vocal fold masses

Otolaryngol Clin N Am

40 (2007) 1091–1108

Vocal Fold Masses

Kenneth W. Altman, MD, PhD, FACSDepartment of Otolaryngology, The Mount Sinai School of Medicine, One Gustave L.

Levy Place, Box 1189, New York, NY 10029, USA

Althoughmany performers consider vocal foldmasses, such as nodules, thebane of their existence, it is rare that these lesions are true career-breakers. It isessential, however, that the many issues contributing to the development ofthese lesions be identified and a multidisciplinary approach instituted toobtain the best possible and most consistent outcome. In the context of theprofessional voice, lesions are generally benign and inflammatory, but profes-sional voice users often engage in carcinogenic activities, such as smoking, al-cohol abuse, and use or abuse of recreational drugs. Such behaviors increasethe risk for malignancies and the possibility of such cannot be overlooked.Also, the title of this article, vocal fold masses, has been chosen to reinforcethe concept that these inflammatory conditions add weight to the vocal foldsand impair vocal closure. This article reviews the multifactorial contributionsto voice disorders with emphasis on the pathophysiology of vocal masses, de-scribes the resulting effects on voice function, and elaborates on the types ofmasses encountered in professional voice users.

Multifactorial contributions to developing vocal masses

Voice use demands (overuse) and vocal technique (misuse) are central tothe trauma and pathogenesis of vocal fold masses in professional voiceusers. Common to performers and other professionals is a passion for com-munication that often pushes the scope of voice use relating to amount oftime, intensity, frequency of use, vocal range, and more advanced tech-niques. Young performers, in particular, usually use their voices in manydifferent roles that include self-management and day jobs also requiringtheir voices. The blossoming use of cellular telephones, especially in loudpublic environments, significantly adds to this sustained and repetitive vocaltrauma. Trauma and subsequent inflammation manifest as vocal limitations

E-mail address: [email protected]

0030-6665/07/$ - see front matter � 2007 Elsevier Inc. All rights reserved.

doi:10.1016/j.otc.2007.05.011 oto.theclinics.com

mailto:[email protected]

1092 ALTMAN

that frustrate the professional voice user, and there is a tendency to try toexceed these limitations.

Paying tribute to these personality factors in the pathogenesis of nodulesand polyps, Yano and colleagues 1982 [1] recognized significantly higher ex-troversion scores on Maudsley Personality Inventory in these patients. Morerecently, Roy and colleagues [2] used the Multidimensional PersonalityQuestionnaire to evaluate personality features distinct to functional dyspho-nia and those who have vocal nodules. They determined that the functionaldysphonia 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 medicalconditions,medications, and the environment add to the synergy in pathogen-esis of vocal foldmasses.With the larynx at the epicenter, the significant inter-relations of the respiratory and upper gastrointestinal tracts also predisposethe vocal folds to further damage. These contributing diseases include rhinitis,allergy, sinusitis, asthma, bronchitis, laryngopharyngeal reflux, and othersdiscussed elsewhere in this issue. Environmental factors include allergens,dust and other particulates, tobacco smoke, and a host of occupationalirritants.

Principal to medical conditions that contribute to inflammatory vocal le-sions is laryngopharyngeal reflux (LPR). There are many examples in the lit-erature; Kuhn and colleagues [3] studied 11 patients who had vocal nodulesusing 24-hour simultaneous three-site pharyngoesophageal pH monitoring.They found pharyngeal acid reflux events in 7 patients in that 24-hour pe-riod (one to four episodes) compared with 2 of 11 controls studied (oneto two episodes). In a follow-up study by Ulualp and colleagues [4], 9 pa-tients who had vocal nodules and posterior laryngitis underwent similarevaluation, in which 78% were found to have pharyngeal acid reflux (signif-icantly higher than controls). It is believed that the baseline inflammationresulting from LPR episodes predisposes the vocal folds to the stressesfrom vocal overuse and misuse.

In a series of allergy patients who had laryngeal disease, Hocevar-Boltezarand colleagues [5] found that treatment of 70 patients who had laryngitis andpositive allergy skin tests resulted in an improved outcome compared with 5patients who did not receive treatment, suggesting that hypersensitivity to in-halatory and nutritional allergens makes laryngeal mucosa more susceptibleto the adverse action of other factors. This example also reinforces the syner-gistic 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 vocalfold masses, it is important to understand how biomechanical factors work

1093VOCAL FOLD MASSES

on the membranous vocal folds to produce such lesions. Jiang and col-leagues [6] developed a mathematical computer-based model to describethe vibratory response of the vocal folds during phonation using the finiteelement method. They found that in normal phonation, mechanical stresswas the least at the midpoint of the membranous vocal fold and highestat tendon attachments. In contrast, during hyperfunctional dysphonia therewas an increase in the second mode of vibration, resulting in incomplete ap-proximation of the vocal folds posteriorly and increased stress at the loca-tion between vibratory segments. In other words, when there wasincreased stiffness in the body of the vocal folds, the midpoint of the mem-branous vocal folds encountered higher shearing stresses.

