New insights into the pathomechanism of postintubation arytenoid subluxation.

BACKGROUND: Impaired movement of the cricoarytenoid joint with hoarseness and immobility of the vocal ligament can occur as a consequence of endotracheal intubation. The biomechanics and pathomechanism of cricoarytenoid subluxation have not been demonstrated to date.

METHODS: The present study attempts to simulate the trauma that has been associated with arytenoid cartilage subluxation in intubation trials on 37 unfixed larynges in cadavers from persons aged 25 to 89 years. Larynges were intubated or extubated according to former conceptions of arytenoid subluxation, which assume that the arytenoid tip enters the lumen of the tracheal tube, or that a deflection of the arytenoid occurs during withdrawal of the endotracheal tube with the cuff of the tube only partially deflated. Also, manual attempts were carried out to subluxate the arytenoid cartilage. Subsequently after dissecting the left and right cricoarytenoid joint from each larynx, the morphologic changes induced experimentally were analyzed using gross microscopic and histologic methods.

RESULTS: Within the scope of the experiment, it proved impossible to produce any subluxation of a cricoarytenoid joint. Histologic analysis revealed injuries of synovial folds, joint-surface impressions of the articular cartilage, and fractures in the area of the subchondral bone in some joints.

CONCLUSIONS: Based on the morphologic results, it was concluded that intubation trauma of the cricoarytenoid joint does not cause subluxation per se, but rather that formation of a hemarthros or fractures of the joint bodies lead to fixation of the joint surfaces in an abnormal position. Subsequent ankylosis may occur.