Otolaryngol Clin N Am 40 (2007) 1091–1108

Vocal Fold Masses
Kenneth W. Altman, MD, PhD, FACS
Department of Otolaryngology, The Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1189, New York, NY 10029, USA

Although many performers consider vocal fold masses, such as nodules, the bane of their existence, it is rare that these lesions are true career-breakers. It is essential, however, that the many issues contributing to the development of these lesions be identified and a multidisciplinary approach instituted to obtain the best possible and most consistent outcome. In the context of the professional voice, lesions are generally benign and inflammatory, but professional voice users often engage in carcinogenic activities, such as smoking, alcohol abuse, and use or abuse of recreational drugs. Such behaviors increase the risk for malignancies and the possibility of such cannot be overlooked. Also, the title of this article, vocal fold masses, has been chosen to reinforce the concept that these inflammatory conditions add weight to the vocal folds and impair vocal closure. This article reviews the multifactorial contributions to voice disorders with emphasis on the pathophysiology of vocal masses, describes the resulting effects on voice function, and elaborates on the types of masses encountered in professional voice users.

Multifactorial contributions to developing vocal masses Voice use demands (overuse) and vocal technique (misuse) are central to the trauma and pathogenesis of vocal fold masses in professional voice users. Common to performers and other professionals is a passion for communication that often pushes the scope of voice use relating to amount of time, intensity, frequency of use, vocal range, and more advanced techniques. Young performers, in particular, usually use their voices in many different roles that include self-management and day jobs also requiring their voices. The blossoming use of cellular telephones, especially in loud public environments, significantly adds to this sustained and repetitive vocal trauma. Trauma and subsequent inflammation manifest as vocal limitations
E-mail address: kenneth.altman@mountsinai.org 0030-6665/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.otc.2007.05.011




that frustrate the professional voice user, and there is a tendency to try to exceed these limitations. Paying tribute to these personality factors in the pathogenesis of nodules and polyps, Yano and colleagues 1982 [1] recognized significantly higher extroversion scores on Maudsley Personality Inventory in these patients. More recently, Roy and colleagues [2] used the Multidimensional Personality Questionnaire to evaluate personality features distinct to functional dysphonia and those who have vocal nodules. They determined that the functional dysphonia group was introverted, stress-reactive, alienated, and unhappy. In contrast, the vocal nodules group was considered to be socially dominant, stress-reactive, aggressive, and impulsive. Based on the multifactorial nature of voice disorders, underlying medical conditions, medications, and the environment add to the synergy in pathogenesis of vocal fold masses. With the larynx at the epicenter, the significant interrelations of the respiratory and upper gastrointestinal tracts also predispose the vocal folds to further damage. These contributing diseases include rhinitis, allergy, sinusitis, asthma, bronchitis, laryngopharyngeal reflux, and others discussed elsewhere in this issue. Environmental factors include allergens, dust and other particulates, tobacco smoke, and a host of occupational irritants. Principal to medical conditions that contribute to inflammatory vocal lesions is laryngopharyngeal reflux (LPR). There are many examples in the literature; Kuhn and colleagues [3] studied 11 patients who had vocal nodules using 24-hour simultaneous three-site pharyngoesophageal pH monitoring. They found pharyngeal acid reflux events in 7 patients in that 24-hour period (one to four episodes) compared with 2 of 11 controls studied (one to two episodes). In a follow-up study by Ulualp and colleagues [4], 9 patients who had vocal nodules and posterior laryngitis underwent similar evaluation, in which 78% were found to have pharyngeal acid reflux (significantly higher than controls). It is believed that the baseline inflammation resulting from LPR episodes predisposes the vocal folds to the stresses from vocal overuse and misuse. In a series of allergy patients who had laryngeal disease, Hocevar-Boltezar and colleagues [5] found that treatment of 70 patients who had laryngitis and positive allergy skin tests resulted in an improved outcome compared with 5 patients who did not receive treatment, suggesting that hypersensitivity to inhalatory and nutritional allergens makes laryngeal mucosa more susceptible to the adverse action of other factors. This example also reinforces the synergistic effects contributing to the development of vocal fold masses.

