Vocal Fold Lesions

Anatomy & Pathophysiology:

The paired vocal folds (VFs) are highly specialized glottic structures that enable the production of sound (phonation) through oscillatory motion. In addition, adduction of the vocal folds serves as a protective mechanism to prevent aspiration of material into the airway. For a detailed review of vocal fold and associated laryngeal anatomy, see The Larynx. Briefly, the vocal folds are attached posteriorly to the arytenoid cartilages. Movement of the arytenoids by the intrinsic muscles of the larynx enables abduction and adduction of the vocal folds, as well as changes in their length and tension. Anteriorly, the vocal folds meet at the anterior commissure and attach to the thyroid cartilage. The space between the medial (free) edges of the vocal folds is called the rima glottidis and varies depending on how closely the vocal folds are approximated. The vocal fold consists of a muscular core (vocalis muscle) and a multilayered mucosa consisting of stratified squamous epithelium over three layers of lamina propria. The two deepest layers of lamina propria (intermediate and deep lamina propria) are collectively referred to as the vocal ligament. The elastic nature of the mucosa allows it to slide smoothly over the underlying muscle (mucosal wave) during vocal fold oscillation. This delicate and precise process can be significantly disrupted by changes in vocal fold morphology, such as those caused by vocal fold lesions.

Benign lesions of the vocal fold include polyps, cysts, nodules, and granulomas, as well as conditions such as polypoid corditis, recurrent respiratory papillomatosis, and sulcus vocalis. Most benign vocal fold lesions occur in the superficial mucosa (epithelium and superficial lamina propria). A brief overview of the pathophysiology of each of these lesions is addressed below.

Vocal fold polyps: the etiology of VF polyps is uncertain, but they are thought to arise as a result of rupture of capillaries in Reinke's space (the potential space between the epithelium and the superficial lamina propria), causing hemorrhage with subsequent local edema and organization with hyalinized stroma. These lesions are edematous outpouchings of mucosa. They tend to occur unilaterally, most commonly at the point of maximal VF vibration (the junction of the anterior one-third and posterior two-thirds of the VF). They can be pedunculated or sessile. There can be a hyperkeratotic reactive lesion of the corresponding region on the contralateral VF (which can lead to confusion with vocal fold nodules).

Vocal fold cysts: these are collections of fluid within epithelium-lined spaces. Intracordal cysts may be mucous retention cysts or epidermoid (keratin-containing) cysts. They typically occur unilaterally in the middle third of the vocal cord. Presence of a VF cyst often causes a hyperkeratotic reaction or depression deformity of the corresponding region on the contralateral VF. Analysis of VF motion with videostroboscopy reveals a diminished mucosal wave in the area of the lesion.

Vocal fold nodules: sometimes referred to as "singer's nodules" or VF nodes, these lesions represent the effects of chronic overuse of the voice. They are by definition bilateral and symmetric and are most commonly located at the junction of the anterior one-third and posterior two-thirds of the vocal fold.

Vocal process granulomas: granulomas occur on the vocal process of the arytenoid cartilages. They may be caused by irritation from vocal abuse, severe cough, trauma (such as from intubation), or laryngopharyngeal reflux.

Polypoid corditis: also referred to as Reinke's edema or smoker's polyposis, this condition involves bilateral diffuse edema of the superficial lamina propria (also known as Reinke's layer). It is strongly associated with cigarette smoking.

Recurrent respiratory papillomatosis: this condition is associated with human papillomavirus (HPV) infection and typically causes multiple papillomas throughout the respiratory tract.

Sulcus vocalis: this is a groove in the vocal fold caused by scarring and retraction of the superficial layers of the VF mucosa, which become tethered to the underlying vocal ligament. There are many possible etiologies for vocal fold scarring, including vocal trauma, infection, prior VF surgery, and progression of other benign VF lesions.

