In Reply:—

The background of our study was to show a new understanding of the pathomechanism leading to arytenoid dislocation. Based on our experiments we concluded that intubation trauma of the cricoarytenoid joint does not cause subluxation per se , but rather that formation of a hemarthros or serosynovitis lead to fixation of the joint surfaces in an abnormal position. 1 

We agree that our study may exclude forces from singular endotracheal tube placement as the culprit in subluxation and we also agree that in a living patient the larynx undergoes movements during insertion of a laryngoscope which we were unable to simulate in our experiments. But this is not the point. Analyzing the anatomy of the human cricoarytenoid joint in several studies 2–4we were able to show that the joint can be compared with diarthrodial joints at the limbs and that the joint capsule consists of unexpected large and intensively vascularized synovial folds projecting into the joint cavity. Laxity of the joint capsule and the large synovial folds are predisposing factors for intubation trauma of the cricoarytenoid joint, potentially leading to hemarthrosis and finally to cricoarytenoid joint dysfunction. 5 

Naturally, a postmortem study is not able to show what happens in a living patient but our experiments give us hints about the probable pathomechanism of arytenoid dislocation. Our concept with the occurrence of joint cavity hemorrhage or serosynovitis and after muscle contractures is able to explain all contradictions in the literature regarding arytenoid subluxation.

How would Professor Kempen explain cases of arytenoid dysfunction that occurred some days after easy intubation. In these cases phonation was normal directly after extubation and arytenoid dislocation primary occurred after some days. 6,7How will he explain the experience of laryngologists 8treating dislocated arytenoids who report that the arytenoid was movable when touching it with a spatula under light pressure but moved back in its starting position after release.

We do not contradict Professor Kempen that arytenoid subluxation may exist under intra vitam forces and conditions. But our experiments speak against this concept and allow the conclusion that arytenoid dislocation is based on the pathomechanism mentioned above 1and therefore we should speak of “postintubation cricoarytenoid joint dysfunction.”

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