Pathophysiology, shearing stress, and compensation Because vocal overuse and misuse are central to the development of vocal fold masses, it is important to understand how biomechanical factors work



on the membranous vocal folds to produce such lesions. Jiang and colleagues [6] developed a mathematical computer-based model to describe the vibratory response of the vocal folds during phonation using the finite element method. They found that in normal phonation, mechanical stress was the least at the midpoint of the membranous vocal fold and highest at tendon attachments. In contrast, during hyperfunctional dysphonia there was an increase in the second mode of vibration, resulting in incomplete approximation of the vocal folds posteriorly and increased stress at the location between vibratory segments. In other words, when there was increased stiffness in the body of the vocal folds, the midpoint of the membranous vocal folds encountered higher shearing stresses. Furthermore, when there was already a nodule or mass, it produced a high mechanical stress at its base during vibration. The authors concluded that intraepithelial stress plays an important role in the pathogenesis of nodules and other masses, and that an abnormal vibratory mode may be more damaging than a high intensity of vibration [6]. In a follow-up study using a self-oscillating model, mechanical stress was noted to periodically undulate with the vibration of the vocal folds, and that vocal impact caused a jump in the normal stress value [7]. The model was also able to confirm that stress was significantly higher on the surface of the vocal folds compared with that under the surface. These models reinforce the concept of how vocal impact results in vibratory trauma to the vocal folds, and that stresses are compounded once a lesion is present. Many lesions can result (at least in part) from this process, including nodules, polyps, and cysts, but other pathology should be considered, such as reactive lesions, intracordal scarring, feeding varices, and reparative granuloma. The direct effect of the vocal mass is to add weight to the vocal fold, which decreases its vibratory qualities and frequency as demonstrated on strobolaryngoscopy. There is a clinical decrease in phonatory pitch along with an abbreviated pitch range, as demonstrated on voice function testing. The presence of the mass causes impaired vocal phase closure during phonation, resulting in excess air egress. Clinically, this adds to a breathy quality of the voice, but also contributes to vocal fatigue. Disruption of vocal fold vibration and phase closure often leads to phase asymmetry (depending on the specific lesion), which adds to a grainy quality of the voice. At this point in the development of the vocal mass, there is a self-perpetuating cycle of inflammation and trauma. Although behavioral qualities contribute to the initial vocal trauma that leads to the development of this process, the presence of a lesion can result in compensatory muscle tension in an effort to reduce excess air flow through the glottis. Altman and colleagues [8] reviewed 150 patients who had muscle tension dysphonia, in which 34 had polyps, 20 had nodules, and 12 had vocal cysts. They found a significant degree of compensatory muscle hyperconstriction in this population. Nevertheless, the multifactorial contributions and spectrum of lesions that may result emphasize the importance of strobolaryngoscopy in



assessment and multidisciplinary approach with speech and voice therapy, medical, and surgical options.

Prevalence of vocal masses and dysphonia in voice professionals Teachers are perhaps the largest group of voice professionals who seem to be at higher risk for the development of hoarseness and vocal masses. Sulkowski and Kowalska [9] analyzed 1261 cases of occupational voice disorders referred for otolaryngologic evaluation in Poland over a 5-year period. Some 66% of these patients were primary school teachers, and 55% of referrals were 51 to 60 years of age. Overall, vocal nodules were found in 4.2%. In a Finnish study, Smolander and Huttunen [10] surveyed 181 teachers, of whom 42% reported frequent voice symptoms, and 10% had history of vocal nodules. Because the evolution of these lesions is complex and the laryngologist initially evaluates patients after they have experienced voice limitations over a period of time, it is uncommon to have an isolated lesion without concomitant or confounding findings. Similarly, nodules are often a ‘‘wastebasket’’ diagnosis for those clinicians unskilled to differentiate between nodules, polyps, cysts, reactive lesions, and intracordal scarring. Although it may be a matter of semantics what to name a lesion, the description is nevertheless helpful in considering prognosis and therapeutic plan. Nagata and colleagues [11] reviewed their 10-year experience with 1156 patients and found 372 who had nodules and 784 who had polyps. Sataloff and colleagues [12] reviewed their experience with videostroboscopy on 377 patients and found nodules in 32, polyps in 4, cysts in 8, granulomas in 3, Reinke edema in 4, and scar in 32. An in-depth discussion of these vocal fold masses follows. Discussion about each of these masses follows with relevance to diagnosis and prognosis.

