Phonotraumatic Lesions

Vocal Fold Nodules

Vocal fold nodules are defined as bilateral symmetric epithelial swellings of the anterior/mid third of the true vocal folds² (Fig. 1). Predilection of this location is due to phonotrauma at this site of maximum excursion and forceful contact.³ These are seen in children, adolescents and predominantly females working in professions with high vocal demands.² In the pediatric age-group, incidence is higher in boys.⁴

Incessant phonotrauma disrupts and hyalinizes the superficial lamina propria (SLP) with consequent basement membrane zone (BMZ) injury and leads to epithelial hyperplasia and thickening of BMZ with increased deposition of type IV collagen and fibronectin.³ It has been noted that an abnormal vibratory pattern may be more damaging than a high intensity vibration.⁵ This explains the higher incidence of vocal nodules in untrained voice users, compared to formally trained performing artists.

Patients who have vocal nodules may have irregular vibration of the surface mucus layer, perhaps resulting in drying, leading to impaired lubrication and exacerbation of the surface stresses leading to formation of nodules.⁶ Personality traits and psychological factors may also come into play in the formation of nodules. It has been documented using Multidimensional Personality Questionnaire⁷ and Maudsley Personality Inventory⁸ studies that patients with vocal nodules tend to be extroverts with greater social activity, aggression and impulse. Most children with nodules tend to be screamers, incessant and loud talkers.³ In a study by Nerurkar et al it was found that people with type A personality were more likely to develop vocal pathologies.⁹

Laryngopharyngeal reflux (LPR) has emerged as a major contributing factor to the development of nodules. This association is well documented on the basis of ambulatory, three-site pharyngoesophageal pH monitoring as well as barium esophagography.¹⁰ The baseline inflammation resulting from episodes of LPR adds to the stress of vocal folds during overuse and misuse.³ Preponderance of nodules in patients with congenital microwebs has also been documented.^11,12

Immunohistochemical studies have shown that fibronectin, a glycoprotein present in the extracellular matrix, is increased in the SLP of patients with nodules.¹³ Gray et al., in a study of nodules of human vocal folds, showed important disarrangement of the BMZ where the overall thickness appeared markedly increased. The anchoring fibers were oriented in multiple directions and were not always linking the lamina densa to the lamina propria. In addition, some of them seemed partially formed, truncated, and rudimentary, incapable of forming secure attachment.¹⁴ Allergy may also contribute to nodule formation along with other risk factors like vocal abuse and reflux.¹⁵

The pathophysiology of vocal nodules relies on the mid-membranous vocal fold experiencing maximal shearing and collision forces resulting in localized vascular congestion with edema. Eventually, hyalinization of Reinke’s space with BMZ injury and thickening of overlying epithelium occurs with development of epithelial hyperplasia. There is increased deposition of type IV collagen and fibronectin. Continued phonotrauma over the early nodule thus formed, leads to fibrosis and callus formation in the long run, resulting in hard and permanent nodules^2,16 Histologically, they are generally acellular with thickening of epithelium over a matrix with abundant fibrin and organized collagen.¹⁷ The principal histological features of nodules are epithelial hyperplasia, thickening of basement membrane, edema and fibrosis.¹⁸ Classical immunohistochemical features are thickened BMZ rich in fibronectin and more intense fibronectin staining.¹³ Patients present with varying degrees of dysphonia, ranging from hoarse, husky to breathy voice. Singers may complain of loss of ability to sing high notes softly, frequent voice breaks, increased breathiness and vocal fatigue.²

Strobolaryngoscopy will show bilateral, usually symmetric superficial swellings at the striking zone junction of the anterior and middle thirds. The typical hourglass phonatory closure (Fig. 2) accounts for the breathiness. Mucosal waves are usually not impeded, however, may be slightly altered in harder nodules. Nodules may vary in size, symmetry, contour and color. Early, young nodules may appear as tiny, soft and pink swellings, whereas more mature, chronic nodules have hard, whitish appearance, being more fibrotic in nature.¹⁹ A simple analogy of a carpenter using a hammer over a long period of time without gloves and consequently developing calluses at the areas of maximal impact with the hand can be applicable in the case of vocal nodules.

Voice therapy is the primary treatment for vocal nodules. Therapy aims to optimize vocal hygiene, eliminate behavior aggravating phonotrauma and correct maladaptive practices.³ Voice therapy can be indirect (vocal education, vocal hygiene) and direct (specific exercises to correct the undue physical colliding forces).³ These exercises are also designed to achieve a balance between pulmonary support and vibratory forces.²⁰ Treatment of contributory medical factors such as reflux and allergy should be considered. Psychological issues should be addressed wherever applicable. It is well documented that voice therapy can resolve nodules in up to 90% of cases.²¹ Complete resolution may not occur in all patients in spite of achieving satisfactory voice quality which is usually due to irreversible changes in the BMZ.²⁰ A meta-analysis of studies assessing acoustic voice parameters before and after voice therapy for vocal fold nodules showed a statistically significant improvement in fundamental frequency and jitter after treatment.²²