Furthermore, when there was already a nodule or mass, it produceda high mechanical stress at its base during vibration. The authors concludedthat intraepithelial stress plays an important role in the pathogenesis of nod-ules and other masses, and that an abnormal vibratory mode may be moredamaging than a high intensity of vibration [6].

In a follow-up study using a self-oscillating model, mechanical stress wasnoted to periodically undulate with the vibration of the vocal folds, and thatvocal impact caused a jump in the normal stress value [7]. The model wasalso able to confirm that stress was significantly higher on the surface ofthe vocal folds compared with that under the surface. These models rein-force the concept of how vocal impact results in vibratory trauma to the vo-cal folds, and that stresses are compounded once a lesion is present.

Many lesions can result (at least in part) from this process, including nod-ules, polyps, and cysts, but other pathology should be considered, such asreactive lesions, intracordal scarring, feeding varices, and reparative granu-loma. The direct effect of the vocal mass is to add weight to the vocal fold,which decreases its vibratory qualities and frequency as demonstrated onstrobolaryngoscopy. There is a clinical decrease in phonatory pitch alongwith an abbreviated pitch range, as demonstrated on voice function testing.The presence of the mass causes impaired vocal phase closure during pho-nation, resulting in excess air egress. Clinically, this adds to a breathy qual-ity of the voice, but also contributes to vocal fatigue. Disruption of vocalfold vibration and phase closure often leads to phase asymmetry (dependingon 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-perpet-uating cycle of inflammation and trauma. Although behavioral qualitiescontribute to the initial vocal trauma that leads to the development ofthis process, the presence of a lesion can result in compensatory muscle ten-sion in an effort to reduce excess air flow through the glottis. Altman andcolleagues [8] reviewed 150 patients who had muscle tension dysphonia, inwhich 34 had polyps, 20 had nodules, and 12 had vocal cysts. They founda significant degree of compensatory muscle hyperconstriction in this popu-lation. Nevertheless, the multifactorial contributions and spectrum of le-sions that may result emphasize the importance of strobolaryngoscopy in

1094 ALTMAN

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 seemto be at higher risk for the development of hoarseness and vocal masses. Sul-kowski and Kowalska [9] analyzed 1261 cases of occupational voice disor-ders referred for otolaryngologic evaluation in Poland over a 5-yearperiod. Some 66% of these patients were primary school teachers, and55% of referrals were 51 to 60 years of age. Overall, vocal nodules werefound in 4.2%. In a Finnish study, Smolander and Huttunen [10] surveyed181 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 laryngologistinitially evaluates patients after they have experienced voice limitationsover a period of time, it is uncommon to have an isolated lesion withoutconcomitant or confounding findings. Similarly, nodules are often a ‘‘waste-basket’’ diagnosis for those clinicians unskilled to differentiate between nod-ules, polyps, cysts, reactive lesions, and intracordal scarring. Although itmay be a matter of semantics what to name a lesion, the description is nev-ertheless helpful in considering prognosis and therapeutic plan.

Nagata and colleagues [11] reviewed their 10-year experience with 1156patients and found 372 who had nodules and 784 who had polyps. Sataloffand colleagues [12] reviewed their experience with videostroboscopy on 377patients 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 vocalfold masses follows. Discussion about each of these masses follows with rel-evance to diagnosis and prognosis.

Nodules

Vocal nodules are defined as bilateral symmetric epithelial swelling of theanterior/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 predomi-nantly female adults working in professions with high voice demands. Sar-fati [13] evaluated 90 French teachers referred for vocal disorders, andpathology was found in two thirds overall, with pseudocysts or nodules inone third overall.

De Bodt and colleagues [14] characterized evolution of these nodulesfrom childhood to adolescence. They examined a group of 34 post-

http://dx.doi.org/10.1016/j.otc.2007.05.011

http://www.Oto.TheClinics.com



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. Thedegree of dysphonia in childhood and the presence of allergy were also pre-dictors of persisting voice complaints in adolescence. This study reinforcesmultifactorial contributions to the development of these lesions, includingbehavior. The female preponderance from childhood to adolescence, cou-pled with adult female preponderance in other studies, further confirmsthat females are at particular risk. Perhaps the softer intensity of female voi-ces leads to more hyperfunction in adult professional environments withlouder background noise.