Nodules Vocal nodules are defined as bilateral symmetric epithelial swelling of the anterior/mid third of the true vocal folds.
(Access Video on Nodules in online version of this article at: http://www.Oto.TheClinics. com.)

Demographically, these are seen in children, adolescents, and predominantly female adults working in professions with high voice demands. Sarfati [13] evaluated 90 French teachers referred for vocal disorders, and pathology was found in two thirds overall, with pseudocysts or nodules in one third overall. De Bodt and colleagues [14] characterized evolution of these nodules from childhood to adolescence. They examined a group of 34 post-



mutational adolescents who had a prior diagnosis of vocal fold nodules. These nodules were still present in 47% of girls but only 7% of boys. The degree of dysphonia in childhood and the presence of allergy were also predictors of persisting voice complaints in adolescence. This study reinforces multifactorial contributions to the development of these lesions, including behavior. The female preponderance from childhood to adolescence, coupled with adult female preponderance in other studies, further confirms that females are at particular risk. Perhaps the softer intensity of female voices leads to more hyperfunction in adult professional environments with louder background noise. One additional note is made of preponderance of nodules in patients who have congenital microweb. Ruiz and colleagues [15] reviewed a sample of 107 patients who had vocal nodules and recognized microweb in 9.4%, although the presence of microweb did not affect nodule location. Although this is a small portion of those patients who develop nodules, it does imply that the clinician should have a heightened awareness of the presence of microwebs, which may have additional implications of treatment and prognosis. The pathophysiology of vocal nodules relies on the mid-membranous vocal fold experiencing maximal shearing and collision forces. This location corresponds to the junction of the anterior to middle vocal folds (because the posterior third of the vocal folds is coupled to the vocal process of the arytenoids). This repeated collision initially results in localized vascular congestion with edema. Eventually hyalinization of Reinke space with thickening of overlying epithelium occurs with the development of epithelial hyperplasia. Consequently, the histology of nodules is distinct from polyps and other vocal lesions. Kotby and colleagues [16] collected 11 patients who had nodules (all female) to characterize this histology. Nodules are generally acellular, with thickening of epithelium over a matrix with abundant fibrin and organized collagen. Polyps also have a more pronounced epithelial reaction and a more dense fibrous stroma than polyps. Immunohistochemical characterization of nodules reveals a thickened basement membrane zone rich in collagen type IV and more intense fibronectin staining [17]. Patients who have vocal nodules present with chronic hoarseness, often with repeated episodes of more severe voice loss. Singers may complain of a loss of ability to sing high notes softly, with frequent voice breaks, increased breathiness, and vocal fatigue. Strobolaryngoscopy reveals bilateral symmetric superficial swelling of the vocal folds at the striking zone junction of the anterior to middle thirds (Fig. 1A). There is slightly decreased amplitude of the mucosal wave, but the wave is generally symmetric. Because there is hourglass-shaped glottal closure, there is consequently decreased phase closure (Fig. 1B). The mucus layer on the surface of the vocal folds is also important for lubrication and reducing friction. Patients who have vocal nodules may



