Arytenoid Subluxation

Etiology

Arytenoid subluxation is multifactorial, with endotracheal intubation representing the most common precipitating factor in contemporary practice.[8][9] Risk factors may be categorized as procedure- or patient-related. Procedure-associated factors include improper endotracheal tube insertion, difficult intubation requiring multiple attempts, prolonged intubation, use of specific airway devices such as bougies, blind intubation techniques, insertion of large-bore double-lumen tubes, head and neck movement during intubation, and the experience level of the intubating physician.[10][11] Patient-specific factors include younger age, female sex, taller stature, and higher body mass index (BMI).[12] The use of a stylet during intubation is protective, associated with a reduced risk of arytenoid dislocation.[13]

Abdominal surgery accounts for a disproportionate number of cases, with a study reporting that 88.1% of arytenoid dislocation cases followed major abdominal procedures. Cardiovascular surgery has also emerged as a significant risk factor, with a large retrospective study demonstrating an odds ratio of 9.9 for arytenoid dislocation.[14] Head and neck positioning during surgery is a particularly important and modifiable risk factor, with an incidence rate ratio of 3.10 for arytenoid subluxation. The experience level of the intubating physician is a significant determinant, with 1st-year anesthesia residents demonstrating an incidence rate ratio of 2.30 compared to more experienced practitioners.[15]

External laryngeal trauma constitutes the 2nd most common etiology of arytenoid subluxation, although it accounts for a substantially smaller proportion of cases than iatrogenic injury.[16] Less frequent causes include severe coughing, the use of laryngeal mask airways, and rare instances of spontaneous subluxation.[17][18][17] Although laryngeal mask airways are traditionally considered safer than endotracheal intubation, their use has been associated with occasional cases of arytenoid dislocation, indicating that even supraglottic airway devices can produce laryngeal injury under specific circumstances.[19]

Epidemiology

The epidemiology of arytenoid subluxation has been clarified through recent systematic reviews and large-scale studies.[20] Contemporary meta-analysis data indicate a pooled incidence of 0.093% (confidence interval: 0.045%-0.14%) among patients undergoing endotracheal intubation, representing a substantial update from earlier estimates suggesting rates as low as 0.009%. This discrepancy likely reflects improved diagnostic awareness and more sophisticated detection methods rather than an actual increase in incidence.

Demographic patterns demonstrate consistent trends across multiple studies. Female sex is a significant risk factor, with incidence rate ratios of 3.05. Younger age is associated with increased risk in some analyses. BMI has emerged as an independent epidemiological factor, with higher BMI correlating with elevated risk. A dedicated case-control study confirmed BMI as an independent risk factor with statistical significance (P = 0.025).

Geographic and institutional variations indicate that factors beyond patient demographics influence occurrence. Institutions performing high volumes of complex procedures, particularly cardiovascular and major abdominal operations, report higher rates of arytenoid subluxation. Temporal patterns suggest a higher incidence when less experienced residents perform intubations. International differences likely reflect variations in diagnostic practices, reporting systems, and clinical awareness rather than true population differences.

Pathophysiology

The pathophysiology of arytenoid subluxation involves disruption of normal anatomical relationships within the cricoarytenoid joint, resulting in altered laryngeal function and impaired voice production (see Image. Anatomy of the Laryngeal Cartilages and Vocal Folds).[21] The cricoarytenoid joint is a synovial articulation between the base of the arytenoid cartilage and the superior surface of the cricoid cartilage lamina, permitting complex 3-dimensional movements essential for vocal fold positioning during respiration, phonation, and airway protection.[22] The joint capsule is reinforced by ligaments, including the posterior cricoarytenoid and vocal ligaments, which provide stability while allowing physiological mobility.[23]

Arytenoid subluxation typically occurs when external forces exceed the joint’s normal range of motion or stability limits. During endotracheal intubation, factors contributing to excessive force include direct instrument contact with the arytenoid cartilage, forceful manipulation during difficult intubation, and suboptimal head and neck positioning.[24] Traumatic extubation with a partially inflated cuff can produce posterolateral arytenoid displacement, as the inflated cuff may engage laryngeal structures during removal.

A cascade of secondary pathophysiological changes may occur following the initial injury. Hemarthrosis with subsequent fibrosis and RLN paresis can develop after the primary insult.[25] Joint inflammation may progress to cricoarytenoid joint ankylosis, resulting in permanent arytenoid fixation and irreversible functional impairment if not addressed promptly.