Indications for microsurgical treatment include longstanding nodules, refractory to maximal and compliant voice therapy. It is imperative to preserve normal anatomy, keeping the plane of dissection superficial, and to minimize trauma to the lamina propria. Sataloff has cautioned that surgery for vocal nodules should be avoided whenever possible and should virtually never be performed without an adequate trial of expert voice therapy.²¹ Postoperative voice therapy helps maintain a healthy phonatory behavior, which plays a crucial role in minimizing recurrence. Béquignon et al. retrospectively analyzed 62 patients who had undergone surgical therapy for vocal fold nodules, with or without postoperative voice therapy.²³ The rate of recurrent dysphonia without postoperative voice therapy was 56% compared to 22% for those receiving postoperative voice therapy. It has been reported that patients treated with an integrated approach involving both a speech pathologist and otolaryngologist tend to show greater progress than those who underwent therapy alone.²⁴

Newer management options include intralesional steroid injections either at the time of laryngeal microsurgery (after excision of lesion) or as an office procedure. Mortenson and Woo discussed the role of in-office steroid injection to reduce granulation tissue to promote primary healing, reduce hypertrophic scar formation and to reduce inflammation to avoid surgical intervention in patients of vocal nodules, polyps, scars and granulomas.²⁵

Vocal Fold Polyps

Vocal fold polyps are benign, exophytic lesions with a thin mucosal covering which are typically unilateral but may be bilateral (Fig. 3). They are often found in men between 30-40 years of age. True polyps are found only on the vocal folds and no other part of the larynx. They are usually acellular and pathologically have been categorized as gelatinous, transitional and telangiectatic, each representing different stages of polyp formation. The telangiectatic type looks like a blister initially and then advances to look grape-like convolutes of blood vessels with a growing peduncle. The transitional form is the most common one with a nucleus of tortuous vessels embedded in a gelatinous substance covered by squamous epithelium.²⁶

The most common etiological factor in the formation of vocal fold polyp is phonotrauma after intense intermittent voice abuse.³ Additional factors such as smoking, reflux, long-term use of oral anticoagulants and other trauma such as endotracheal intubation also predispose to polyp formation.³ Polyps are also found to be preceded by the formation of a varix or ectasia. The localized edema which follows such vascular lesions, organizes to a hyalinized stroma and present as a polyp.

Patients present with varying degrees of hoarseness, inability to raise their pitch, loss of range and vocal fatigue. The degree of hoarseness corresponds to the bulk of the polyp and the phonatory gap and secondary compensatory mechanisms. On videostroboscopy, the polyp may be sessile or pedunculated and may appear white or red depending on their primary content. They are usually found attached to the medial free margin of the vocal fold but may also be found along the superior and inferior margins. A ‘contact lesion’ is often found on the opposite vocal fold.²⁶ The amplitude of the mucosal wave depends on the location of the polyp. A polyp in supraglottic region, does not usually cause any decrease in the amplitude, whereas polyps attached to the medial vibratory edge with a resultant phonatory gap, may cause a reduced amplitude. Telangiectatic polyps often have a feeding vessel found running along the superior surface of the vocal fold³ (Fig. 4).

Polyps rarely tend to resolve with conservative treatment. Acute hemorrhagic polyps may reduce in size with voice rest and low dose oral steroids.³ There is a definitive role of voice therapy even when surgery has been planned. Voice therapy not only teaches a healthy phonatory practice, it also aims to correct the compensatory maladaptive behaviors. The aim of surgical excision is to create a smooth vibrating surface of the vocal fold with maximal preservation of overlying epithelium and normal SLP. The principle of microflap technique may be applied in both cold steel and laser assisted excision of polyps. Laser has an advantage in dealing with the feeding blood vessels especially in case of a hemorrhagic polyp. Hemoangiolytic lasers with flexible delivery systems, such as KTP, pulse dye and 445 nm blue laser have found popularity in many voice centers in the recent past for office excision of small polyps, though the constant movement of the larynx in an awake patient may hamper the precision.²⁷

Vascular Lesions

Commonly found vascular lesions have been classified by Hochman et al. as varix, papillary ectasia and spider telangiectasia.¹ A varix is prominent, enlarged and acutely tortuous vein. Varices are normally found parallel to the vibratory margin. A papillary ectasia is a blood-filled venous enlargement that looks like a coalescent hemangioma. A spider telangiectasia is a delicate network of inappropriately arranged blood vessels.²⁸ (Fig. 5- used with permission from Nupur Nerurkar, Atlas on Phonomicrosurgery, Jaypee publications, chapter 4, page 27, figure 4.72 A)

Vocal fold varices are more common in women than men. This predisposition suggests a hormonal contribution to the varix formation with possible enlargement in the pre-menstrual period. Higher incidence of vascular lesions of the vocal fold is seen in professional voice users, both men and women, making vocal trauma a major etiological factor.²⁹

The increased blood flow or reactive hyperemia after intensive vocal usage has been postulated to lead to varix formation which is similar to the vascular engorgement of extremities after vigorous exercise.²⁹ Though blood vessels are sparse in normal vocal folds, when present they run parallel to the vibratory margin and are tortuous. The microcirculatory system of the vocal fold mucosa is maintained by this parallel arrangement during shearing movements of phonation. The tortuosity of vessels helps maintain their patency when the vocal fold length changes with pitch variations. There is little or no connection between the microvasculature of the superficial lamina propria and thyroarytenoid muscle. This enables mucosal cover’s flexibility during the shearing motions of a normal mucosal wave without causing a vascular accident. However, when these delicate blood vessels are subjected to unconventional forces, vascular pathologies occur.²⁸

The individual may be completely asymptomatic or may have subtle changes of vocal fatigue or decreased vocal range. Dysphonia occurs due to the mass effect and disruption of mucosal wave with acute subepithelial hemorrhage (Fig. 6) causing severe dysphonia which may occur in women during the pre-menstrual period. Professional voice users often seek evaluation sooner for subtle changes in voice.