Fig. 1. Vocal nodules in a classical singer (A) during inspiration, and (B) during phonation. Note the hourglass configuration with pinpoint phase closure on strobolaryngoscopy.

subsequently have irregular vibration of the surface mucus layer, perhaps resulting in drying, leading to impaired lubrication and an exacerbation of the surface stresses leading to the formation of nodules [18]. In addition, abnormal or excess mucus has been anecdotally noted by the author to be responsible for increased voice breaks in singers when transitioning through the passaggio (ascending glissando from the chest voice into the head voice). When considering treatment options for a patient who has vocal nodules, it is useful to discuss with the patient a simple analogy of a carpenter using a hammer over a long period of time without gloves. As a result, calluses form at the areas of maximal impact with the hand. Using this analogy, one may expect that conservative (nonsurgical) treatment would be applicable to the patient who has true vocal nodules. Hogikyan and colleagues [19] recognized a consensus among otolaryngologists, speech pathologists, and teachers of singing regarding the treatment of singers who have nodules. Addressing voice use demands, improper technique, optimizing other contributing factors, and coordinating care were believed to be paramount. Indications for microsurgical treatment include longstanding nodules, particularly when other factors, including speech therapy, have been maximized, and suspicion of a primary lesion with a reactive callus on the other vocal fold. Microsurgical technique is addressed elsewhere; it is imperative to preserve normal anatomy, keeping the plane of dissection superficial, and to minimize trauma to the lamina propria. Polyps Vocal polyps are unilateral, occasionally pedunculated masses encountered on the true vocal fold. They occur more often in males, after intense intermittent voice abuse, history of aspirin or anticoagulant use, or other vocal trauma, such as endotracheal intubation. Kotby and colleagues [16] reviewed 19 patients who had polyps, of whom 16 (84%) were male. The pathophysiology is believed to be attributable to breakage of a capillary in Reinke space



(superficial lamina propria) with subsequent extravasation of blood, resultant local edema, and ultimate organization with hyalinized stroma. The resulting mass may be broad-based or pedunculated, and hemorrhagic versus nonhemorrhagic (Fig. 2).
(Access Video on Pre-op Excision of Bilateral Polyps in online version of this article at: http://www.Oto.TheClinics.com)

Hemorrhagic polyps may also have a feeding blood vessel, or varix.
(Access Video on Hemorrhagic Polyp in online version of this article at: http://www.Oto. TheClinics.com)

Although the gross appearance may vary, the lesion is generally considered to be an outpouching of inflamed and organized Reinke space. A superficial nonhemorrhagic, broad-based polyp may therefore be interpreted as or called a pseudocyst. Pathologically, polyps are acellular, with thickened epithelium over superficial lamina propria and increased vascularity in an abundant delicate fibrin stromal matrix. They have more vasculature and less organized collagen than nodules, but the distinction may be difficult for the pathologist [20]. Immunohistochemistry studies reveal clustered fibronectin and disruption of laminar pattern suggesting diffuse injury in the region of the polyp [17]. On strobolaryngoscopy, vocal folds with small polyps generally have intact mucosal waves but phase asymmetry because of the impaired phase closure and the mass effect of the polyp. Vocal folds with larger polyps have more prominent decreased mucosal wave amplitude. Thibeault and colleagues [21] characterized gene expression in vocal polyps compared with Reinke edema. They found evidence of enhanced expression of extracellular matrix proteins in vocal polyps corresponding to increased mucosal wave stiffness observed on strobolaryngoscopy. Both nodules and polyps result in excess air egress during phonation (with a relatively breathy voice), and earlier vocal fatigue, frequent voice breaks in

Fig. 2. Vocal polyps. (A) Hemorrhagic. (B) Broad-based, nonhemorrhagic.