Dynamic CT studies demonstrate significant differences in bilateral vocal cord height and laryngeal chamber area between patients with arytenoid dislocation and healthy controls, with structural characteristics evolving as the condition progresses. Understanding these pathophysiological mechanisms has important implications for prevention and treatment, highlighting the importance of early closed reduction techniques to restore normal joint anatomy before fibrotic changes become established.

History and Physical

Arytenoid subluxation typically presents within hours of the precipitating event, most commonly endotracheal intubation or laryngeal trauma. Voice changes vary according to the severity and type of displacement, ranging from mild hoarseness to complete aphonia. The most frequently reported symptoms include persistent hoarseness, breathy voice quality, vocal fatigue, and markedly reduced vocal projection. A systematic review reported dysphonia in 27% of cases with laryngeal injury.

The temporal relationship between the inciting event and symptom onset is critical for diagnosis, as voice changes typically persist beyond the expected duration of routine postintubation hoarseness. Dysphagia and odynophagia are common, with difficulty swallowing liquids more pronounced than solids and sensations of food sticking in the throat. Pain occurs in 38% of patients and may localize to the throat or radiate to the ears, often exacerbated by swallowing or phonation. Coughing affects 32% of patients and may result from aspiration, laryngeal irritation, or altered sensory feedback mechanisms.

Physical examination should include a comprehensive head and neck assessment, with focused evaluation of laryngeal tenderness, asymmetry, or crepitus. Direct laryngoscopy or flexible fiberoptic laryngoscopy reveals the hallmark finding of arytenoid malposition, typically presenting as anterior and medial displacement in anterior subluxation. In anteromedial dislocation, the affected vocal fold appears shortened and bowed, whereas posterolateral dislocation produces a straightened and lengthened vocal fold. The absence of the "jostle sign," defined as displacement of an immobile arytenoid by the mobile contralateral arytenoid during phonation, distinguishes arytenoid subluxation from vocal fold paralysis.

Videostroboscopy provides additional diagnostic information. Asymmetric vocal fold vibration, altered mucosal wave patterns, and differences in vocal fold tension are commonly observed using this technique.[26]

Evaluation

Accurate diagnosis of arytenoid subluxation requires a multimodal approach integrating clinical assessment with imaging studies and specialized testing. Diagnostic evaluation must differentiate arytenoid subluxation from other causes of vocal fold immobility, particularly RLN paralysis, which can present with similar findings. Flexible laryngoscopy serves as the initial diagnostic tool, allowing direct visualization of laryngeal structures and assessment of vocal fold mobility. However, laryngoscopy alone is insufficient to distinguish mechanical dislocation from nerve injury.

Key laryngoscopic findings suggestive of arytenoid subluxation include asymmetric arytenoid positioning, altered vocal fold length and tension, and absence of the "jostle sign" during phonation. High-resolution CT provides detailed anatomical information regarding arytenoid cartilage position and cricoarytenoid joint integrity. Dynamic CT allows quantitative evaluation of laryngeal structural changes throughout respiratory and phonatory cycles. Bedside ultrasound offers a noninvasive method to assess cricoarytenoid joint position and motion in real time.

Laryngeal electromyography differentiates mechanical dislocation from RLN paralysis, with normal muscle activity observed in dislocation and characteristic denervation changes in nerve injury. Quantitative movement analysis using vector-based measurement reveals greater arytenoid mobility in dislocation compared to paralysis.[27] Voice assessment should combine subjective and objective methods, including acoustic analysis and patient-reported outcome measures, to characterize functional impact.

Treatment / Management

The primary treatment for arytenoid subluxation is closed reduction, which entails manual repositioning of the displaced arytenoid cartilage under direct laryngoscopic visualization. Recent meta-analysis data report success rates of 77% (confidence interval: 62%-87%) under general anesthesia and 89% (confidence interval: 70%-97%) under local anesthesia. These findings suggest that regional anesthesia may improve outcomes, potentially by enhancing patient cooperation, minimizing tissue trauma, and allowing intraoperative assessment of voice quality.

The timing of intervention is a critical determinant of treatment success. Evidence indicates that closed reduction performed within 21 days of the presumed dislocation consistently produces superior outcomes. Recent innovations include modified laryngeal forceps, which reduce treatment duration compared to traditional instruments, with a median time to return of normal voice of 17.92 days (standard deviation: 3.83 days) versus 31.08 days (standard deviation: 10.56 days) using conventional forceps.

