Reinke's edema: phonatory mechanisms and management strategies

• Published in: Annals of otology, rhinology & laryngology Vol. 106; no. 7 Pt 1; p. 533
• Main Authors: Zeitels, S M, Hillman, R E, Bunting, G W, Vaughn, T
• Format: Journal Article
• Language: English
• Published: United States 01-07-1997
• Subjects: Edema - complications; Female; Follow-Up Studies; Humans; Laryngitis - complications; Laryngoscopy; Male; Microsurgery - methods; Recurrence; Severity of Illness Index; Smoking - adverse effects; Speech Acoustics; Treatment Outcome; Voice Disorders - diagnosis; Voice Disorders - etiology; Voice Disorders - physiopathology; Voice Disorders - surgery
• ISSN: 0003-4894
• DOI: 10.1177/000348949710600701

Reinke's edema (RE) has been associated typically with smoking and sometimes with vocal abuse, but aspects of the pathophysiology of RE remain unclear. To gain new insights into phonatory mechanisms associated with RE pathophysiology, we used an integrated battery of objective vocal function tests to analyze 20 patients (19 women) who underwent phonomicrosurgical resection. Preoperative stroboscopic examinations demonstrated that the superficial lamina propria is distended primarily on the superior vocal fold surface. Acoustically, these individuals have an abnormally low average speaking fundamental frequency (123 Hz), and they generate abnormally high average subglottal pressures (9.7 cm H2O). The presence of elevated aerodynamic driving pressures reflects difficulties in producing vocal fold vibration that are most likely the result of mass loading associated with RE, and possibly vocal hyperfunction. Furthermore, it is hypothesized that in the environment of chronic glottal mucositis secondary to smoking and reflux, the cephalad force on the vocal folds by the subglottal driving pressure contributes to the superior distention of the superficial lamina propria. Surgical reduction of the volume of the superficial lamina propria resulted in a significant elevation in fundamental frequency (154 Hz) and improvement in perturbation measures. In almost all instances, both the clinician and the patient perceived the voice as improved. However, these patients continued to generate elevated subglottal pressure (probably a sign of persistent hyperfunction) that was accompanied by visually observed supraglottal strain despite the normal-sized vocal folds. This finding suggests that persistent hyperfunctional vocal behaviors may contribute to postsurgical RE recurrence if therapeutic strategies are not instituted to modify such behavior.