Videostroboscopy helps in defining the extent of the lesion, its mobility or fixation to the underlying tissues, presence of surrounding areas of stiffness that may have resulted from previous traumatic hemorrhage. Most common site for varices and ectasias is the superior surface of the vocal fold near the mid-membranous portion where the shearing forces are greatest. As the lesions may occur on or below the vibratory margin, it is helpful to view the vocal fold tangentially during office evaluation and intraoperatively to map the vasculature accurately.

In case of acute subepithelial hemorrhage, the patient is advised a strict voice rest of 7–10 days, a course of oral steroids, cessation of oral anticoagulants (if possible) and avoidance of nonsteroidal anti-inflammatories. In case the subepithelial hemorrhage persists, an incision may be made laterally on the superior surface of the vocal fold to evacuate the blood under GA. Laser is avoided in this situation to avoid scarring.

Vascular lesions may be resected using cold steel instruments, CO₂ laser or haemongiolytic lasers. The CO₂ laser is used in defocused mode at low power settings of 1-2 W to coagulate the blood vessel. With Hemoangiolytic lasers such as the KTP or Blue laser, the beam is delivered through a flexible optical fiber and is well absorbed by hemoglobin, thus allowing photocoagulation of microvascular lesions with minimal damage to the epithelium, in a non-contact mode. Photocoagulation is stopped when the vessel is shrunk³⁰ or darkened due to thrombus formation.³¹ Post-operative voice therapy is required in either of the modes of treatment of vascular lesions.

Office-based Pulsed Dye Laser is relatively contraindicated for treating varices and ectasias as vessel wall rupture due to the procedure is difficult to control. Moreover, majority of the patients require phonomicrosurgical resection of associated lesions.³¹ Postoperative vocal fold scarring is extremely rare with excision of vascular lesions but can occur after laser treatment of vascular lesions. Scarring may disrupt the mucosal wave and worsen dysphonia. It can be avoided with minimal operative trauma using either cold or laser techniques.²⁸

Vocal Fold Cysts

A cyst is defined as a benign, well-encapsulated collection of fluid of variable consistency. Vocal fold cysts (Fig. 7) lie freely in the superficial lamina propria under the epithelial layer and may be adherent to the overlying epithelium or may extend into the vocal ligament. Anterior and posterior fibrotic tethering bands in long standing cysts, after dissection, give ‘a pearl on a string’ appearance.³² Glottic cysts can typically be either epidermoid or mucous retention cysts. These subepithelial cysts along with sulci and mucosal bridges are often found in association with one another and may be labeled as belonging to one family.

A study done in the University of Essen in 1984 showed that the submucosa of the true vocal folds contains a large number of mixed serous and mucous glands.³³ The secretion of the mucous glands provides lubrication and enables viscosity of these folds and it is felt that mucous retention cysts occur when the ducts of the mucous glands are blocked. This may occur following aerodynamically induced shearing stress due to phonatory abuse. Inadequate laryngeal hydration may affect the stiffness and viscosity of the lamina propria, predisposing to the formation of thick secretions, which may plug the mucous gland duct, forming a mucous retention cyst.³⁴ A mucous retention cyst is usually lined by a thin capsule formed by respiratory epithelium (cuboidal or columnar) and typically contains clear or yellow colored fluid. They may vary in their sizes and can wax and vane over a period of time. Mucous retention cysts are usually found on the medial vibrating edge of the vocal fold or in the infraglottic region where there is abundance of the mucous glands.

The epidermoid cysts are also referred to as squamous inclusion cysts. They have a thick capsule lined by stratified squamous epithelium. The contents within it are usually pultaceous, containing keratin debris or cholesterol. They are believed to arise either from phonotraumatic fissures developing on the vocal fold epithelium with ingrowth of some epithelium into the superficial lamina propria, or to be congenital.³⁵ The congenital theory suggests that epidermoid cysts constitute remnants of the fourth and sixth branchial arches.³⁵ These lesions are most often found on the superior surface of the striking zone of vocal folds and tend to grow centripetally, eliciting an inflammatory response in the surrounding normal tissue.

Shvero et al.³⁶ have proposed a histological classification for vocal fold cysts which is called the Koren classification:

• Cysts lined by non ciliated columnar epithelium with mucous content.

• Cysts lined by ciliated columnar epithelium with mucous content.

• Cysts lined by squamous epithelium without keratinization.

• Cysts lined by squamous epithelium with keratinization.