Voice therapy can serve as an adjunct to closed reduction or, in selected cases, as primary treatment.[28] A recent study demonstrated that combining voice therapy with closed reduction under local anesthesia produced superior outcomes compared to closed reduction alone, with significant improvements in acoustic parameters and patient-reported outcomes. Conservative management with voice therapy alone has been reported successfully in select patients, particularly older adults or people with significant comorbidities.

Botulinum toxin injection may be employed as an adjunct, especially in anteromedial dislocation, where adductor muscle forces contribute to persistent arytenoid displacement.[29] Management of failed primary reduction requires evaluation of the interval since the initial injury, the extent of fibrosis, and patient-specific factors influencing the likelihood of success with repeat intervention.

Differential Diagnosis

The primary differential diagnosis for arytenoid subluxation is unilateral vocal fold paralysis due to RLN injury, as both conditions present with similar voice changes and apparent vocal fold immobility on laryngoscopy. Accurate differentiation is essential because treatment strategies differ. Arytenoid subluxation requires mechanical reduction, whereas vocal fold paralysis may necessitate voice therapy, injection laryngoplasty, or medialization procedures.

Several features aid distinction between the 2 conditions. In arytenoid subluxation, the vocal fold typically retains restricted and asymmetric movement, whereas complete nerve paralysis produces an immobile vocal fold. Direct visualization reveals malposition of the arytenoid cartilage, with anterior and medial displacement in anteromedial dislocation or posterior and lateral displacement in posterolateral cases. The "jostle sign" is typically present in vocal fold paralysis but absent in arytenoid subluxation.

Laryngeal electromyography provides definitive differentiation between mechanical and neurological causes of vocal fold immobility. Pure arytenoid subluxation demonstrates normal muscle activity and innervation, whereas RLN injury produces characteristic denervation changes, including fibrillation potentials, positive sharp waves, and reduced recruitment. Quantitative movement analysis using vector-based assessment of arytenoid motion during respiration has emerged as a novel diagnostic tool, demonstrating significantly greater cuneiform movement in dislocation compared to paralysis. Other differential diagnoses include vocal fold scarring, posterior glottic stenosis, cricoarytenoid joint arthritis, laryngeal edema, vocal fold hemorrhage, laryngeal fractures, functional voice disorders, and laryngeal neoplasms.

Prognosis

Prognosis for arytenoid subluxation depends primarily on the timing of diagnosis and intervention, with early recognition and prompt treatment associated with excellent outcomes and complete restoration of voice function. Meta-analysis evidence indicates that timing significantly influences results, with intervention within the first few weeks after injury producing complete or near-complete recovery of voice and restoration of arytenoid mobility. Contemporary case series report favorable outcomes when treatment is provided promptly. In a prospective study of 22 consecutive patients, 86% demonstrated recovery of arytenoid motion accompanied by concomitant voice improvement following closed reduction.

Treatment outcomes may be categorized using multidimensional evaluation criteria. A study of 57 patients classified results as "recovered" (42%), "improved" (26%), and "ineffective" (32%). The use of modified laryngeal forceps is associated with faster recovery and superior outcomes compared to traditional instruments. Long-term prognosis remains excellent for patients receiving successful reduction within the optimal time window, with sustained improvement in voice and arytenoid mobility. Delayed intervention beyond several weeks is associated with reduced recovery due to fibrosis and joint stiffening.

Complications

The most significant complication of untreated arytenoid subluxation is permanent voice impairment resulting from chronic arytenoid malposition and subsequent fibrosis of the cricoarytenoid joint. Cricoarytenoid joint ankylosis represents the most serious long-term consequence, characterized by permanent fixation of the arytenoid cartilage due to intra-articular fibrosis and scarring. Aspiration risk constitutes an important complication, particularly in the acute phase when glottal closure is compromised by arytenoid malposition.

Secondary pathophysiological changes may include hemarthrosis, fibrosis, and RLN paresis. Failed reduction attempts increase scarring and reduce the likelihood of success with subsequent interventions. Additional complications include psychological effects related to voice dysfunction, recurrence following successful reduction, bilateral arytenoid subluxation with potential airway compromise, chronic pain syndromes, and development of compensatory voice behaviors that may persist despite successful treatment.[30]