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Summary Table

Feature	Details
Risk Factors	Voice overuse (singers, teachers, coaches), smoking, alcohol use, chronic GERD/LPR, HPV infection (types 6 and 11), male sex and age >40 for malignancy
Etiology	Benign: mechanical trauma, mucosal irritation, HPV infection. Malignant: squamous cell carcinoma driven by tobacco and alcohol synergy
Patient Presentation	Progressive or persistent hoarseness (dysphonia) lasting >2 weeks; may include globus sensation, throat clearing, vocal fatigue, dysphagia, referred otalgia, or stridor in advanced cases
Classic Physical Exam	Hoarse or breathy voice quality; indirect or flexible laryngoscopy reveals a visible lesion on the vocal fold; cervical lymphadenopathy in malignancy
Key Diagnostic Results	Flexible fiberoptic laryngoscopy for visualization; videostroboscopy for mucosal wave assessment; biopsy and histopathology for any suspicious or persistent lesion; CT/MRI for staging malignant disease
Management	Benign lesions: voice therapy, smoking cessation, anti-reflux treatment, microlaryngeal surgery if refractory. Malignant lesions: early stage treated with radiation or laser excision; advanced stage treated with chemoradiation or laryngectomy
Keywords	"Singer's nodules," "smoker's polyp," "Reinke's edema," "recurrent respiratory papillomatosis," "leukoplakia," "hoarseness >2 weeks in a smoker," "stroboscopy," "mucosal wave"

1. Pathophysiology

Vocal cord masses arise from the layered microanatomy of the vocal fold. The vocal fold is composed of the epithelium, the superficial lamina propria (Reinke's space), the deeper layers of the lamina propria (vocal ligament), and the vocalis muscle. Normal phonation depends on the pliability of the superficial lamina propria, which allows the "mucosal wave" to propagate during vibration. Any lesion that alters the mass, tension, or regularity of this mucosal cover will disrupt vibration and produce dysphonia.

Vocal cord nodules develop from chronic mechanical stress at the junction of the anterior one-third and posterior two-thirds of the membranous vocal fold, the point of maximal vibratory contact. Repeated collision causes localized edema, then progressive fibrosis of the superficial lamina propria. Because the trauma is bilateral and symmetric, nodules are characteristically bilateral. This is why they are strongly associated with voice overuse in singers, teachers, and young children who shout frequently.

Vocal cord polyps result from a similar phonotraumatic mechanism but tend to follow an acute vocal insult (a single episode of intense voice abuse or a hemorrhagic event within Reinke's space). Unlike nodules, polyps are usually unilateral and arise from a localized vascular injury that produces edema, fibrin deposition, and sometimes thrombosis. Smoking potentiates polyp formation by increasing vascular fragility in the lamina propria.

Reinke's edema (polypoid corditis) is a diffuse, bilateral accumulation of gelatinous fluid within Reinke's space. It is almost exclusively seen in chronic smokers, and often in combination with laryngopharyngeal reflux (LPR). The diffuse swelling of both vocal folds lowers the fundamental frequency of the voice, producing a characteristically deep, husky voice quality, particularly noticeable in women.

Laryngeal papillomas are caused by HPV types 6 and 11 (the same low-risk strains that cause anogenital warts). In children, vertical transmission from the birth canal leads to juvenile-onset recurrent respiratory papillomatosis (RRP), which typically presents before age 5 with progressive hoarseness, stridor, and potential airway compromise. In adults, the disease is usually less aggressive and often presents with isolated hoarseness. Papillomas are exophytic, cauliflower-like growths that can seed throughout the airway. Despite being histologically benign, they are notorious for recurrence after excision.

Contact granulomas form on the vocal process of the arytenoid cartilage, the posterior portion of the vocal fold where the cartilaginous framework is covered only by thin mucosa. Chronic irritation from GERD/LPR, endotracheal intubation, or habitual throat clearing causes mucosal ulceration followed by exuberant granulation tissue formation. The location (posterior glottis, overlying the arytenoid) is the key anatomic discriminator from nodules and polyps, which occur on the membranous fold.

Laryngeal squamous cell carcinoma accounts for the vast majority of malignant vocal cord masses. The synergistic carcinogenic effects of tobacco and alcohol drive squamous metaplasia, dysplasia, and eventual invasive carcinoma. Precursor lesions such as leukoplakia (white mucosal patches) and erythroplakia (red patches, which carry a higher malignant potential) may be seen on laryngoscopy. Glottic carcinoma (arising from the true vocal folds) presents early with hoarseness because even a small lesion disrupts vibration. In contrast, supraglottic carcinoma presents later with dysphagia, muffled voice, referred otalgia, or neck mass because the supraglottic region is less sensitive to small changes in mass.