Dysphonia, which is often disproportionate to the apparent size of the cyst, is not uncommon. Coexistence of sulci may cause an increase in pitch of the voice, while most patients present with a rough and breathy voice. Upon stroboscopy, phase asymmetry of the mucosal wave and hour-glass closure pattern are commonly seen. The mass of the cyst, depending upon its size, may cause minimal to extreme disruption of the mucosal wave vibratory pattern. One may also note the movement of the overlying epithelium and possible contralateral traumatic changes in the opposite vocal fold. Small subepithelial cysts may be picked up by narrow band imaging due to the color differentiation where the cyst will typically appear white against a light blue backdrop.³⁷

It has been observed that cysts are very unlikely to resolve without surgical intervention and generally remain stable in size, but approximately 30% of them are equally likely to grow or shrink, with corresponding effect on voice. A very small number may also rupture and yield permanent hoarseness.³⁸

Surgery is performed by the microflap technique (Fig. 8) as per the principles of phonomicrosurgery. Phonomicrosurgery is based on the notion that surgery should be designed to remove the pathology without promoting scar formation (i.e., without stimulating fibroblasts in the intermediate layer of the lamina propria or deeper).³⁹ The incision is made immediately lateral to the lateral edge of the cyst (mini-microflap) such that minimum amount of epithelial elevation is needed.

Epithelial cordotomy is followed by a blunt dissection to separate the cyst from the surrounding structures. If the cyst is attached to the vocal ligament, the dissection and elevation may be tricky. Sharp dissection and cutting of the anterior and posterior tethering bands is performed to free the cyst attachments. Ideally the cyst is delivered in-toto and the infraglottic flap is reposited on the medial vibrating edge. However every attempt to completely excise the cyst must be made in the not so uncommon situation of the cyst “popping” open. Even if the cyst contents entirely leak out, an attempt must be made to remove the entire cyst wall, using dissectors or the laser, so as to prevent cyst recurrence.⁴⁰ Complete cyst wall removal takes preference over attempts to preserve epithelial cover as regeneration of epithelium will eventually take place over time. However, unaffected SLP must be preserved as this will not regenerate once removed. If the cyst wall is breached during dissection, the area of breach may be held with curved crocodile forceps plugging the leak and at the same time providing traction medially, thus helping in further dissection. Mucous retention cysts tend to rupture more often compared to epidermoid cysts which have a thicker cyst wall.

Voice therapy helps to overcome wrong compensatory techniques and decreases any acute swelling that maybe present postoperatively. Good vocal hygiene, adequate hydration and reflux management aids in the postoperative healing process which in turn can provide satisfactory vocal outcome. For patients who have not undergone surgery, voice therapy may improve daily phonatory function but it does not affect the chances of lesion resolution.³⁸

Pseudocyst

A pseudocyst, also termed as paresis podules⁴¹ is a discrete, unilateral, localized area of Reinke’s edema that usually occurs at the mid-membranous part of the vocal fold.³⁷ They generally do not involve the deeper layers of the lamina propria.⁴¹ These lesions have been universally found to be associated with unilateral vocal fold paresis.⁴¹

Etiological factors contributing to the development of pseudocysts include asymmetrical muscular activity, glottal incompetence, mucosal fragility and/or concomitant inflammatory disease. Preponderance of pseudocysts in females may be due to estrogen and progesterone hormone receptors known to exist within the cells in the vocal fold.^42,43 This edematous lesion appears as a cystic bulge, but without a true capsule⁴¹ and are therefore termed as ‘pseudo’- cysts.

Pseudocysts retain the pliability of the vocal fold more than other phonotraumatic lesions and therefore cause less severe symptoms. Laryngeal videostroboscopy aids in diagnosis of these lesions. Sometimes, laryngeal EMG may be needed to rule out coexisting unilateral vocal fold paresis.

Recent studies show that behavioral interventions such as increased hydration, control of laryngeal reflux and quitting smoking along with voice therapy is sufficient for most patients.⁴⁴ Patients who fail conservative management maybe offered microsurgical removal of the lesion with or without treatment of underlying glottic insufficiency. Evacuation of the pseudocyst contents is done by the microflap technique. For glottic insufficiency, medialization laryngoplasty or lipo-injection will reduce the phonatory gap and in turn decrease the shearing stress of the vocal folds. Most patients who undergo surgical intervention for vocal fold pseudocyst are unlikely to experience recurrence, regardless of demographic characteristics, vocation, or concurrent clinical factors. When it occurs, recurrence appears to evolve relatively briskly in a matter of months.⁴⁵

Reactive Lesions

Lesions that occur as a reaction to the shearing stress caused by a primary pathology on the opposite vocal fold are referred to as reactive lesions. A reactive vocal fold lesion usually occurs exactly opposite a cyst or polyp, typically in the mid-portion of the contralateral membranous vocal fold. These lesions are often confused with vocal fold nodules. However, it is important to differentiate reactive lesions from vocal fold nodules since both of them have different course of management.