One additional note is made of preponderance of nodules in patients whohave congenital microweb. Ruiz and colleagues [15] reviewed a sample of107 patients who had vocal nodules and recognized microweb in 9.4%, al-though the presence of microweb did not affect nodule location. Althoughthis is a small portion of those patients who develop nodules, it does implythat the clinician should have a heightened awareness of the presence of mi-crowebs, which may have additional implications of treatment andprognosis.

The pathophysiology of vocal nodules relies on the mid-membranous vo-cal fold experiencing maximal shearing and collision forces. This locationcorresponds to the junction of the anterior to middle vocal folds (becausethe posterior third of the vocal folds is coupled to the vocal process of thearytenoids). This repeated collision initially results in localized vascular con-gestion with edema. Eventually hyalinization of Reinke space with thicken-ing of overlying epithelium occurs with the development of epithelialhyperplasia.

Consequently, the histology of nodules is distinct from polyps and othervocal lesions. Kotby and colleagues [16] collected 11 patients who had nod-ules (all female) to characterize this histology. Nodules are generally acellu-lar, with thickening of epithelium over a matrix with abundant fibrin andorganized collagen. Polyps also have a more pronounced epithelial reactionand a more dense fibrous stroma than polyps. Immunohistochemical char-acterization of nodules reveals a thickened basement membrane zone rich incollagen type IV and more intense fibronectin staining [17].

Patients who have vocal nodules present with chronic hoarseness, oftenwith repeated episodes of more severe voice loss. Singers may complain ofa loss of ability to sing high notes softly, with frequent voice breaks, in-creased breathiness, and vocal fatigue. Strobolaryngoscopy reveals bilateralsymmetric superficial swelling of the vocal folds at the striking zone junctionof the anterior to middle thirds (Fig. 1A). There is slightly decreased ampli-tude of the mucosal wave, but the wave is generally symmetric. Becausethere is hourglass-shaped glottal closure, there is consequently decreasedphase closure (Fig. 1B).

The mucus layer on the surface of the vocal folds is also important forlubrication and reducing friction. Patients who have vocal nodules may

1096 ALTMAN

subsequently have irregular vibration of the surface mucus layer, perhaps re-sulting in drying, leading to impaired lubrication and an exacerbation of thesurface stresses leading to the formation of nodules [18]. In addition, abnor-mal or excess mucus has been anecdotally noted by the author to be respon-sible for increased voice breaks in singers when transitioning through thepassaggio (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 usinga hammer over a long period of time without gloves. As a result, callusesform at the areas of maximal impact with the hand. Using this analogy,one may expect that conservative (nonsurgical) treatment would be applica-ble to the patient who has true vocal nodules.

Hogikyan and colleagues [19] recognized a consensus among otolaryngol-ogists, speech pathologists, and teachers of singing regarding the treatmentof singers who have nodules. Addressing voice use demands, improper tech-nique, optimizing other contributing factors, and coordinating care were be-lieved to be paramount.

Indications for microsurgical treatment include longstanding nodules,particularly when other factors, including speech therapy, have been maxi-mized, and suspicion of a primary lesion with a reactive callus on the othervocal fold. Microsurgical technique is addressed elsewhere; it is imperativeto preserve normal anatomy, keeping the plane of dissection superficial,and to minimize trauma to the lamina propria.

Polyps

Vocal polyps are unilateral, occasionally pedunculatedmasses encounteredon the true vocal fold. They occur more often in males, after intense intermit-tent voice abuse, history of aspirin or anticoagulant use, or other vocaltrauma, such as endotracheal intubation. Kotby and colleagues [16] reviewed19 patients who had polyps, of whom 16 (84%) were male. The pathophysiol-ogy is believed to be attributable to breakage of a capillary in Reinke space

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.


(superficial lamina propria) with subsequent extravasation of blood, resultantlocal edema, and ultimate organization with hyalinized stroma.

The resulting mass may be broad-based or pedunculated, and hemor-rhagic 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 consid-ered to be an outpouching of inflamed and organized Reinke space. A super-ficial nonhemorrhagic, broad-based polyp may therefore be interpreted asor called a pseudocyst.

Pathologically, polyps are acellular, with thickened epithelium over su-perficial lamina propria and increased vascularity in an abundant delicatefibrin stromal matrix. They have more vasculature and less organized colla-gen than nodules, but the distinction may be difficult for the pathologist [20].Immunohistochemistry studies reveal clustered fibronectin and disruption oflaminar pattern suggesting diffuse injury in the region of the polyp [17].

