Arytenoid Fixation Workup

Updated: Jul 27, 2021
  • Author: Paul C Bryson, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Workup

Imaging Studies

Although CT scanning may help in demonstrating arytenoid dislocation or cartilaginous fracture, the extent of ossification of the laryngeal cartilage and the plane and thickness of the sections limit the sensitivity of CT. In patients in whom the arytenoid is not ossified (ie, children, young adults), CT imaging is relatively unrevealing.

Plain radiography of the neck and larynx occasionally reveals evidence of cricoarytenoid (CA) joint pathology. Joint erosion and blurring may demonstrate active arthritis.

A retrospective study by Ravanelli et al reported that in patients with cT3 laryngeal squamous cell carcinoma (SCC), signal patterns from magnetic resonance imaging (MRI) with surface coils can indicate the etiology of arytenoid fixation. The investigators found that a normal signal pattern and one characterized by T2 hyperintensity, with no diffusion-weighted imaging (DWI) restriction, tend to be associated with arytenoid fixation stemming from mass effect and/or an inflammatory reaction. However, an intermediate T2 signal with DWI restriction strongly suggests arytenoid fixation resulting from neoplastic invasion. [4]

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Diagnostic Procedures

Electromyography of the thyroarytenoid, cricothyroid, and posterior cricoarytenoid (CA) muscles help to clarify the status of laryngeal innervation. In general, a normal pattern of laryngeal-muscle activation and recruitment is expected in a patient with isolated cricoarytenoid (CA) fixation.

Videostroboscopy, electromyography, and CT scanning may help to distinguish a fixed cricoarytenoid (CA) joint from an immobile vocal fold of another cause. Of these examinations, videostroboscopy is the most readily available and useful to determine the exact position of the arytenoid, to assess subtle movements, and to determine the relative positions of the vocal folds, which may help to narrow the differential diagnoses.

With regard to electromyography, however, a retrospective study by Martínez-Martínez et al indicated that in patients with vocal fold immobility but normal laryngeal electromyography results, it is best not to assume that the immobility has resulted from cricoarytenoid (CA) fixation. The investigators found that immobility in such patients stemmed from a variety of causes, including idiopathic and iatrogenic etiologies, as well as central nervous system damage and external compression. [5]

Operative direct laryngoscopy is the criterion standard for clinical evaluation of cricoarytenoid (CA) joint mobility.

  • The recommended technique requires that the patient be under general anesthesia with deep paralysis.

  • In the ideal situation, the patient is in laryngeal suspension, and the examiner uses 1 hand to externally stabilize the larynx while attempting endoscopic manipulation of the arytenoid.

  • This technique is intended to avoid misinterpreting movement of the entire larynx as arytenoid mobility.

  • Surrounding tissues, as well as the arytenoid, should be palpated to determine the presence of scarring or associated lesions.

  • Lateral displacement of 1 arytenoid accompanied by passive medial movement of the other may indicate interarytenoid tethering.

  • Careful attention to the exact placement of the laryngoscope is also important.

  • Placement of the blade too deeply in the laryngeal inlet may artificially restrict motion.

  • Note any associated subglottic stenosis and/or tracheal stenosis at the time of endoscopy.

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Histologic Findings

Histologic involvement of the cricoarytenoid (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.

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