2. Classification and Clinical Manifestation

Lesion	Laterality	Location on Vocal Fold	Voice Quality	Other Symptoms	Key Association
Vocal Cord Nodules	Bilateral, symmetric	Junction of anterior 1/3 and posterior 2/3 of membranous fold	Breathy, rough hoarseness; worse with use	Vocal fatigue	Voice overuse (singers, teachers)
Vocal Cord Polyp	Usually unilateral	Membranous fold (variable)	Intermittent or constant hoarseness	Diplophonia (two simultaneous pitches)	Acute vocal trauma, smoking
Reinke's Edema	Bilateral, diffuse	Entire membranous fold	Low-pitched, husky voice	Globus sensation	Heavy smoking, LPR
Laryngeal Papilloma	Unilateral or bilateral, may be multifocal	Anterior glottis most common	Hoarseness, weak cry in children	Stridor, airway obstruction (children)	HPV 6 and 11
Contact Granuloma	Usually unilateral	Vocal process of arytenoid (posterior glottis)	Mild hoarseness or throat pain	Throat clearing, globus, odynophonia	GERD/LPR, intubation
Leukoplakia/Erythroplakia	Usually unilateral	Variable on vocal fold surface	Progressive hoarseness	May be asymptomatic	Smoking, alcohol (premalignant)
Laryngeal SCC (Glottic)	Unilateral initially	True vocal fold	Progressive, unrelenting hoarseness	Stridor, dyspnea if advanced; vocal fold fixation	Smoking + alcohol synergy
Laryngeal SCC (Supraglottic)	Variable	Epiglottis, aryepiglottic folds, false cords	Muffled or "hot potato" voice	Dysphagia, referred otalgia, neck mass	Smoking + alcohol; presents later

3. Diagnostic Workup

Test	Role	Key Findings
Flexible fiberoptic laryngoscopy	Best initial test for any patient with hoarseness >2 weeks	Direct visualization of lesion morphology, location, and mobility of vocal folds
Videostroboscopy	Most informative functional test	Assesses mucosal wave propagation; absent or reduced wave suggests infiltrative lesion (malignancy) or deep fibrosis
Biopsy with histopathology	Gold standard / confirmatory test	Distinguishes benign from premalignant (dysplasia) and malignant (invasive SCC) lesions
CT neck with contrast	Staging for suspected or confirmed malignancy	Evaluates cartilage invasion, subglottic extension, lymph node involvement
MRI	Adjunct for soft tissue detail	Better than CT for assessing pre-epiglottic space invasion and cartilage involvement
Chest X-ray or CT chest	Metastatic workup for confirmed carcinoma	Lung metastases, second primary lung malignancy (field cancerization)

The evaluation of any vocal cord mass begins with a thorough history. The examiner will look for duration and progression of hoarseness, voice use patterns, smoking and alcohol history, GERD symptoms, history of intubation, and any associated symptoms such as dysphagia, otalgia, weight loss, or hemoptysis. Any patient with hoarseness lasting more than 2 weeks should undergo laryngoscopy to rule out malignancy. This is one of the most tested principles in this topic.

Flexible fiberoptic nasopharyngolaryngoscopy is the best initial test. It is performed in the outpatient setting and allows direct visualization of the vocal folds. The examiner can assess the color, surface texture, size, location, and number of lesions, as well as vocal fold mobility during phonation. Immobility or fixation of one vocal fold raises concern for invasion of the cricoarytenoid joint or the recurrent laryngeal nerve by a malignant process.

Videostroboscopy is the most important functional assessment tool. Stroboscopic light allows slow-motion visualization of the mucosal wave. In benign superficial lesions (nodules, polyps), the mucosal wave is typically present but may be dampened. In malignant or deeply infiltrative lesions, the mucosal wave is absent or markedly reduced because the tumor tethers the mucosa to the deeper structures, eliminating the pliability of Reinke's space. This finding is a critical discriminator between benign and malignant pathology.

Biopsy is mandatory for any lesion that is suspicious for malignancy. Indications include unilateral vocal fold lesions in a smoker, leukoplakia, erythroplakia, an irregularly surfaced or exophytic mass, or any lesion failing to respond to conservative management. Biopsy is typically performed via direct microlaryngoscopy under general anesthesia, which also allows therapeutic excision of benign lesions. Histopathology is the gold standard for definitive diagnosis.