On strobolaryngoscopy, vocal folds with small polyps generally have in-tact mucosal waves but phase asymmetry because of the impaired phase clo-sure and the mass effect of the polyp. Vocal folds with larger polyps havemore prominent decreased mucosal wave amplitude. Thibeault and col-leagues [21] characterized gene expression in vocal polyps compared withReinke edema. They found evidence of enhanced expression of extracellularmatrix proteins in vocal polyps corresponding to increased mucosal wavestiffness observed on strobolaryngoscopy.

Both nodules and polyps result in excess air egress during phonation (witha relatively breathy voice), and earlier vocal fatigue, frequent voice breaks in

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






1098 ALTMAN

singers, and worsening hoarseness with high-pitched soft phonation. As such,this decreased vocal efficiency with decreased mucosal wave phase closure hasbeen quantified with decreased subglottal and acoustic power [22]. Becausepolyps are asymmetric masses of the vocal folds, they are more prone to resultin chaotic vibrations and aperiodic mucosal waves [23].

In the treatment of patients who have vocal polyps, all of the factors thatcontribute to voice disorders should be addressed from a multidisciplinaryperspective, and polyps are usually addressed withmicrosurgery. An evolvingtreatment modality for particularly hemorrhagic polyps is the use of office-based technology using lasers. The wavelength of the lasers is well absorbedby hemoglobin, and damage to the epithelium is minimal. In one recent pilotstudy evaluating the use of the pulsed-dye laser (585 nm), small vascularpolyps showed greater potential for resolution over larger polyps [24].

There have also been reports (and anecdotal observation by the author ofthis article and others) that small vocal polyps may completely resolve withconservative nonsurgical treatment [25]. One would expect that smaller le-sions and those that have been present for shorter periods of time may bemore prone to regression, especially in patients who are more compliantwith treatment.

Cysts

Cysts are subepidermal epithelial-lined sacs locatedwithin the lamina prop-ria, and may be mucus retention or epidermoid in origin. Mucus retentioncysts form when a mucous gland duct becomes obstructed (usually duringanupper respiratory infection orwith 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 subepi-thelium of the fourth and sixth branchial arches or from healing injured mu-cosa 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 ina 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 patientswho have nodules and polyps, but with less vocal limitation than expectedfrom its size. The voice often sounds diplophonic (particularly with epider-moid cysts), whereby there is great pitch instability and there is splitting ofthe fundamental frequency overtones. As with nodules and polyps, this isusually accompanied by vocal hyperfunction, which is often compensatory.







Bouchayer and colleagues [26] reviewed their experience with 157 cases ofcysts, sulci, and mucosal bridges over a 10-year period. Cysts were present in78, and more commonly in females. Female professional singers may noteincreasing vocal limitation and voice roughness when they are premenstrual[27], and there is anecdotal evidence of varying cyst size with the femalemonthly cycle. Consequently, many phonosurgeons exercise caution whenoperating on premenstrual women.

On strobolaryngoscopy, the vocal folds appear asymmetric with occa-sional evidence of the subepithelial mass (Fig. 3). Because of displacementof lamina propria, there is significant decreased or absent mucosal waveon the side of the cyst. Phase closure depends on the cyst size and whetherthere is the development of a contralateral reactive callus.

Shohet and colleagues [28] compared stroboscopic findings between cystsand polyps. They determined that the mucosal wave was the most importantparameter in differentiating cysts from polyps. They also found the mucosalwave to be diminished or absent in 100% of vocal fold cysts, and the waveto be present in 80% of polyps.

Treatment again requires a multidisciplinary approach addressing factorsthat contribute to voice disorders. Although it is imperative to respect vocallimitations, a true cyst does not resolve with conservative management. Thephonosurgical approach is discussed elsewhere in this issue, but requiresmore extensive dissection because the cyst is in the submucosal plane. Thecyst may also be associated with intracordal scarring, requiring a more elab-orate dissection. Consequently, recovery of the mucosal wave is prolongedand may never return to being completely normal.

Furthermore, leaving behind a minute fragment of epithelium in the cystsac may result in recurrence of the cyst. Some vocal professionals have beenknow to have cysts that do not cause substantial limitation to their singingcareers and have been observed without surgery. Consideration of surgery in

Fig. 3. Vocal cyst.

1100 ALTMAN

a vocal professional with this complex lesion should not be taken lightly,therefore, and there should be a lengthy discussion of the risks and alterna-tives to surgery.

