Dysphonia associated with vocal fold scar is one of the most challenging voice disorders to both patients and clinicians. The best treatment of vocal fold scar is prevention. In no medical procedure is the phrase primum non nocere ("first do no harm") more applicable than in surgery of the larynx. Certainly, improperly performed or timed surgical intervention can result in irreversible dysfunction and dysphonia. Benign vocal lesions should be approached conservatively whenever possible; surgery should be reserved for unresolving lesions that result in dysphonia. This requires precise and conservative phonomicrosurgery with proper postoperative voice care. New techniques to prevent or reduce scarring are becoming more widespread; nevertheless, vocal fold scarring following surgery is not uncommon.
This article focuses on surgical and nonsurgical treatment of vocal fold scars. No proven treatment currently exists for every case of vocal fold scarring. Conservative treatment therefore should be exhausted before considering surgical intervention, which then should be based on the modern concepts of the vocal fold microanatomy and histology of the vocal fold physiology.
The image below depicts vocal fold scarring.
Iatrogenic injury to vocal cords typically consists of scarring, fibrosis, webbing, or sulcus formation. The term sulcus vocalis is used to describe a depression or groove in the surface of the vocal fold mucosa that typically is found on the leading edge of the vibratory surface. Along the sulcus, the mucosal cover is scarred down to the underlying vocal ligament and therefore is tethered with limited mobility. 
Iatrogenic injury is likely underreported, and its true incidence is difficult to estimate. The incidence of sulcus vocalis is impossible to determine because of the variation in presentation, etiology, and diagnosis.  Most cases of sulcus are undiagnosed because of subclinical symptoms, lack of awareness, and difficulty in identification because of the relative rarity of videostroboscopy.
Surgical causes include an overresection of the superficial layer of the lamina propria, which results in remucosalization over the deficient area and damage to the vocal ligament and deep layers of the lamina propria. Surgical incisions or abrasions on both true vocal folds can lead to webbing and scarring between the vocal cords. In particular, damage to the anterior commissure may result in scarring and web formation, especially if surgery is performed on the anterior portion of both true cords. With respect to surgical incisions, the depth of injury and the damage to surrounding tissues are the most important predictors of scar formation. Surgical dissection or laser ablation into the zone of the vocal ligament can result in significant fibrosis and scar formation. Injudicious use of the laser may result in vaporization of the mucosa or thermal injury with a zone of damage extending through the mucosa into the vocal ligament or vocalis muscle and surrounding tissue.
A defect in the medial surface of the true vocal fold along the sulcus may produce a glottic gap. More importantly, the vocal cover fibroses to the vocal ligament and the resulting mucosal wave may be significantly diminished or absent. This decreased pliability restricts the Bernoulli and myoelastic effects whereby transglottic airflow medializes the leading edge of the vocal fold. The overall effect is a higher fundamental frequency with significantly reduced harmonics and a harsher voice quality. At the extremes of scarring, glottic closure is impaired, which may lead to a very weak breathy voice and possibly aspiration of liquids.
Patients may have had past vocal cord mucosal stripping or laser surgery. Typically, the patient has a history of surgery for nodules and developed hoarseness postoperatively that never improved. Patients complain of hoarseness and may complain of dysphonia or a higher-pitched, thin voice. Patients often have symptoms of glottal insufficiency, including vocal fatigue, breathiness, and poor volume and projection. The voice may be thin and exhibit a higher fundamental frequency. Patients also may revert to use of the false vocal folds, which results in a strained, low-pitched, dysphonic voice. If vocal fold scarring is severe, patients may complain of shortness of breath caused by excessive loss of air with phonation. In severe cases of glottic insufficiency, patients may experience aspiration of thin liquids or dysphagia.
Examination of the glottis may reveal an anterior web and/or an irregular, fibrotic, and sometimes atrophic vocal fold with mucosal hypertrophy. Videostroboscopy reveals a decreased or absent mucosal wave, and often the medial edge of the injured cord does not approximate the other during phonation. In addition, the cords may be at different levels, leading to incomplete closure. In sulcus vocalis, examination of the true vocal fold reveals a linear depression or an area of incomplete closure. Videostroboscopy reveals an area of decreased mucosal wave corresponding to the sulcus and may demonstrate associated incomplete closure.
Indications for surgical intervention include impaired function secondary to troublesome dysphonia, severe breathiness with vocal fatigue, aspiration, and uncertainty as to the diagnosis.
Awareness of the body-cover principle of vocal fold vibration is essential to the understanding of vocal fold scarring. The vocal fold is composed of a muscle covered by a free mucosal edge that vibrates and can be separated into discrete layers. Each layer has distinct mechanical properties and can be differentiated by the concentration of elastin and collagen fibers that run parallel to the leading edge. The delicate arrangement of the extracellular matrix proteins within the lamina propria permits passive movement of the vocal cover over the body, resulting in the formation of the mucosal wave as air is passed through the glottis as a release of building subglottic pressure.
Fibroblasts are found in high concentrations in the deep layers of the lamina propria and in the vicinity of the vocal ligament. Violation of these layers stimulates fibroblastic activity, which promotes scar and sulcus formation.
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