The morphology of reactive lesions can be variable (Fig. 9). They may appear as a bump or as a ‘cup-and-saucer’ shaped indentation on the medial free edge of the contralateral vocal fold. This occurs at the site of maximum contact with the primary lesion following focal trauma during vocal overuse or misuse.⁴⁶ The excessive shearing forces on the contralateral vocal fold produces a reactive callus with epithelial hyperplasia.^2,47-50 Shorter traumatic periods usually tend to form less indurated lesions. Having a prolonged duration of hoarseness of voice, presence of a vocal polyp or a small primary lesion were found to be independent risk factors for the development of contralateral reactive lesions.⁵¹

The primary pathology (cysts or polyps) often extends till the sub-epithelium and superficial layer of the lamina propria of the vocal fold. The increased mass on one of the vocal folds makes it heavier and there is dampening of the mucosal wave on that side. However, the site of reactive lesion on the contralateral vocal fold remains relatively superficial and there is a mismatch in the mucosal wave pattern causing increased shimmer and variable peak amplitude.⁵²

These reactive lesions can be classified into 2 types based upon their morphology–fibrous or polypoid. Fibrous lesions tend to have opaque consistency with thickened epithelium. They are more likely to persist but may resolve, if at all, with less invasive treatments. Polypoid lesions are more translucent and smooth in nature and usually require surgical excision but are more likely to recur. Based upon their relationship with the normal vocal fold edge, they can also be classified as gradual or steeply transitioning reactive lesions. Gradually transitioning lesions are relatively flush with normal vocal fold edge and upon palpation, the lesion cannot be moved. Patients with gradual lesions are more likely to remain disease free. Steeply transitioning lesions have a palpable step off from the normal edge.⁵³

Reactive lesions have been noted more commonly in females. Patients usually present with variable period of dysphonia. It has been observed that those with contralateral reactive lesions are often more aware of their vocal abnormality.⁵² These lesions more commonly occur opposite unilateral vocal fold polyps as compared to unilateral cysts at the striking zone of the contralateral vocal fold. They are usually seen to coexist with medium sized and broad based polyps.

One of the biggest challenges of contralateral reactive lesions is to be able to distinguish them from bilateral vocal fold nodules. Upon video-laryngo-stroboscopy, presence of significant asymmetric vocal fold vibration is one of the most important diagnostic features. Other notable features include irregular mucosal wave vibration, focal adynamic segments and incomplete glottic closure. Definitive diagnosis is established intraoperatively.

Conservative management includes reducing voice use, speech therapy and maintaining vocal hygiene. This helps to reduce the vocal fold edema and lesion contact. However, this will only help in improving phonatory function over a period of time and is unlikely to lead to complete resolution of the reactive lesion. When managed conservatively, the fibrous type of reactive lesions is more likely to persist while the polypoidal type are expected to improve. However, when excised surgically the polypoidal lesions are more likely to recur.⁵² This indicates that fibrous type of reactive lesions are more recalcitrant compared to typical nodules. Polypoidal lesions have high recurrence likely due to factors other than vocal trauma. These include inherent vulnerability of the vocal fold, manner of voice use, glottal closure patterns and coexisting pathology like allergy or laryngo-pharyngeal reflux.

Simultaneous excision of the primary pathology and the reactive callus may provide better and more rapid voice quality improvement. Also, in situations where voice therapy is not easily available or patient is unlikely to be compliant, simultaneous excision of the lesions is preferred. However, if the lesion is very close to the anterior commissure and its excision in the same sitting may cause anterior commissure webbing, simultaneous removal should be avoided. Subepithelial infiltration at the reactive lesion site helps the surgeon to remain in the superficial plane while excising it. This prevents unnecessary damage to the underlying layers of the vocal fold and prevents formation of scar tissue. Post surgery, voice rest for a week followed by voice therapy is the routine recommended at our center.

Contact Granuloma

Contact granulomas (CGs) are benign and inflammatory lesions of the vocal fold, attached to the vocal process of the arytenoid cartilage (Fig. 10). These result from the continuous hammering of one vocal process against the other vocal process during phonation, especially during loud phonation and hard glottal attacks.⁵⁴ Few other terms for these lesions are vocal process granuloma, laryngeal contact ulcer, laryngeal granuloma, vocal fold granuloma and post- intubation granuloma.⁵⁵ The granulomas may be ulcerative, pedunculated, sessile, white or erythematous in appearance. They may be unilateral or bilateral.⁵⁵ Histologically, the granulomas reveal squamous hyperplasia with a proliferation of capillaries, fibroblasts, collagen fibers and leukocytes.⁵⁵ However, histologically a pyogenic granuloma is different from granulation tissue as it has a lobular arrangement of capillaries in the deep portion of the lesion.⁵⁶

Common etiological factors of CGs are vocal abuse, laryngopharyngeal reflux, excessive glottic attack during initiation of speech, glottal incompetence with severe hyperfunction, chronic cough, habitual throat clearing and intubation (prolonged or traumatic).^28,54 Other causative factors observed are perichondritis of the arytenoid cartilage, allergy, infection and individual susceptibility.

The vocal process of arytenoid cartilage is covered with a thin layer of stratified squamous epithelium. This thin layer of mucosa is susceptible to damage by any unyielding force like opposite arytenoid’s vocal process or endotracheal tube.⁵⁷ Subsequently it causes injury to the perichondrium of the arytenoid cartilage.

Based on size and endoscopic appearance, Farwell et al. have proposed a grading system for CGs (Fig. 11). Grade 1 CGs are sessile and limited to vocal process without any ulceration. Grade 2 CGs are limited to vocal process, are ulcerated or pedunculated. Grade 3 CGs extend beyond the vocal process but do not cross the midline of a fully abducted vocal fold. Grade 4 CGs extend beyond the vocal process and over the midline of a fully abducted vocal fold. CGs are additionally graded as ‘A’ if unilateral and ‘B’ if bilateral.⁵⁵

CGs are more commonly seen in men than in women. Intubation granulomas though not phonotraumatic, are found more in women than in men.⁵⁸ Patients usually complain of hoarseness, foreign body sensation, frequent throat clearing, throat pain. If the CG is extremely large, then the patient might experience shortness of breath and dyspnea on exertion.