singers, and worsening hoarseness with high-pitched soft phonation. As such, this decreased vocal efficiency with decreased mucosal wave phase closure has been quantified with decreased subglottal and acoustic power [22]. Because polyps are asymmetric masses of the vocal folds, they are more prone to result in chaotic vibrations and aperiodic mucosal waves [23]. In the treatment of patients who have vocal polyps, all of the factors that contribute to voice disorders should be addressed from a multidisciplinary perspective, and polyps are usually addressed with microsurgery. An evolving treatment modality for particularly hemorrhagic polyps is the use of officebased technology using lasers. The wavelength of the lasers is well absorbed by hemoglobin, and damage to the epithelium is minimal. In one recent pilot study evaluating the use of the pulsed-dye laser (585 nm), small vascular polyps showed greater potential for resolution over larger polyps [24]. There have also been reports (and anecdotal observation by the author of this article and others) that small vocal polyps may completely resolve with conservative nonsurgical treatment [25]. One would expect that smaller lesions and those that have been present for shorter periods of time may be more prone to regression, especially in patients who are more compliant with treatment.

Cysts Cysts are subepidermal epithelial-lined sacs located within the lamina propria, and may be mucus retention or epidermoid in origin. Mucus retention cysts form when a mucous gland duct becomes obstructed (usually during an upper respiratory infection or with overuse), retaining glandular secretions.
(Access Video on Pre-op Subepithelial/Mucous Retention Cyst in online version of this article at: http://www.Oto.TheClinics.com.)

Epidermoid cysts develop either from congenital cell rests in the subepithelium of the fourth and sixth branchial arches or from healing injured mucosa burying epithelium.
(Access Video on Left Cyst, Right Nodule in online version of this article at: http://www. Oto.TheClinics.com.)

A ruptured cyst may result in scarring within the lamina propria or in a sulcus. A cyst may also irritate the contralateral vocal fold, producing a reactive lesion on that vocal fold. The history of a patient who has a vocal cyst is similar to those of patients who have nodules and polyps, but with less vocal limitation than expected from its size. The voice often sounds diplophonic (particularly with epidermoid cysts), whereby there is great pitch instability and there is splitting of the fundamental frequency overtones. As with nodules and polyps, this is usually accompanied by vocal hyperfunction, which is often compensatory.



Bouchayer and colleagues [26] reviewed their experience with 157 cases of cysts, sulci, and mucosal bridges over a 10-year period. Cysts were present in 78, and more commonly in females. Female professional singers may note increasing vocal limitation and voice roughness when they are premenstrual [27], and there is anecdotal evidence of varying cyst size with the female monthly cycle. Consequently, many phonosurgeons exercise caution when operating on premenstrual women. On strobolaryngoscopy, the vocal folds appear asymmetric with occasional evidence of the subepithelial mass (Fig. 3). Because of displacement of lamina propria, there is significant decreased or absent mucosal wave on the side of the cyst. Phase closure depends on the cyst size and whether there is the development of a contralateral reactive callus. Shohet and colleagues [28] compared stroboscopic findings between cysts and polyps. They determined that the mucosal wave was the most important parameter in differentiating cysts from polyps. They also found the mucosal wave to be diminished or absent in 100% of vocal fold cysts, and the wave to be present in 80% of polyps. Treatment again requires a multidisciplinary approach addressing factors that contribute to voice disorders. Although it is imperative to respect vocal limitations, a true cyst does not resolve with conservative management. The phonosurgical approach is discussed elsewhere in this issue, but requires more extensive dissection because the cyst is in the submucosal plane. The cyst may also be associated with intracordal scarring, requiring a more elaborate dissection. Consequently, recovery of the mucosal wave is prolonged and may never return to being completely normal. Furthermore, leaving behind a minute fragment of epithelium in the cyst sac may result in recurrence of the cyst. Some vocal professionals have been know to have cysts that do not cause substantial limitation to their singing careers and have been observed without surgery. Consideration of surgery in

Fig. 3. Vocal cyst.