Reactive lesions

The presence of a unilateral vocal fold lesion results in hourglass-shapedclosure of the membranous vocal folds during phonation. Consequently,there are extra shearing forces on the contralateral vocal fold that may pro-duce a reactive callus with epithelial hyperplasia. A unilateral lesion with re-active callus formation may appear as bilateral lesions, such as nodules, thatmay confound the diagnosis, prognosis, and ultimate management.

Rosen and colleagues [29] evaluated a series of 85 patients who had bilat-eral vocal fold lesions and found 21 to have nodules and 64 to have a unilat-eral vocal fold lesion with a contralateral reactive lesion (UVFL/RL). Whencomparing patients who had nodules to those who had UVFL/RL, theyfound statistically significant differences in (1) symmetry of vocal fold vibra-tion, (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 pri-mary lesion with reactive callus, from the standpoint of prognosis and sur-gical planning.

(Access Video on Left Cyst, Right Nodule in online version of this article at: http://www.


Fig. 4A shows an example of a singer who has a left vocal polyp and re-active right vocal fold broad-based edema/callus. After a 1-month period ofreducing voice use, speech therapy, and treatment of LPR, Fig. 4B showssignificant improvement in the right reactive callus. As such, contralateralreactive lesions are often not removed in microsurgery for the primary le-sion, because the reactive lesion tends to resolve with conservativemanagement.

Intracordal scarring

Repeated inflammation, vocal trauma, vocal hemorrhage, and the pres-ence of an intracordal cyst predispose to scarring in Reinke space. Intracor-dal scarring is often found in association with a cyst, particularly if it isepidermoid in origin and has ruptured. Intracordal scarring may also befound after vocal surgery involving the lamina propria, with the use ofthe CO2 laser, and after repeated epithelial procedures, such as those for ma-lignancy, leukoplakia, and papilloma.

(Access Video on Left Vocal Fold Scar in online version of this article at: http://www.Oto.

TheClinics.com.)








Discussion on vocal sulcus (epithelial scarring) goes beyond the scope ofthis article, although it can certainly affect the professional voice [30].

Intracordal scarring is suspected on strobolaryngoscopy when there ismarkedly reduced or absent mucosal wave (usually asymmetric), which oftenaffects phase closure. From a professional voice standpoint, it is crucial to dif-ferentiate between an uncomplicated subepithelial cyst and an intracordalscar, because the latter is a more complex problem with worse prognosis forprofessional voice rehabilitation. A convex subepithelial fullness of the mem-branous vocal foldmaywarrant exploratorymicroflap surgery to tease out re-maining cyst sac and adynamic fibrous components. Because the extracellularmatrix components of the lamina propria largely determine the biomechanicalproperties of the vocal folds (and subsequent voice quality), there has been sig-nificant 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 microcir-culation within the superficial lamina propria. Although they are not truemasses, they develop as a result of the same multifactorial and shearingforces that lead to masses, and they also predispose to the development ofpolyps and vocal hemorrhage. Fig. 5A and B show strobolaryngoscopicexamples of a varix and hemorrhage.

Treatment options for these aberrant vessels have traditionally includedmicrodissection and the use of the CO2 laser, which lead to an increased riskfor postoperative scarring or sulcus. More recently, there has been renewedinterest in the use of pulsed angiolytic lasers that have a wavelength withinthe specific absorption of oxyhemoglobin, because this has the potential of se-lectively ablating microvessels without damage to the overlying epithelium.Hirano and colleagues [32] demonstrated the use of the KTP laser (532 nm

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 treat-

ment of LPR.

1102 ALTMAN

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

Granulomas

Although vocal process granulomas are not on themembranous vocal foldand often do not cause vocal symptoms, it is important for the clinician to un-derstand differences with other vocal fold masses. Vocal process granulomasoccur in response to trauma,most commonly fromLPR, exacerbating chroniccough, or throat clearing. They may also occur after endotracheal intubationresulting in contact ulceration, or by forceful glottal closure when compensat-ing for vocal paresis or presbylaryngia. Kiese-Himmel and Kruse [34] docu-mented a male predominance with 27 out of 28 patients who had contactgranuloma being male.

The granuloma may appear as solitary or bilobed (Fig. 6) and often doesnot affect mucosal wave or phase closure on strobolaryngoscopy (unlessthere is underlying vocal paresis, presbylaryngia, or sulcus).

(Access Video on Vocal Process Granuloma in online version of this article at: http://www.


