Vocal Polyps and Nodules

Updated: Aug 31, 2023
  • Author: Candace M Hrelec, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Practice Essentials

Vocal fold nodules (VFNs), depicted in the video below and sometimes called singer's nodules or nodes, are localized, benign, superficial growths on the medial surface of the true vocal folds (TVFs) that are commonly believed to result from phonotrauma. Nodules are bilateral, with a classic location at the junction of the anterior and middle third of the vocal fold (ie, the midpoint of the membranous vocal fold). Nodules are most often observed in women aged 20-50 years, but they are also found commonly in children (more frequently in boys than in girls), who are prone to excessive shouting or screaming. [1, 2, 3, 4, 5]

In this patient with hoarseness, opposing nodules are clearly seen at the anterior one third of the true vocal cords. These responded nicely to outpatient nonsurgical treatment (voice therapy). Video courtesy of Vijay R Ramakrishnan, MD.

Vocal fold polyps (VFPs) are generally unilateral and have a broad spectrum of appearances, from hemorrhagic to edematous, pedunculated to sessile, and gelatinous to hyalinized. VFPs are believed to result from phonotrauma; however, they are also recognized to potentially arise from a single episode of hemorrhage. In 1995, Dikkers et al found that the combination of signs of recent bleeding and depositions of fibrin and iron pigment in macrophages resided almost exclusively in polyps when compared with other benign lesions. Moreover, approximately a third of the vocal polyps in their sample showed evidence of capillary proliferation, further lending credence to the theory of bleeds as the inciting event. [6] VFPs can also be caused by smoking and/or reflux such as in polypoid corditis (Reinke edema). The video below depicts a pedunculated hemorrhagic polyp along the anterior right true vocal fold.

Along the anterior right true vocal fold, a pedunculated hemorrhagic polyp is seen. Surgical treatment is indicated. Video courtesy of Vijay R Ramakrishnan, MD.

VFPs typically involve the free edge of the vocal fold mucosa, although they may also be found along the superior or inferior borders. Occasionally, a more diffuse pattern termed polypoid degeneration is observed as well and is generally considered a separate pathologic entity. For the purposes of this article, comments are limited to isolated focal lesions of the TVF.

Videostroboscopy can be used to detect laryngeal lesions and characterize them. Both nodules and polyps may interrupt the vibratory patterns of the vocal fold by increasing the mass and reducing the pliability of the overlying cover (ie, cover/body theory of vocal fold vibration), as well as by impeding proper closure of the membranous folds throughout the glottic cycle

Treatment options for VFNs and VFPs include invasive and noninvasive techniques, [7]  although surgery for VFNs is rare (fewer than 5% of cases).

Confronted with symptoms of dysphonia, the clinician is charged with accurate diagnosis and timely institution of appropriate therapeutic intervention. Vocal fold lesions are a common cause of hoarseness. A more thorough understanding of these benign lesions has been the goal of laryngologists and voice scientists over the last several decades, since Hirano's description of the complex layered microanatomy of the human vocal fold.

Several distinct pathologic entities are encompassed in this broad category, including laryngeal papillomatosis, vocal fold cysts, intracordal cysts, sulcus vocalis, and vascular ectasia, as well as VFNs and VFPs. Each of these entities has an attendant clinical presentation; each presents diagnostic and treatment challenges. This article focuses specifically on vocal fold nodules VFNs and VFPs. [8]

Signs and symptoms of vocal fold polyps and nodules

The clinical presentation of benign vocal fold lesions is most commonly associated with voice change. [9] Typical presenting symptoms include generalized and persistent hoarseness, change in voice quality, and increased effort in producing the voice. The laryngeal examination may show either unilateral or bilateral lesions of the TVF.

Workup in vocal fold polyps and nodules

Videostroboscopy is far more sensitive for detecting laryngeal lesions when compared with other indirect laryngoscopy techniques. Measurements within a voice laboratory, including aerodynamic, acoustic, and videostroboscopic baselines (as well as a high-quality audio recording of the patient's voice) are all helpful for appropriate pretreatment and posttreatment documentation of VFNs and VFPs. Also, clinician and patient perceptual measures are commonly performed to more subjectively gauge the impact of the vocal disability and improvement.