On laryngoscopy, CGs are globular or lobulated of various sizes and found attached to the vocal process of the arytenoids (Fig. 12). It is important to thoroughly examine the vocal folds for a second lesion caused due to phonotrauma.

As CGs have multifactorial etiology, their treatment is also multidimensional. Medical treatment of the underlying cause includes antacids, proton pump inhibitors, alginates, steroids (systemic or inhaled), cough suppressants and antibiotics. Voice therapy is helpful to correct the faulty technique of phonation and to relax the vocal folds to avoid hitting the opposite arytenoid with force. If patients are resistant to these modalities of treatment, then percutaneous injection of Botulinum toxin is considered to cause paresis of the vocal fold and put voice at rest. A dose in the range of 2.5 to 30 U is injected into the adductors (thyroarytenoid and lateral cricoarytenoid muscles) to relax them and decrease the trauma of one vocal process to the other.⁵⁴ It maybe performed as an office procedure, preferably EMG guided via the percutaneous route through the cricothyroid membrane or under general anesthesia during MLS and after surgical excision of the grade 3 or 4 CG.

Grade 1 and grade 2 CGs are usually treated conservatively with proton pump inhibitors, voice therapy and botulinum injection. In cases of recurrent CG or a large CG causing airway obstruction (grade 3 or 4) or a CG resistant to the above modalities of treatment, surgical excision under general anaesthesia is considered. Excision can be done using either cold steel instruments or laser. The goal is to remove the CG in an atraumatic fashion, maintaining as much normal mucosa surrounding the surgical site as possible and minimizing any possible trauma to the underlying arytenoid cartilage perichondrium. To achieve this, the granuloma is not excised flush to its base and a small stump is left attached to the vocal process to prevent perichondrial exposure or damage. After the excision, botulinum toxin can be injected into the ipsilateral thyroarytenoid muscle to weaken the vocal fold. Post operatively, laryngopharyngeal reflux is treated with medical and lifestyle changes along with voice rest followed by vocal therapy.⁵⁴

Sulcus Vocalis

It is a fibroplastic anomaly of the normally pliable vocal fold cover, where there is migration of the vocal fold epithelium into the normally convex SLP, or deeper, parallel to its free edge⁵⁹ (Fig. 13).

Some authors consider it to be of congenital origin,⁶⁰ with a postulation of faulty genesis of the fourth and sixth branchial arches⁶¹ or a degeneration of fibroblasts in the macula flavae similar to age-related degeneration of vocal folds.⁶² Some have suggested a familial occurrence.⁶³ An acquired origin such as following chronic upper respiratory tract infection⁶⁴ phonotrauma⁶⁵ or rupture of vocal cyst⁶⁶ is also suggested. Both factors may play a role.

Sulcus causes alteration of the physical and viscoelastic properties of the vocal fold due to loss or derangement of lamina propria. There is disruption of normal mucosal wave as a result of varying deficiency to the vocal fold architecture.⁶⁷ Histopathologic evaluation studies have demonstrated that tissues adjacent to a sulcus are found to have a proliferation of fibrous tissue and blood vessels; findings that are characteristic of a chronic inflammatory process.⁶⁸ Sato and Hirano⁶² performed electron microscopy and noted increased thickness of the basement membrane, decreased elastic tissue, degeneration of fibroblasts in the macula flava which is the structure responsible for ensuring synthesis of lamina propria fibrous components and dense collagen fibers. Lee and colleagues evaluated the histopathology specimens of sulcus vocalis patients and noted marked epithelial thickening, parakeratosis, and dyskeratosis.⁶⁹

The various classifications for sulcus vocalis include:

• Bouchayer et al.⁶¹:

• Sulcus vergeture: Corresponding to atrophy of mucosa covering the vocal ligament.

• Sulcus Vocalis: Corresponding to an open epidermoid cyst with thickened epithelium with the bottom of the cystic pouch adherent to the vocal ligament.

• Nakayama et al.⁶⁸:

• Type I: Superficial sulcus, confined to SLP

• Type IIa: Deep sulcus, approximating the vocal ligament

• Type IIb: Pouch type

• Ford et al.⁷⁰:

• Type I: Physiological sulcus, depression does not reach the vocal ligament and can be distinguished clinically by preservation of vocal fold vibratory activity on videostroboscopy.

• Type II: Full length depression up to or deeper to the vocal ligament

• Type III: Deep focal indentation not involving the entire length

• Pontes et al.⁷¹:

• Occult sulcus

• Sulcus striae minor

• Sulcus striae major

• Sulcus Pocket

Nerurkar et al.⁷² —based on depth as well as length of sulcus under microscopic magnification following palpation and subepithelial infiltration (Fig. 14)

Length classification—single sulcus along length of half or more of the membranous vocal fold (types A, B, C) and focal pit with length less than half of the membranous vocal fold (types D, E, F)

Depth classification—Type A & D: depth into SLP; Type B & E: depth into ligament and Type C & F: depth into muscle.