a vocal professional with this complex lesion should not be taken lightly, therefore, and there should be a lengthy discussion of the risks and alternatives to surgery. Reactive lesions The presence of a unilateral vocal fold lesion results in hourglass-shaped closure of the membranous vocal folds during phonation. Consequently, there are extra shearing forces on the contralateral vocal fold that may produce a reactive callus with epithelial hyperplasia. A unilateral lesion with reactive callus formation may appear as bilateral lesions, such as nodules, that may confound the diagnosis, prognosis, and ultimate management. Rosen and colleagues [29] evaluated a series of 85 patients who had bilateral vocal fold lesions and found 21 to have nodules and 64 to have a unilateral vocal fold lesion with a contralateral reactive lesion (UVFL/RL). When comparing patients who had nodules to those who had UVFL/RL, they found statistically significant differences in (1) symmetry of vocal fold vibration, (2) amplitude perturbations, (3) estimated subglottic pressure, and (4) voice handicap index as tools to differentiate nodules from UVFL/RL. It is important to distinguish bilateral lesions, such as nodules, from a primary lesion with reactive callus, from the standpoint of prognosis and surgical planning.
(Access Video on Left Cyst, Right Nodule in online version of this article at: http://www. Oto.TheClinics.com.)

Fig. 4A shows an example of a singer who has a left vocal polyp and reactive right vocal fold broad-based edema/callus. After a 1-month period of reducing voice use, speech therapy, and treatment of LPR, Fig. 4B shows significant improvement in the right reactive callus. As such, contralateral reactive lesions are often not removed in microsurgery for the primary lesion, because the reactive lesion tends to resolve with conservative management. Intracordal scarring Repeated inflammation, vocal trauma, vocal hemorrhage, and the presence of an intracordal cyst predispose to scarring in Reinke space. Intracordal scarring is often found in association with a cyst, particularly if it is epidermoid in origin and has ruptured. Intracordal scarring may also be found after vocal surgery involving the lamina propria, with the use of the CO2 laser, and after repeated epithelial procedures, such as those for malignancy, leukoplakia, and papilloma.
(Access Video on Left Vocal Fold Scar in online version of this article at: http://www.Oto. TheClinics.com.)



Fig. 4. (A) Left vocal polyp (on right of image) with reactive callus on the right vocal fold. (B) Resolution of the reactive callus after 1 month of voice reduction, speech therapy, and treatment of LPR.

Discussion on vocal sulcus (epithelial scarring) goes beyond the scope of this article, although it can certainly affect the professional voice [30]. Intracordal scarring is suspected on strobolaryngoscopy when there is markedly reduced or absent mucosal wave (usually asymmetric), which often affects phase closure. From a professional voice standpoint, it is crucial to differentiate between an uncomplicated subepithelial cyst and an intracordal scar, because the latter is a more complex problem with worse prognosis for professional voice rehabilitation. A convex subepithelial fullness of the membranous vocal fold may warrant exploratory microflap surgery to tease out remaining cyst sac and adynamic fibrous components. Because the extracellular matrix components of the lamina propria largely determine the biomechanical properties of the vocal folds (and subsequent voice quality), there has been significant recent interest in functional soft tissue replacement substances [31]. Feeding varices and hemorrhage Varices and ectasias of the vocal fold are aberrant vessels of the microcirculation within the superficial lamina propria. Although they are not true masses, they develop as a result of the same multifactorial and shearing forces that lead to masses, and they also predispose to the development of polyps and vocal hemorrhage. Fig. 5A and B show strobolaryngoscopic examples of a varix and hemorrhage. Treatment options for these aberrant vessels have traditionally included microdissection and the use of the CO2 laser, which lead to an increased risk for postoperative scarring or sulcus. More recently, there has been renewed interest in the use of pulsed angiolytic lasers that have a wavelength within the specific absorption of oxyhemoglobin, because this has the potential of selectively ablating microvessels without damage to the overlying epithelium. Hirano and colleagues [32] demonstrated the use of the KTP laser (532 nm



Fig. 5. (A) Vocal varix, and (B) vocal fold hemorrhage (both on the patient’s right; left of the figure)

wavelength) on 12 patients who had microvascular and hemorrhagic lesions and found no adverse scarring or reduction in the mucosal wave postoperatively. Zeitels and colleagues [33] also recognized the potential for the pulsed KTP and the 585-nm pulsed-dye laser in a series of 39 patients.