Management of vocal fold polyps and nodules

Intervention in the form of voice therapy to correct vocal use issues may be all that is required to address the vast majority of VFNs, as well as some small VFPs.

Although the surgical removal of VFNs is relatively uncommon, recommendations for such a procedure include minimal normal tissue disruption, with an endpoint of a straight medial TVF edge without divots or remaining excess tissue.

Much debate continues regarding the relative merits of cold steel versus carbon dioxide laser removal of benign laryngeal pathology. Both techniques have the known potential to cause scarring with disruption of the lamina propria (LP). Despite the advent of high-magnification operative microscopes, microlaryngeal instrumentation, and the refinement of microspot manipulators for the carbon dioxide laser, both techniques require extreme care and a skilled surgeon to avoid vocal complications.



Nonneoplastic lesions of the vocal folds are presumed to represent a response to vocal trauma (more specifically, phonotrauma in the case of vocal fold polyps and vocal fold nodules). A 1999 survey performed by Hogikyan et al elicited opinions of the professional groups most involved with the care of the voice (including laryngologists, speech language pathologists, and singing teachers) to gauge the prevalence of opinions regarding the specific entity of VFNs. [10] The survey found that the prevailing and nearly unanimous belief follows: "Practices that constitute either abuse or misuse of the speaking and/or singing voice were felt by all groups to be of greatest importance in causing vocal fold nodules in singers."

For the sake of clarity, vocal abuse refers to vocal behaviors that are practiced under circumstances that lead to trauma of the laryngeal mucosa. Excessive talking, prolonged and excessive loudness, use of inappropriate pitch, excessive cough, and throat clearing are some of these vocally abusive behaviors.

Vocal misuse involves abnormal vocal behaviors that cause stress or trauma to the larynx. Such practices include the use of excessive tension and effort while phonating, hard glottal attacks, and ventricular phonation. The concept of vocal overuse is self-explanatory.

In the effort to substantiate these traditional clinical beliefs regarding the etiology of vocal lesions, in 1987 Gray et al undertook the task of creating an animal model in which to study the pathologic process. [11] In an experiment designed to simulate phonotrauma, canines were hyperphonated artificially for periods of 2, 4, and 6 hours, after which the ultrastructure of their vocal fold was examined under electron microscopy to determine early anatomic changes related to phonotrauma.

With 2 hours of persistent phonation, Gray et al demonstrated reproducible structural changes that were absent in the control animals. The inherent shortcoming of such studies lies in the inability to perform longitudinal follow-up of the pathologic changes due to phonotrauma and, more importantly, the uncertainties of extrapolating data to humans (ie, given the behavioral differences between the canines in Gray's study protocol and normal human vocal behaviors as well as differences in vocal fold microanatomy).

In 2000, Andrade tested these causal behavioral assumptions by designing a retrospective study that attempted to correlate the frequency of specific, observed, vocally traumatic behavior (ie, hard glottal attack) with the type and extent of clinically visible vocal pathology. [12] The investigators hypothesized that a higher frequency of hard glottal attack would be found in patients exhibiting muscle tension dysphonia (MTD) and/or vocal fold lesions than would be found in normal speakers.

Further, investigators hypothesized that the frequency of these behaviors would correlate positively with the presence and severity (unilateral versus bilateral) of the observed vocal fold pathology. Results of Andrade's study confirmed a higher frequency of hard glottal attack in the disordered groups than in the controls. On the other hand, the study did not demonstrate a difference in frequency between the purely MTD group and those with lesions or between the unilateral and bilateral lesion groups.