In this classification the presence of a polyp within a sulcus is denoted as (p), keratin within a sulcus as (k) and associated mucosal bridge as mb.

The superficial sulci are often phonotraumatic in origin and may be associated with other lesions such as varices, cysts or polyps on the same or opposite vocal fold. Patients usually present with hoarseness of voice, effortful voice production, easy vocal fatigability, reduced intensity and raised pitch.⁷²

Diagnosis of sulcus vocalis can be difficult. Ideal evaluation should consist of a multidisciplinary approach with a laryngologist and a certified speech and language pathologist. Vocal folds may appear normal on regular laryngoscopy so the use of videostroboscopy is essential. However, discrepancy between office stroboscopy and suspension microlaryngoscopy (MLS) exists. This may be due to the tangential views of the medial surface of the vocal folds during office endoscopy which limits diagnostic ability known as “umbrella effect.”⁷³ Findings of sulcus vocalis on stroboscopy include reduced amplitude of mucosal wave, bowed or curved aspect to the free edge of the involved vocal fold, glottic incompetence and hyperfunction of ventricular folds in some cases of compensation. The term “spindle shaped glottis” is often used in literature to describe the glottic closure pattern associated with sulcus vocalis; however, this is not pathognomic and can be found in other entities.⁷⁴ Asymmetric phonatory gap on white light laryngoscopy with no obvious structural or neuromuscular glottic pathology should make the laryngologist suspect a sulcus vocalis.⁷⁵

A conclusive diagnosis of sulcus vocalis can be obtained by performing a microlaryngoscopy (MLS). MLS with palpation of vocal folds revealed a sulcus in 61.7 % of stroboscopically undiagnosed lesions⁷² (Fig. 15 and ¹⁶). A systematic examination of the supraglottic, glottic and subglottic subsites should be undertaken with detailed photo documentation using rigid 0° and 70° telescopes. Coexisting lesions are commonly found along with sulcus, the most common one being a vocal cyst.

As with most benign vocal fold lesions, nonsurgical therapy should be tried first, and then therapeutic treatment options should progress in a stepwise manner from least invasive to most invasive. Co-morbid conditions affecting the voice should be addressed. A patient’s functional limitations and goals should be clearly defined with reasonable expectations with regard to vocal improvement.

It is targeted to improve the incorrect compensatory techniques which develop due to glottic insufficiency and poor mucosal waves. The goals of therapy are to encourage vocal hygiene, avoid hyperfunctional activity, and improve forward focus of voice.⁷² it involves relaxation therapy followed by strengthening exercises to reduce the phonatory gap. Studies have shown improvement in acoustic, aerodynamic, perceptual, and voice handicap index (VHI) scores with voice therapy for sulcus vocalis.^76,77

When trials with maximal voice and singing therapy have proved unsuccessful and functional limitations persist, the patient can be considered a candidate for surgical interventions. The surgical methods may be broadly divided as epithelial surgeries, augmentation of SLP, and medialization techniques.

Epithelial surgeries include Sulcussectomy described by Hirano,⁷⁸ sliding down technique by Saito,⁷⁹ partial sulcussectomy by Roch et al.⁸⁰ Undermining the sulcus with cold instruments or laser followed by redraping of epithelium without suturing or gluing has also been described.⁷⁰ The slicing mucosa technique was described by Pontes and Behlau with the purpose of interrupting the fibrotic and tension lines of the sulcus to yield a free mucosal vibration by using the principles of scar contracture repair.⁸¹ A parallel incision is made 1 mm above the superior lip of the sulcus and mucosa is detached without touching the vocal ligament. Multiple incisions of different lengths are made in the detached mucosa perpendicular to the sulcus, producing mucosal slices which are positioned without suturing. Laser-assisted sulcus release surgery (LASR) (Fig. 17) described by Nerurkar et al⁷² is based on the principle of the slicing mucosa technique as well as the principle underlying radial incisions for subglottic stenosis with a CO₂ laser.⁸² By making multiple small but complete epithelial incisions on the overlying epithelium of the medial and lateral lips of superficial sulci and focal pits (type A and D), the aim is to break the fibrous bands and release the tension enough to flatten the sulcus and allow normal epithelium to grow into the incised raw portions that are created between interspersed normal mucosa. The epithelium is not elevated from its bed in this technique in order to avoid increasing inflammation and scarring during the recovery phase.

Medialization of the vocal fold may be performed by external thyroplasty for closure of the glottal gap,⁸³ by injecting fat into the paraglottic space,⁸⁴ or by augmentation of SLP using various materials. Fat implantation into SLP was reported by Sataloff et al. in 1997 and can be used as an adjunct along with medialization thyroplasty.⁸⁵ The use of temporalis fascia as a superficial and deep implant into the vocal fold has been reported.^86-88 Ford introduced Alloderm strips longitudinally within the Reinke’s space to restore pliability and tissue loss in SLP.⁸⁹

Office based injection laryngoplasty using materials such as collagen, hyaluronic acid, hydroxyapatite is a relatively safe and effective method to close the glottal gap.⁹⁰