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

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

figure)





Papilloma

Respiratory papillomatosis is an infection caused by human papillomavi-rus (HPV), which is also known tomore commonly cause cervical, vaginal, pe-nile, and anal warts. Although relatively uncommon in the larynx, it is stillconsidered to be among the most common laryngeal neoplasms. There aremore than 50 strains of HPV, but HPV 6 and 11 are among the most commonin the larynx.Aswith genitalwarts, there is an approximately 2% likelihood ofmalignant degeneration in laryngeal papilloma, most commonly found withstrains HPV 16 and 18. Once the wart is manifested, there is overall abouta 10% likelihoodof spread to the tracheaor other sites, depending on the num-ber of surgical procedures necessary to control the disease.

HPV appears as a cauliflower-like exophytic protuberance, most com-monly found at the transition between columnar and squamous epithelium(Fig. 7). Because pathologic specimens reveal multiple fronds of fibrovascu-lar stalks, papilloma also has vascular stippling on the mass. Early formsmay have a superficial spreading presentation, again with vascular stipplingseen 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 ofthickened diseased epithelium can present with a decreased mucosal wave.

There are many controversies related to papilloma and HPV, includinga high prevalence of greater than 40% with HPV-positive serology but stillrelatively low overt infection rates, suggesting an important role of host im-mune recognition [35]. The many treatments for papilloma go beyond thescope of this discussion, although shaver excision and CO2 laser excisionare also used in select instances. The greater depth of penetration of the laser

Fig. 6. Left vocal process granuloma.




1104 ALTMAN

than is visibly apparent increases the risk for scarring and implantation ofthe virus (an epithelial disease) into deeper tissues of the vocal fold anduse of the CO2 laser is avoided in most centers. Pulsed-dye lasers are nowconsidered the mainstay. The emerging use of the HPV vaccine for themost common strains and cidofovir injections to control regrowth are excit-ing options for protection from acquiring the disease and for treatment.

Polypoid corditis

Polypoid corditis, vocal polyposis, and Reinke edema are terms that referto a proliferation or redundancy of the superficial lamina propria (Reinkespace). It is often seen in patients who have chronic irritant exposure,such as tobacco smoke, laryngopharyngeal reflux, and sometimes occupa-tional exposures. Polypoid corditis appears as an outpouching of the mem-branous vocal folds with an edematous, almost water-balloon appearance(Fig. 8). Strobolaryngoscopy reveals decreased mucosal wave because ofthe mass effect of the edema, often with phase asymmetry because ofball-valving and asymmetric edema. Treatment is aimed at reducing airwayobstruction while preserving voice quality. Surgically, it is paramount topreserve some epithelium and remaining superficial lamina propria so thatpatients may maintain some degree of mucosal wave postoperatively. It isalso imperative to stage procedures in patients who have bilateral diseaseto reduce the likelihood of postsurgical anterior web formation [36] Cessa-tion of smoking and control of reflux disease are important factors in pre-venting recurrence of the disease after surgical excision and should beinstituted before surgery to maximize the postoperative outcome.

Leukoplakia and dysplasia

Leukoplakia, or white plaque, refers to a spectrum of diseases affectingthe vocal fold epithelium, and includes hyperkeratosis, dysplasia, and early

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


verrucous changes. Overall, when leukoplakia is present there is an 8% to14% likelihood of developing malignancy in such lesions. The pathophysi-ology is still unknown, but it is likely that chronic irritation and genetic pre-disposition form a synergy in such patients. The plaque may present initiallywith subtle hyperkeratotic epithelium resulting in decreased or sluggish mu-cosal wave on strobolaryngoscopy (Fig. 9A). Progression, particularly withdysplastic or premalignant changes, may be exophytic in a surrounding bedof erythema (Fig. 9B). Microflap excision, carbon-dioxide lasers, andpulsed-dye lasers are all treatment options, but appropriate pathologic stag-ing must be performed because the visual appearance does not always cor-respond to the degree of dysplasia [37]. Treatment of hyperkeratosis andmild dysplasia is centered on eradication of disease while preserving neigh-boring normal anatomy and voice quality. Severe dysplasia and carcinomain situ must be treated more aggressively.

Fig. 8. Bilateral polypoid corditis.

Fig. 9. (A) Broad superficial leukoplakia blanketing bilateral vocal folds, and (B) discrete leu-

koplakia with severe dysplasia and microinvasion seen in a bed of erythematous vocal folds.

