Abstract
Tracheotomy is playing a very important role in daily clinic. However, inability of decannulation or closing tracheostoma is not so seldom seen. When no anatomic laryngotracheal abnormality can be demonstrated, the inability to decannulate a prolonged tracheotomiged patient may in fact be explained by the temporary loss of laryngeal abductor function. This study was carried out to see if the phasic inspiratory activity of the laryngeal abductors may be altered by tracheotomy.
Eleven dogs were used for this study. Motor action potentials of the posterior cricoarytnoid muscle were electromyographically studied while varying the resistance of the upper airway and after acute and/or chronic tracheotomy. The loss of abductor activity persists as long as air way resistance remains severely reduced. Prolonged reduction of airway resistance by, for example, tracheotomy, resulted in difficulty of reestablishment of abductor function. It seems most likely that gradual reduction of tracheotomy bore or increasing ventilatory resistance by partial cannula occlusion is very effective in restoring the phasic activity of the posterior cricoarytenoid muscle in a patient with problem of decannulation due to affected abductive movement of the vocal cord.
In fact, we had a tracheotomized patient with inability of closing the tracheostoma due to sever stridor and dyspnoea.
Laryngobronchoscopic examination revealed that there was no significant anatomical and organic abnormality but for loss of laryngeal abductor function. Supported by the present experimental data, gradual reduction of the bore of tracheostoma was carried out while careful checking blood gas values.
Finaliy, laryngeal abductor function was obtained enough to inspirate respiratory air. In this paper, this case was reported and discussed in terms of the present experimental data.
