[Phonosurgery of chronic vocal cord edema]

Chronic (Reinke's) oedema of the vocal folds is a frequent and declicate objective of phonosurgery. It is characterized by a marked bilateral subepithelial oedema, which develops by degrees, as a non-specific reaction of the vocal folds to various irritative noxious agents (especially smoking), in patients with some predisposition. It is found, by the light and electron microscopes and immunohistochemistry, that oedema is characterized by subepithelial fissure-like spaces, which accumulate a protein-rich fluid, and develops like neobursae. Therefore, mechanical factors and functional influences may also contribute to the development of Reinke's oedema. The voice is low pitched and with various degrees of hoarseness. Reinke's oedema alters the mechanical properties of the cover, which becomes very pliable and with reduced stiffness, incapacitating the vocal fold for production of high tones. Hoarseness is induced in subject with associated laryngitis, or disbalance in mechanical properties of the vocal folds. Hyperkinetic pattern of voice production can often be seen in patients with Reinke's oedema, which is a compensatory results of reduced functional capability of the vocal folds. Stroboscopy reveals a prolonged closed phase of the vibratory cycles and strikingly marked mucosal waves.

A series of 371 patients with Reinke's oedema was operated by direct microlaryngoscopy, under the general anaesthesia. The "excessive" mucosa was removed by bimanual micro-procedure, while the care was not taken to severe layers deeper than a superficial part of the intermediate layer of the vocal fold (Reinke's space). In this procedure we used the micro-forceps and scissors, to detach oedema parallel to the free edge of the vocal fold, at its upper and lower demarcation lines, beginning from the posterior part of oedema. Another 27 patients were operated by indirect procedures. Microstroboscopy (IMS) was used in subjects, while videostroboscopy (IVS) was carried out in another 18 patients. These procedures were used when general anaesthesia was contraindicated, and in patients with Reinke's oedema of the first degree (initial oedema). In these patients only a mucosal strip was removed from the upper surface of the vocal fold, apart from the free edge. Oedema was removed bilaterally, while the formation of the postoperative web was prevented by regular examinations of the patient. In several cases of adherence between the two folds in their anterior commissure, the problem was solved indirectly by the use of a curved forceps and under the topical anaesthesia. Postoperative voice rest and administration of steroids were mandatory. Surgical and functional results were followed-up by stroboscopy over the period of at least three years after surgery. The majority of patients were additionally treated by the voice therapy, while the decision about its use was made three weeks after surgery.

Functional results of our therapeutic strategy were satisfactory in our series of 398 subjects with Reinke's oedema. In comparison with other benign lesions of the vocal folds, it was more time-consuming and required a more frequent use of the postoperative voice therapy (Table 1). Thus, we have not encountered recurrences.

During the last 10 years we operated on 1550 patients with various benign lesions of the vocal folds, including 398 subjects with Reinke's oedema (25.7%). Excision of the "excessive" mucosa may appear today as a procedure which is too radical if compared with many techniques which have been offered during the last decades: conservative excision and suction, squeezing technique, laser. Nevertheless, the histological structure of Reinke's oedema, with subepithelial fissure-like spaces indicated that the latter procedures can hardly be expected to prevent recurrences. It was found that the use of laser was not favourable in this area for its deteriorative local effect.