1106 ALTMAN

Vocal fold carcinoma

Squamous call carcinoma is by far the most common form of laryngealmalignancy. Those patients who have a history of tobacco smoking accountfor about 90% of cases, and the likelihood is far greater with a concurrenthistory of excess alcohol consumption. There are also anecdotal and indirectdata to support the role of laryngopharyngeal reflux in causing and com-pounding the development of vocal fold carcinoma. Any mass lesion in a pa-tient who has such a history should therefore raise the appropriate level ofsuspicion.

Features of squamous carcinoma include exophytic, ulcerative, and infil-trative. Consequently, one may see on strobolaryngoscopy an area of focallydecreased mucosal wave at the site of an exophytic epithelial lesion (Fig. 10).This area is distinguished from papilloma, which remains an epithelial dis-ease, whereas carcinoma tends to infiltrate into the lamina propria, account-ing for the decreased mucosal wave. Also, the fibrovascular fronds seen inpapilloma are generally softer than the exophytic mass produced in carci-noma, so carcinoma would have more of a detrimental effect on phase clo-sure seen in strobolaryngoscopy. Distinguishing carcinoma fromleukoplakia is more challenging because leukoplakia may form a continuumfrom keratosis to severe dysplasia to microinvasive disease. Nevertheless,the degree of clinical suspicion and evidence of microinvasion with focallydecreased mucosal wave should mandate further evaluation [38].

Summary

There are several vocal masses that can affect the professional voice. It isimportant to understand the multifactorial contributions and pathogenesisof each to determine prognosis. Strobolaryngoscopy plays a crucial role indifferentiating the spectrum of masses and in guiding optimal management.

Fig. 10. Vocal fold squamous cell carcinoma.


References

[1] Yano J, Ichimura K, Hoshino T, et al. Personality factors in pathogenesis of polyps and

nodules of vocal cords. Auris Nasus Larynx 1982;9:105–10.

[2] Roy N, Bless DM, Heisey D. Personality and voice disorders: a multitrait-multidisorder

analysis. J Voice 2000;14(4):521–48.

[3] Kuhn J, Toohill RJ, Ulualp SO, et al. Pharyngeal acid reflux events in patients with vocal

cord nodules. Laryngoscope 1998;108(8 Pt 1):1146–9.

[4] Ulualp SO, Toohill RJ, Shaker R. Pharyngeal acid reflux in patients with single andmultiple

otolaryngologic disorders. Otolaryngol Head Neck Surg 1999;121(6):725–30.

[5] Hocevar-Boltezar I, Radsel Z, Zargi M. The role of allergy in the etiopathogenesis of laryn-

geal mucosal lesions. Acta Otolaryngol (Stockh) 1997;527(Suppl):134–7.

[6] Jiang JJ, Diaz CE, Hanson DG. Finite element modeling of vocal fold vibration in normal

phonation and hyperfunctional dysphonia: implications for the pathogenesis of vocal nod-

ules. Ann Otol Rhinol Laryngol 1998;107:603–10.

[7] Tao C, Jiang JJ. Mechanical stress during phonation in a self-oscillating finite-element vocal

fold model. J Biomech 2007;40:2191–8.

[8] Altman KW, Atkinson C, Lazarus C. Current and emerging concepts in muscle tension

dysphonia: a 30-month review. J Voice 2005;19:261–7.

[9] Sulkowski WJ, Kowalska S. Occupational voice disorders: an analysis of diagnoses made

and certificates issued in 1999–2004. Int J Occup Med Environ Health 2005;18(4):341–9.

[10] Smolander S, Huttunen K. Voice problems experienced by Finnish comprehensive school

teachers and realization of occupational health care. Logoped Phoniatr Vocol 2006;31(4):

166–71.

[11] Nagata K, Kurita S, Yasumoto S, et al. Vocal fold polyps and nodules. A 10-year review of

1,156 patients. Auris Nasus Larynx 1983;10(Suppl):S27–35.

[12] Sataloff RT, Speigel JR, Hawkshaw MJ. Strobovideolaryngoscopy: results and clinical

value. Ann Otol Rhinol Laryngol 1991;100:725–7.

[13] Sarfati J. Readaptation vocale des enseignants. Rev Laryngol Otol Rhinol (Bord) 1989;110:

393–5.

[14] DeBodtMS,KetelslagersK, Peeters T, et al. Evolution of vocal fold nodules from childhood

to adolescence. J Voice 2007;21:151–6.

[15] Ruiz DM, Pontes P, BehlauM, et al. Laryngeal microweb and vocal nodules. Clinical study

in a Brazilian population. Folia Phoniatr Logop 2006;58(6):392–9.