For confirmed malignancy, CT of the neck with contrast is the primary imaging modality for staging. It assesses depth of invasion, cartilage involvement (particularly the thyroid and cricoid cartilages), paraglottic and pre-epiglottic space invasion, and cervical lymph node metastasis. A chest X-ray or CT chest is obtained to evaluate for pulmonary metastases and to screen for a synchronous second primary malignancy, which occurs with notable frequency due to field cancerization from shared tobacco exposure.

4. Management and Treatment

Lesion	Initial Management	Surgical Management	Additional Considerations
Vocal Cord Nodules	Voice therapy (speech-language pathology), vocal hygiene	Microlaryngeal surgery only if refractory to 6-12 weeks of therapy	Surgery alone without voice therapy leads to recurrence
Vocal Cord Polyp	Smoking cessation, voice therapy (may help but less likely to resolve polyp)	Microlaryngeal excision is usually definitive	Distinguish hemorrhagic polyps from malignancy with biopsy
Reinke's Edema	Smoking cessation (essential), anti-reflux therapy	Microflap surgery or suction stripping if no improvement	Will not resolve without smoking cessation
Laryngeal Papilloma	Observation if mild and not obstructing	Repeated microlaryngeal debulking with CO2 laser or microdebrider	Cidofovir injection or bevacizumab as adjuncts for aggressive recurrence; tracheostomy avoided if possible due to seeding risk
Contact Granuloma	Anti-reflux therapy (PPI), voice therapy, avoidance of throat clearing	Surgical excision only as last resort (high recurrence)	Botulinum toxin injection to reduce vocal fold contact force is an emerging option
Early Glottic SCC (T1-T2)	Radiation therapy OR transoral laser microsurgery	Comparable cure rates; choice depends on patient preference, tumor characteristics, and voice preservation goals	Radiation: typically 60-66 Gy over 6-7 weeks
Advanced Glottic SCC (T3-T4)	Concurrent chemoradiation (organ-preservation protocol)	Total laryngectomy if chemoradiation fails or for very advanced T4a with cartilage destruction	Cisplatin $100\ mg/m^2$ q3 weeks concurrent with radiation is the standard regimen
Supraglottic SCC	Radiation or chemoradiation with neck dissection for nodal disease	Supraglottic laryngectomy for select cases	Higher rate of nodal metastasis than glottic SCC due to rich lymphatic drainage

Benign lesions are managed with a conservative-first approach. The cornerstone of treatment for vocal cord nodules is voice therapy with a speech-language pathologist. Voice therapy addresses the underlying phonotraumatic behavior that caused the nodules. If the patient adheres to therapy and proper vocal hygiene (hydration, avoidance of irritants, rest), nodules frequently resolve or improve significantly within 6 to 12 weeks. Surgery is reserved for nodules that are fibrotic and refractory to therapy. It is critical to understand that excision without addressing the vocal behavior will result in recurrence.

For vocal cord polyps, voice therapy alone is less likely to produce resolution because polyps often contain organized fibrin, vascular proliferation, or hemorrhage. Microlaryngeal surgery (phonosurgery) is the definitive treatment. This is performed under general anesthesia with direct laryngoscopy and microsurgical instruments, carefully excising the polyp while preserving the underlying lamina propria to protect the mucosal wave.

Reinke's edema will not resolve without smoking cessation. This is a non-negotiable prerequisite. Anti-reflux therapy with proton pump inhibitors (e.g., omeprazole 20-40 mg daily) is added if LPR is suspected. If the voice remains unacceptable after smoking cessation and medical optimization, surgical reduction via microflap technique can restore a more normal vocal fold contour.

Recurrent respiratory papillomatosis requires repeated debulking procedures because there is no cure. The virus persists in adjacent-appearing normal mucosa, driving recurrences. The goal of surgery is to maintain a safe airway and acceptable voice without causing scarring of the vocal folds. CO2 laser ablation and microdebrider techniques are standard. Tracheostomy is avoided whenever possible because the surgical stoma creates a new mucosal surface where papillomas can seed, potentially extending the disease into the lower airway. Adjuvant therapies such as intralesional cidofovir or systemic bevacizumab (anti-VEGF) are considered in cases with aggressive, frequently recurring disease.

Contact granulomas are managed primarily with anti-reflux therapy (high-dose PPI, twice daily dosing for 3 to 6 months), voice therapy to reduce forceful glottal closure, and cessation of throat clearing. Surgical excision carries a high recurrence rate (up to 70%) and is therefore reserved for cases where airway compromise is present or biopsy is needed to exclude granular cell tumor or other pathology.