Epidemiology:

The incidence of benign vocal fold lesions varies according to the type of lesion. Vocal fold polyps are more common in men, particularly those with a history of voice abuse or cigarette smoking. Because of their association with excessive voice use, vocal fold nodules are more prevalent in professions that rely on the voice, as well as in children (who are more prone to voice abuse). Vocal fold nodules are the most common cause of persistent dysphonia in the pediatric population. Vocal process granulomas are more commonly seen in patients with a history of prior endotracheal intubation. Polypoid corditis is strongly associated with cigarette smoking and is most common in perimenopausal women.

Natural History:

Lesions that are caused by vocal trauma may persist or worsen with continued overuse of the voice. Similarly, conditions that are exacerbated by irritant exposure (such as polypoid corditis) will persist in the continued presence of the irritant. Untreated, some vocal fold lesions may produce scarring of the vocal fold mucosa, further impacting voice production.

Presentation:

Vocal fold lesions most frequently present with dysphonia, although the specific symptoms may vary widely. Patients may experience hoarseness, breathiness, or other change in voice quality, as well as voice fatigue and increased effort for voice production. Patients may experience worsening dysphonia with prolonged voice use or voice breaks at certain pitches. In some patients, only the singing voice is affected, while the speaking voice is not. Rarely, if the lesion size is large enough, patients may present with globus sensation, dysphagia, aspiration, or symptoms of airway compromise.

Differential Diagnosis of Dysphonia:

Evaluation:

History

The patient history should include the timing of symptom onset and progression, vocal use patterns, and irritant exposure (such as cigarette smoking, alcohol use, reflux, or postnasal drip). Any prior endotracheal intubations should be noted, including duration of intubation.

Physical Examination

The physical examination should include characterization of voice quality, noting the presence of hoarseness, breathiness, voice breaks, tremor, or vocal fatigue. The primary diagnostic technique for identifying vocal fold lesions is flexible fiberoptic laryngoscopy (FFL), which allows for visualization of the vocal folds. Many VF lesions can be distinguished on the basis of laterality, location on the VF, and gross appearance as assessed by FFL.

Videolaryngostroboscopy

Videolaryngostroboscopy allows for the characterization of vocal fold movement during phonation. By using a strobe light that flashes at a rate slightly offset from that of VF vibration, stroboscopy produces the illusion of slow motion. This allows for a detailed analysis of vocal fold properties that may otherwise be difficult to ascertain by FFL, such as symmetry, pliability, and mucosal wave amplitude and propagation. The presence of vocal fold lesions can change or attenuate the mucosal wave, or produce incomplete glottic closure.

Lesion	Laterality	Location	Gross Appearance	Stroboscopic Findings
Polyp	Usually unilateral	Junction of anterior one-third and posterior two-thirds of VF	Pedunculated or sessile, often with vascular markings	Asymmetric vibratory pattern in the two VFs, reduced vibration in the area of the polyp
Intracordal cyst	Unilateral	Often in the middle one-third of the VF	Fullness of vocal fold, may be translucent	Decreased pliability and mucosal wave deficit over the area of the cyst
Nodules	Bilateral	Junction of anterior one-third and posterior two-thirds of VF	Pale, symmetric	Usually no disruption of mucosal wave; hour-glass shaped glottic closure
Granuloma	Usually unilateral	Vocal process of arytenoid cartilage	Inflamed granulomatous tissue, may be ulcerated	Mucosal wave deficit and incomplete glottic closureif lesion is large enough
Polypoid corditis	Bilateral	Diffuse	Diffuse edema of the vocal folds, may have polypoid appearance	Varies; may include asymmetry in the vibratory patterns of the two VFs, increase in mucosal wave amplitude, incomplete glottic closure
Sulcus vocalis	Unilateral or bilateral	Close to the medial margin of the VF, may extend along the entire length of the VF	Groove or furrow parallel to the free edge of the VF	Area of decreased mucosal wave with incomplete glottic closure

Treatment:

The diagnosis of vocal fold polyp should be confirmed by direct laryngoscopy and excision, as large polyps may harbor early glottic carcinoma. The polyp may be excised using microinstruments or with the carbon dioxide laser. When operating on the vocal fold, care must be taken to cause as little disruption as possible to the VF microstructure. The subepithelial microflap is a direct excision method that spares the VF epithelium overlying the lesion. Details regarding direct laryngoscopy with phonomicrosurgical interventions, including microflap dissection, are given in Microdirect Laryngoscopy with Phonomicrosurgery.

