralysis. Left-sided displacements/dislocations occur more often because most anesthesiologists insert the endotracheal tube from the right side of the mouth and oropharynx, placing undue force on the left arytenoid by the convex curvature of the endotracheal tube. After the lesion occurs, hemarthrosis with subsequent fibrosis and paresis of the recurrent laryngeal nerve may occur.
Patients typically present with hoarseness, difficulty swallowing and pain in the anterior region of the neck after a recent traumatic tracheal intubation or upper airway instrumentation. There are reports of rare instances of severe cough, external blunt trauma, or spontaneous events that lead to this presentation. The development of respiratory problems, dyspnea, and pseudo asthma are also possible.
The clinician must first rule out life-threatening conditions such as stridor, dyspnea, and internal and external hematomas of the neck. The physical examination must include flexible fiber-optic laryngoscopy and videostroboscopy to allow direct and dynamic evaluation of the laryngeal structures.
There is no gold standard for diagnosis. All patients who develop hoarseness after extubation must be evaluated with a flexible fiberoptic laryngeal examination, videostroboscopy and computed tomography, focusing on the position and mobility of the vocal fold and arytenoid cartilage as well as traumatic injury to the larynx.
Flexible fiberoptic laryngoscopy can reveal the arytenoid displacement or dislocation with or without glottic edema. Videostroboscopy allows better visualization of any discrepancy in the lengths of the vocal cord and height of the vocal processes during phonation. It helps to differentiate cricoarytenoid subluxation from vocal cord palsy.
Computed tomography with thin-section and multiplanar reformation will reveal disparities in the height of the vocal cords, a unique finding for arytenoid dislocation, but its value is limited in young patients, as the cartilage may not yet be ossified.
Laryngeal electromyography may help distinguish between cricoarytenoid joint subluxation and vocal palsy. A dislocated arytenoid cartilage would most probably show normal EMG patterns while in the case of recurrent laryngeal nerve palsy, the EMG pattern will be abnormal. However, both dislocation/subluxation and hematoma can occur with recurrent laryngeal nerve paresis and can lead to misdiagnosis.
The most common treatment is direct laryngoscopy with closed arytenoid reduction. The arytenoid cartilage should be repositioned on top of the cricoid while ensuring that the vocal process is placed as symmetrically as possible to the contralateral vocal process. The scheduling of this procedure must take place as soon as the diagnosis is made to improve the outcome. This process can be performed under sedation while assessing phonation in real time. Immediate improvement of symptoms confirms the diagnosis. Concomitant nerve injury is usually associated with delayed or no improvement.
With a delayed diagnosis, fibrosis and scarring may develop, making treatment more challenging. Open procedures such as thyroplasty and arytenoidopexy are options in selected cases.  Botox and voice therapy are important adjuvants in the treatment of arytenoid subluxation. For patients with surgical contraindications, an alternative is vocal cord augmentation procedures such as injection laryngoplasty with temporary injectable materials such as absorbable gelatin powder or long lasting and permanent agents such as polytetrafluoroethylene past and voice therapy. Vocal cord augmentation procedures allow for better phonation and alleviate the risk of aspiration.
Conservative management with voice therapy, which entails voice exercises, relaxation techniques of the larynx and voice compensation mechanisms have also shown good results.
The most important differential diagnosis is vocal cord paralysis due to recurrent laryngeal nerve paralysis. Laryngeal electromyography is an important diagnostic test to differentiate between arytenoid subluxation and recurrent laryngeal nerve paralysis. Further, it may offer some prognostic information regarding potential vocal fold paralysis recovery.
It may have some limitations since a transient paresis may be present with both a subluxation or a hematoma.
In about 19% of patients, spontaneous reduction, and resolution occur without treatment. Early treatment is associated with better outcomes with almost all patients regaining normal voice and vocal fold mobility immediately after closed reduction. Adequate voice recovery can be obtained even with late intervention. Patients with delayed or no improvement often have associated nerve injury, and in some instances may recover with time. If not promptly reduced, an arytenoid joint can become fibrosed and fixed in an unfavorable position.
Patients can develop cricoarytenoid ankylosis and scarring with persistent hoarseness, dysphagia, and even respiratory complications if the condition persists.
Postoperatively voice therapy is a possible adjunct, or it can serve as a valid and effective intervention in patients who prefer conservative therapy.
An otolaryngologist should be alerted immediately if an arytenoid subluxation is suspected. A screening flexible laryngeal endoscopy with stroboscopy (specialized viewing of vocal cord vibration) should be done to confirm the diagnosis to prevent treatment delays.
All patients undergoing endotracheal intubation must be made aware of possible complications of the procedure and must be advised to seek medical attention if acute, persistent hoarseness or dysphagia develop.
The inclusion of arytenoid subluxation/dislocation must be a consideration in the differential diagnosis of prolonged postoperative hoarseness after endotracheal intubation. Although rare, it is a complication that can cause significant distress to patients. It has an excellent prognosis if diagnosed and treated promptly.
Gentle instrumentation of the airway and completely deflating the endotracheal tube cuff before extubation may prevent this injury. The use of a stylet appears to protect against arytenoid dislocation.
Arytenoid dislocation is not an uncommon complication of orotracheal intubation, and when the diagnosed is missed or delayed, it carries high morbidity. Thus, an interprofessional team should participate in diagnosis and management.
The anesthesiologist and anesthesia nurse have to communicate with an ENT surgeon if they believe the patient has suffered arytenoid dislocation during intubation. Clinicians (MDs, DOs, NPs, PAs) need to all consider this in their differential in intubated patients, as well as those who present with sudden unexplained hoarseness, dysphagia, and anterior neck pain. In the event of confirmed arytenoid dislocation, the entire team (clinicians, nursing, and afterward, voice therapists) need to communicate both during and following the corrective procedures.
It is crucial during the transfer of care for anesthesiologists to communicate any difficulties encountered during intubation with an emphasis on direct trauma during laryngoscopy. The diagnosis is not straightforward and may require several imaging studies. Acute dislocations are reducible during surgery, but chronic cases may require botulinum toxin and gel foam injection. A speech therapist must be involved in the care as the outcomes appear to be much better when combining the above treatments with voice therapy. Nursing can monitor post-procedure, and report to the clinician or even the voice therapist any findings of note.
The entire interprofessional team, including the clinicians, nursing, and therapists need to work collaboratively to manage the case through to a successful outcome. [Level V]
Early treatment is associated with better outcomes with almost all patients regaining normal voice and vocal fold mobility immediately after closed reduction. Adequate voice recovery can be obtained even with late intervention. Patients with delayed or no improvement often have associated nerve injury, and in some instances may recover with time. If not promptly reduced, an arytenoid joint can become fibrosed and fixed in an unfavorable position.
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