Granulomas Although vocal process granulomas are not on the membranous vocal fold and often do not cause vocal symptoms, it is important for the clinician to understand differences with other vocal fold masses. Vocal process granulomas occur in response to trauma, most commonly from LPR, exacerbating chronic cough, or throat clearing. They may also occur after endotracheal intubation resulting in contact ulceration, or by forceful glottal closure when compensating for vocal paresis or presbylaryngia. Kiese-Himmel and Kruse [34] documented a male predominance with 27 out of 28 patients who had contact granuloma being male. The granuloma may appear as solitary or bilobed (Fig. 6) and often does not affect mucosal wave or phase closure on strobolaryngoscopy (unless there is underlying vocal paresis, presbylaryngia, or sulcus).
(Access Video on Vocal Process Granuloma in online version of this article at: http://www. Oto.TheClinics.com.)

Treatment relies on addressing the underlying LPR, other factors, and vocal process impact on cough or phonation. Botox to the thyroarytenoid muscle has also been shown to be helpful in reducing the glottal impact in cases refractory to LPR treatment and speech therapy. Because there is a high recurrence rate after surgical excision, surgery is reserved for cases in which the lesion is (1) enlarging; (2) compromising the voice, breathing, or swallowing; or (3) suspicious for malignancy.



Fig. 6. Left vocal process granuloma.

Papilloma Respiratory papillomatosis is an infection caused by human papillomavirus (HPV), which is also known to more commonly cause cervical, vaginal, penile, and anal warts. Although relatively uncommon in the larynx, it is still considered to be among the most common laryngeal neoplasms. There are more than 50 strains of HPV, but HPV 6 and 11 are among the most common in the larynx. As with genital warts, there is an approximately 2% likelihood of malignant degeneration in laryngeal papilloma, most commonly found with strains HPV 16 and 18. Once the wart is manifested, there is overall about a 10% likelihood of spread to the trachea or other sites, depending on the number of surgical procedures necessary to control the disease. HPV appears as a cauliflower-like exophytic protuberance, most commonly found at the transition between columnar and squamous epithelium (Fig. 7). Because pathologic specimens reveal multiple fronds of fibrovascular stalks, papilloma also has vascular stippling on the mass. Early forms may have a superficial spreading presentation, again with vascular stippling seen on laryngoscopy, providing a clue to the underlying disease.
(Access Videos on bilateral papilloma in online version of this article at: http://www.Oto. TheClinics.com.)

Strobolaryngoscopy is exceptionally helpful in making an early diagnosis, especially when recurring disease is suspected, because the mass effect of thickened diseased epithelium can present with a decreased mucosal wave. There are many controversies related to papilloma and HPV, including a high prevalence of greater than 40% with HPV-positive serology but still relatively low overt infection rates, suggesting an important role of host immune recognition [35]. The many treatments for papilloma go beyond the scope of this discussion, although shaver excision and CO2 laser excision are also used in select instances. The greater depth of penetration of the laser



Fig. 7. Vocal fold papilloma involving the left vocal fold.