In a large retrospective study of pediatric voice patients, Shah et al (2005) found that hyperfunctional vocal behaviors correlated with vocal fold nodule size, but the presence or absence of signs of reflux disease did not. [13] With a parent-rated standardized scale Roy et al (2006) confirmed that children with vocal fold nodules rate as "outgoing" or "extroverted" and scored significantly higher than controls on the "social scale." [14]

The literature notes other clinical associations with VFNs. Some authors have mentioned an anecdotal association between the presence of anterior glottic microwebs and nodules. Additionally, the contributory role of gastroesophagopharyngeal reflux in the pathogenesis of VFN has been studied.

In 1998, Kuhn et al compared a small cohort of patients with VFN against volunteers with normal health. [15] Both groups were studied with barium esophagography and ambulatory, 24-hour, 3-site pharyngoesophageal pH monitoring. Kuhn found that the prevalence of pharyngeal reflux events was significantly higher in patients with VFN compared with normal controls. Vibration-induced elevations in capillary pressure have also been hypothesized to cause vocal nodules and associated edema. [16] These results supports voice therapy aimed at reducing vibratory amplitude.

A literature review by Lechien et al indicated that laryngopharyngeal reflux increases the risk of VFN or VFP formation or development of Reinke edema, via caustic mucosal injury that makes the vocal fold mucosa more susceptible to injury. However, the investigators noted that data limitations hampered their ability to derive definitive conclusions. [17]



Indications for surgical intervention in benign TVF mucosal lesions are relative. Even in the most casual of voice users, the proposition of surgical intervention should never be taken lightly, especially given the ever-present potential for poor healing or irreversible scarring, which causes permanent change in the speaking/singing voice.

In general, vocal fold microsurgery is considered for cases in which the patient remains unacceptably vocally impaired despite compliance with a medical treatment and voice therapy regimen. Rare instances may also occur, in which the lesion (typically, a large polyp) threatens the patency of the airway. In these cases, the polyp's vocal impact is a distant secondary consideration. In other specific instances (eg, extremely long history of voice limitations, mucosal injury clearly resulting from a one-time event, clearly irreversible pathology), surgery may appropriately be considered at initial diagnosis. Even in this setting, however, the patient may benefit from one or more voice therapy sessions or from optimal preoperative education and postoperative compliance with the rehabilitative regimen.

The importance of careful patient selection cannot be overstated. At a minimum, rudimentary vocal education and a commitment to compliance with a preoperative and postoperative vocal regimen is required of any surgical candidate. This regimen routinely includes limitation of vocally damaging behavior and observance of improved vocal hygiene with respect to alcohol, caffeine, tobacco, and hydration. The patient must be committed to the recommended courses of both preoperative and postoperative voice therapy (and singing instruction as appropriate) and to the prescribed course of perioperative vocal rest that allows for optimal surgical healing and results. In the most general of terms, patients who do not meet these criteria are poor operative candidates; therefore, surgery is relatively contraindicated.


Relevant Anatomy

Advances in modern phonomicrosurgical techniques have largely stemmed from improved understanding of the complex microarchitecture of the TVF as described by Hirano. More specifically, understanding of the role of the layered architecture to normal voice production has led to surgical techniques designed for maximal preservation of the normal structure.

The TVF is composed of 5 individually identifiable layers. The deepest layer consists of the thyroarytenoid muscle body. This muscle is capable of contraction and serves to voluntarily stiffen and thicken the vibratory margin of the cord. Overlying the muscle is a region referred to as the lamina propria (LP), which can be divided into 3 portions (ie, superficial, middle, deep) based on the molecular compositions of each. The deep layer of the LP is largely comprised of densely crowded collagen fibers. The middle layer has some collagen but is distinguished by its high elastin content.

The deep and middle layers of the LP blend imperceptibly on operative dissection to form a structure commonly referred to as the vocal ligament, a recognized and important landmark in vocal fold surgery, as well as a transition zone between the body (muscle) and the cover (epithelium and superficial LP) of the TVF.

The superficial LP is composed of mostly amorphous ground substance and a few fibrils. The importance of this layer (which is not well appreciated on traditional hematoxylin and eosin [H&E] staining) to normal vibratory behavior of the TVF has been progressively elucidated over the last 30 years. The most superficial of the layers is the stratified squamous epithelial cover that overlies the LP.