Intracordal cysts are treated with surgical excision. The microflap technique is preferred to minimize damage to the surrounding vocal fold layers.

The initial approach to treatment of vocal fold nodules is via speech therapy. Surgical treatment for vocal fold nodules is rare, but may be considered in cases where voice quality remains unacceptable despite compliance with adequate voice therapy regimens. In such cases, nodules may be excised using microsurgical instruments or with carbon dioxide laser.

Conservative treatment of vocal process granulomas involves voice therapy with anti-reflux medication. In cases of severe inflammation or underlying chondritis of the arytenoid cartilage, antibiotics and corticosteroids may be prescribed as well. Recently, botulinum toxin injection has also been proposed as a therapeutic measure; the vocal fold paresis induced by the injection reduces the forcefulness of contact between the vocal folds during glottic closure, reducing trauma and further irritation of the granuloma. Granulomas can be excised if there is airway compromise or if conservative measures are ineffective; however, they have a high rate of recurrence after surgical therapy.

The most important component of treatment for polypoid corditis is smoking cessation, as continued exposure to tobacco smoke exacerbates the condition. Voice therapy may produce a modest improvement in voice quality, as patients typically also exhibit voice overuse, in addition to cigarette smoking. More severe cases may be treated with microlaryngeal surgery to reduce the edematous polyps. The VF mucosa is incised, allowing drainage or suctioning of the transudative fluid. If redundant mucosa is present after the polyp has been drained, it may then be trimmed. This technique results in minimal disturbance to the VF microstructure, as opposed to traditional polypectomy, where the mucosa is stripped from the vocal fold.

Sulcus vocalis is treated surgically. Although voice therapy is not effective in improving symptoms in patients with the condition, it may be prescribed for individuals with a history of voice overuse. In such patients, the goal is to prevent development of use-associated lesions that could again result in VF scarring after surgery. Since sulcus vocalis involves the deeper layers of the vocal fold, surgical excision is more challenging than for superficial VF lesions. Removal may entail a submucosal injection to achieve hydrodissection, incising the VF around the sulcus, and dissecting the area of scarring from the underlying vocal ligament. Others have suggested injecting fat or inserting fascia under the superficial mucosa to physically separate it from the vocal ligament.

Complications, Prognosis & Follow-Up:

Voice improvement after VF surgery typically occurs over the course of 1-3 months. Anti-reflux medication is prescribed after the procedure to minimize the risk of postoperative inflammation and scarring. Voice therapy may also be recommended to achieve optimal results. Patients are generally evaluated at regular intervals during the postoperative period with FFL and videostroboscopy to assess VF appearance and function.

The primary complication after vocal fold surgery is postoperative dysphonia. This may occur as a result of excessive tissue excision or scar formation that tethers the mucosa to the vocal ligament. In such cases, rigorous voice therapy is typically recommended. With time, the patient may be able to develop adaptive mechanisms, such as using the laryngeal muscles to compensate for decreased VF mucosal oscillation. In certain cases, revision surgery may be possible; the option is typically not considered until 6-12 months after the original procedure to allow ample time for voice improvement and resolution or stabilization of iatrogenic VF defects.

Surgical outcomes for intracordal cyst excision are good, with up to 85% of patients exhibiting restoration of normal mucosal waves after the procedure. Outcomes after microlaryngeal removal of vocal cord nodules and polyps are similarly positive, provided that patients maintain adequate vocal behavior and avoid voice abuse after surgery. While the initial response rate for vocal process granuloma excision may be high, 30-50% of granulomas recur after surgery. The success rate for surgical treatment of polypoid corditis is variable, but may be as high as 80% with smoking cessation and attention to vocal hygiene. Results of sulcus vocalis excision depend on the extent of scarring; the thinner the mucosa and the more adherent it is to the vocal ligament, the more technically difficult the surgery. Although most patients gain some improvement in voice quality relative to their preoperative state, a complete return to normal voice quality is unlikely, particularly if considerable disruption of the VF microstructure has occurred.