than is visibly apparent increases the risk for scarring and implantation of the virus (an epithelial disease) into deeper tissues of the vocal fold and use of the CO2 laser is avoided in most centers. Pulsed-dye lasers are now considered the mainstay. The emerging use of the HPV vaccine for the most common strains and cidofovir injections to control regrowth are exciting options for protection from acquiring the disease and for treatment. Polypoid corditis Polypoid corditis, vocal polyposis, and Reinke edema are terms that refer to a proliferation or redundancy of the superficial lamina propria (Reinke space). It is often seen in patients who have chronic irritant exposure, such as tobacco smoke, laryngopharyngeal reflux, and sometimes occupational exposures. Polypoid corditis appears as an outpouching of the membranous vocal folds with an edematous, almost water-balloon appearance (Fig. 8). Strobolaryngoscopy reveals decreased mucosal wave because of the mass effect of the edema, often with phase asymmetry because of ball-valving and asymmetric edema. Treatment is aimed at reducing airway obstruction while preserving voice quality. Surgically, it is paramount to preserve some epithelium and remaining superficial lamina propria so that patients may maintain some degree of mucosal wave postoperatively. It is also imperative to stage procedures in patients who have bilateral disease to reduce the likelihood of postsurgical anterior web formation [36] Cessation of smoking and control of reflux disease are important factors in preventing recurrence of the disease after surgical excision and should be instituted before surgery to maximize the postoperative outcome. Leukoplakia and dysplasia Leukoplakia, or white plaque, refers to a spectrum of diseases affecting the vocal fold epithelium, and includes hyperkeratosis, dysplasia, and early



Fig. 8. Bilateral polypoid corditis.

verrucous changes. Overall, when leukoplakia is present there is an 8% to 14% likelihood of developing malignancy in such lesions. The pathophysiology is still unknown, but it is likely that chronic irritation and genetic predisposition form a synergy in such patients. The plaque may present initially with subtle hyperkeratotic epithelium resulting in decreased or sluggish mucosal wave on strobolaryngoscopy (Fig. 9A). Progression, particularly with dysplastic or premalignant changes, may be exophytic in a surrounding bed of erythema (Fig. 9B). Microflap excision, carbon-dioxide lasers, and pulsed-dye lasers are all treatment options, but appropriate pathologic staging must be performed because the visual appearance does not always correspond to the degree of dysplasia [37]. Treatment of hyperkeratosis and mild dysplasia is centered on eradication of disease while preserving neighboring normal anatomy and voice quality. Severe dysplasia and carcinoma in situ must be treated more aggressively.

Fig. 9. (A) Broad superficial leukoplakia blanketing bilateral vocal folds, and (B) discrete leukoplakia with severe dysplasia and microinvasion seen in a bed of erythematous vocal folds.



Fig. 10. Vocal fold squamous cell carcinoma.

Vocal fold carcinoma Squamous call carcinoma is by far the most common form of laryngeal malignancy. Those patients who have a history of tobacco smoking account for about 90% of cases, and the likelihood is far greater with a concurrent history of excess alcohol consumption. There are also anecdotal and indirect data to support the role of laryngopharyngeal reflux in causing and compounding the development of vocal fold carcinoma. Any mass lesion in a patient who has such a history should therefore raise the appropriate level of suspicion. Features of squamous carcinoma include exophytic, ulcerative, and infiltrative. Consequently, one may see on strobolaryngoscopy an area of focally decreased mucosal wave at the site of an exophytic epithelial lesion (Fig. 10). This area is distinguished from papilloma, which remains an epithelial disease, whereas carcinoma tends to infiltrate into the lamina propria, accounting for the decreased mucosal wave. Also, the fibrovascular fronds seen in papilloma are generally softer than the exophytic mass produced in carcinoma, so carcinoma would have more of a detrimental effect on phase closure seen in strobolaryngoscopy. Distinguishing carcinoma from leukoplakia is more challenging because leukoplakia may form a continuum from keratosis to severe dysplasia to microinvasive disease. Nevertheless, the degree of clinical suspicion and evidence of microinvasion with focally decreased mucosal wave should mandate further evaluation [38]. Summary There are several vocal masses that can affect the professional voice. It is important to understand the multifactorial contributions and pathogenesis of each to determine prognosis. Strobolaryngoscopy plays a crucial role in differentiating the spectrum of masses and in guiding optimal management.



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