[16] Kotby MN, Nassar AM, Seif EI, et al. Ultrastructural features of vocal fold nodules and

polyps. Acta Otolaryngol (Stockh) 1988;105:477–82.

[17] Courey MS, Shohet JA, Scott MA, et al. Immunohistochemical characterization of benign

laryngeal lesions. Ann Otol Rhinol Laryngol 1996;105:525–31.

[18] HsiungMW.Videolaryngostroboscopic observation ofmucus layer during vocal cord vibra-

tion in patients with vocal nodules before and after surgery. Acta Otolaryngol 2004;124(2):

186–91.

[19] HogikyanND, Appel S, Guinn LW, et al. Vocal fold nodules in adult singers: regional opin-

ions about etiologic factors, career impact, and treatment. A survey of otolaryngologists,

speech pathologists, and teachers of singing. J Voice 1999;13(1):128–42.

[20] Michaels L. Pathology of the larynx. New York: Springer-Verlag; 1984.

[21] Thibeault SL, Gray SD, Li W, et al. Genotypic and phenotypic expression of vocal fold

polyps and Reinke’s edema: a preliminary study. Ann Otol Rhinol Laryngol 2002;111(4):

302–9.

[22] Jiang J, Stern J, Chen HJ, et al. Vocal efficiency measdasurements in subjects with vocal

polyps and nodules: a preliminary report. Ann Otol Rhinol Laryngol 2004;113(4):277–82.

[23] ZhangY, Jiang JJ. Chaotic vibrations of a vocal fold model with a unilateral polyp. J Acoust

Soc Am 2004;115(3):1266–9.

1108 ALTMAN

[24] Ivey CM, Woo P, Shapshay SM, et al. "Outcomes of office pulsed dye laser treatment for

benign laryngeal lesions". Presented at the Triological Society 2007 Combined Sections

Meetings. Marco Island (FL), February 14–18, 2007.

[25] Srirompotong S, Saeseow P, Vatanasapt P. Small vocal cord polyps: completely re-

solved with conservative treatment. Southeast Asian J Trop Med Public Health 2004;

35(1):169–71.

[26] Bouchayer M, Cornut G, Witzig E, et al. Epidermoid cysts, sulci and mucosal bridges of the

true vocal cord: a report of 157 cases. Laryngoscope 1985;95:1087–94.

[27] Abitbol J, Abitbol P, Abitbol B. Sex hormones and the female voice. J Voice 1999;13:424–46.

[28] Shohet JA, CoureyMS, Scott MA, et al. Value of videostroboscopic parameters in differen-

tiating true vocal fold cysts from polyps. Laryngoscope 1996;106:19–26.

[29] Rosen CA, Lombard LE, Murry T. Acoustic, aerodynamic, and videostroboscopic features

of bilateral vocal fold lesions. Ann Otol Rhinol Laryngol 2000;109(9):823–8.

[30] Dailey SH, Ford CN. Surgical management of sulcus vocalis and vocal fold scarring.

Otolaryngol Clin North Am 2006;39:23–42.

[31] Hansen JK, Thibeault SL. Current understanding and review of the literature: vocal fold

scarring. J Voice 2006;20(1):110–20.

[32] Hirano S, Yamashita M, Kitamura M, et al. Photocoagulation of microvascular and hem-

orrhagic lesions of the vocal fold with the KTP laser. Ann Otol Rhinol Laryngol 2006;

115(4):253–9.

[33] Zeitels SM, Akst LM, Bums JA, et al. Pulsed angiolytic laser treatment of ectasias and vari-

ces in singers. Ann Otol Rhinol Laryngol 2006;115(8):571–80.

[34] Kiese-Himmel C,Kruse E. Sociodemographic variables of aGerman sample of patients with

contact granuloma. J Voice 1995;9:449–52.

[35] Gerein V, Soldatski IL, Babkina N, et al. Children and partners of patients with recurrent

respiratory papillomatosis have no evidence of disease during long-term observation.

Int J Pediatr Otorhinolaryngol 2006;70:2061–6.

[36] Desloge RB, Zeitels SM. Endolaryngeal microsurgery at the anterior glottal commissure:

controversies and observations. Ann Otol Rhinol Laryngol 2000;109:385–92.

[37] Schweinfurth JM, Powitsky E, Ossoff RH. Regression of laryngeal dysplasia after serial

microflap excision. Ann Otol Rhinol Laryngol 2001;110:811–4.

[38] Colden D, Zeitels SM, Hillman RE, et al. Stroboscopic assessment of vocal fold keratosis

and glottic cancer. Ann Otol Rhinol Laryngol 2001;110:293–8.

vocal fold masses

Documents