Transforming growth factor β3 has been found to have role in vocal fold repair mechanisms.⁹¹ Grafting small intestinal submucosa into vocal fold of canine model resulted in newly generated hyaluronic acid.⁹² Hirano et al in 2018 published their results of the first phase I/II clinical trial for intracordal injection of recombinant HGF for vocal fold scar and sulcus in 18 human patients.⁹³

Mucosal Bridges

Mucosal bridges are rare laryngeal lesions of unknown etiology, which may cause dysphonia of varying degrees. Thin epithelial mucosal bridge is a strip of epithelium that runs parallel to the vocal fold and is connected anteriorly and posteriorly but not attached to the free edge of the vocal fold.⁹⁴ Thick connective tissue mucosal bridge consists of a central axis of connective tissue, covered by a surrounding stratified epithelium. The thickness of this variant may be even half the total bulk of the vocal fold.⁹⁴ The existence of incomplete mucosal bridge was first proposed by Nerurkar et al.⁹⁵ An incomplete mucosal bridge, in the opinion of the authors, is typically identified by palpation of a slit on the superior surface of membranous vocal fold. This slit leads to a subepithelial pocket which lies just below and parallel to the vocal fold epithelium and just stops short of opening up at its medial edge. They may also be thin or thick.

Male or female preponderance of mucosal bridge is not established as such due to small sample studies and fewer mucosal bridge studies so far. They are more commonly found in adults.⁹⁴

According to some authors, they are congenital anomalies of the group referred to as minimum structural lesions of the vocal fold that include sulci, cysts, microwebs and capillary ectasia.^61,96 There are occasional reports of iatrogenic mucosal bridges being developed as complications of laryngeal microsurgery.⁹⁷

Trauma is usually surgical and rarely intubation trauma. Surgical causes include over-resection of the superficial layer of lamina propria, resulting in remucosalization over the deficient area and damage to the vocal ligament and deep layers of the lamina propria.⁹⁸ Non-surgical causes include untreated benign lesions, chronic vocal abuse and repeated intracordal hemorrhage. Microvascular lesions (i.e., varices, capillary ectasia) may also result in scarring secondary to hemorrhage and fibrosis.⁹⁸

Histologically, the thin mucosal bridges consist of non-keratinized stratified epithelium with no or very little connective tissue at the core, with thicker MB consisting of a significant thickness of vascularized dense connective tissue core covered by non-keratinized stratified squamous epithelium that may be accompanied by thick basement membrane.⁹⁴

Most patients experience vocal symptoms since childhood. The occurrence and time of onset of mucosal bridge-induced voice symptoms are determined by several factors, such as lesion thickness, number, site and its association with other lesions. In some cases, vocal symptoms are experienced only when vocal abuse or secondary lesions are present.⁹⁴

Thin mucosal bridges are invariably associated with an underlying sulcus and hoarseness is due to the combination of these two pathologies. Vocal fatigue is another presentation of mucosal bridges.⁹⁹ The mucosal bridge may cause dysphonia and diplophonia of varying degrees because of their separate vibratory characteristics from the main vocal fold, especially if they are associated with cysts or sulci.⁹⁴

A mucosal bridge is described by some as occult as it is not easily identified on flexible laryngoscopy or videostrobolaryngoscopy but is mistakenly diagnosed as sulcus vocalis.¹⁰⁰ In most cases, MB are discovered after close inspection and palpation on microlaryngoscopic examination. Hence, final diagnosis is usually not made until microscopic direct laryngoscopy is performed and palpation of the true vocal fold reveals the mucosal bridge.^99,101 A mucosal bridge should be suspected on videostrobolaryngoscopy, if two parallel sulci are seen on the same vocal fold. This scenario usually represents a single wide sulcus with an overlying thin epithelial mucosal bridge.

When a cyst or polyp develops or co-exists with a MB, the voice dramatically deteriorates. In such cases, surgical management of only the cyst/polyp may suffice. Management of the sulcus may be deferred for a second stage if the voice is not satisfactory a couple of months after surgery. It has been postulated that a thin MB tethers the vocal fold during vibration, possibly resulting in two out of sync vibrating bodies, with no added benefit of providing significant bulk to the vocal fold, and therefore, its excision may be preferable. This does not apply to thicker bridges, which form a large part of the bulk of the vocal fold as their removal would result in a large phonatory gap with air leak.¹⁰²

Removal of coexisting condition (cyst, sulci,polyp) and leaving the MB intact may achieve desirable results if surgery is followed by good speech therapy.¹⁰³ Voice therapy encourages vocal hygiene, enhances breath support and avoids hyperfunctional activity.

In the case of thicker MB, their undersurface and apposing vocal fold epithelium may be freshened and glued to obliterate the bridge. A newer technique, the ‘sandwich flap technique’ has been proposed which involves freshening (by cold steel or laser) and then suturing the mucosal bridge to the vocal folds.¹⁰⁴ Pulse dye laser (PDL) glottoplasties with PDL assisted undermining technique in patients with sulcus vocalis accompanying MB has also been described.¹⁰⁵ For incomplete MB, excision of the subepithelial pocket with or without suturing the apposing surfaces offers good vocal outcomes.⁹⁵

When mucosal bridges are bilateral, vocal improvement after surgery is not always fully satisfactory and immediate. Further studies are needed to standardize a gold standard of care.