For laryngeal carcinoma, early-stage glottic disease (T1-T2, N0) has excellent cure rates exceeding 85-90% with either radiation therapy or transoral laser microsurgery. Both approaches achieve comparable oncologic outcomes; the choice is individualized based on tumor volume, patient preference, and voice quality considerations. Radiation is typically delivered at 60 to 66 Gy in 2 Gy fractions over 6 to 7 weeks.

Advanced-stage disease (T3-T4a or node-positive) is managed with concurrent chemoradiation using the organ-preservation protocol, which avoids total laryngectomy. The standard chemotherapy agent is cisplatin at $100\ mg/m^2$ administered intravenously every 3 weeks during the radiation course. Total laryngectomy with permanent tracheostomy is reserved for patients who fail organ preservation, have T4a disease with thyroid cartilage destruction through and through, or who are not candidates for chemoradiation. Supraglottic cancers have a higher propensity for cervical lymph node metastasis due to the rich lymphatic drainage of the supraglottic region, so neck dissection or elective nodal radiation is routinely incorporated.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Vocal cord nodules vs. polyp	Both present with hoarseness and arise on the membranous fold	Nodules are bilateral and symmetric at the mid-fold junction; polyps are usually unilateral and may have a feeding vessel
Reinke's edema vs. hypothyroidism	Both can cause a low-pitched, husky voice	Reinke's edema shows diffuse translucent swelling of both folds on laryngoscopy; hypothyroidism causes myxedematous changes without a visible vocal fold mass and has systemic features (fatigue, weight gain, cold intolerance)
Laryngeal papilloma vs. laryngeal SCC	Both can appear as exophytic vocal fold masses	Papillomas have a classic "mulberry" or cauliflower-like appearance, occur in younger patients (children or young adults), and are associated with HPV 6/11; SCC occurs in older patients with tobacco/alcohol history and presents as an irregular, ulcerated mass with reduced mucosal wave
Contact granuloma vs. vocal process cyst	Both located in the posterior glottis	Granuloma sits on the surface of the vocal process with ulceration; a cyst is submucosal and smooth without ulceration
Laryngeal SCC vs. laryngeal TB	Both can present with progressive hoarseness, vocal fold mass, and constitutional symptoms	TB causes a pale, edematous "turban-like" epiglottis or posterior glottic involvement, with pulmonary findings and positive AFB; SCC is usually a unilateral, fixed fold lesion in a smoker without pulmonary infiltrates
Vocal cord paralysis vs. glottic SCC	Both cause unilateral hoarseness with a fixed or immobile fold	Paralysis shows a paramedian-positioned fold with intact mucosa (no visible mass); SCC shows a visible lesion with mucosal irregularity and absent mucosal wave
Functional dysphonia vs. organic vocal fold lesion	Both present with hoarseness	Functional dysphonia shows structurally normal vocal folds on laryngoscopy; the diagnosis is established when no organic pathology is found; may demonstrate paradoxical vocal fold motion or glottal insufficiency patterns

6. Traps and High-Yield Pearls

The most common way students get questions about vocal cord masses wrong is by failing to appreciate the significance of hoarseness lasting more than 2 weeks in a patient with risk factors for malignancy. A vignette that describes a 55-year-old smoker with 3 weeks of progressive hoarseness is not asking about voice rest or reflux therapy. The answer is laryngoscopy. Students who jump to "trial of PPI" or "voice therapy" without first visualizing the larynx will miss the diagnosis of carcinoma. The rule is simple: hoarseness beyond 2 weeks requires direct visualization.

A second trap involves confusing bilateral nodules with a unilateral polyp. Both are phonotraumatic, but the management diverges: nodules respond to voice therapy, whereas polyps usually require surgical excision. If the vignette says the lesion is bilateral and symmetric, the answer is voice therapy first. If it says unilateral, think polyp and plan for surgery.

Students also frequently miss the connection between laryngeal papillomatosis and HPV 6/11. The exam loves to present a child with progressive hoarseness and stridor, born via vaginal delivery to a mother with a history of condylomata. The answer is juvenile-onset RRP. The corollary pearl is that tracheostomy is avoided in these patients because of the risk of distal airway seeding.

Another tested concept is the location of contact granulomas on the vocal process of the arytenoid, not on the membranous vocal fold. This posterior location, combined with a history of intubation or chronic GERD, should immediately point to contact granuloma rather than a nodule or polyp.

Finally, for laryngeal carcinoma, students must recognize the distinction between glottic and supraglottic primaries. Glottic tumors present early (hoarseness) and metastasize to lymph nodes late because the true vocal fold has minimal lymphatic drainage. Supraglottic tumors present late (dysphagia, otalgia, neck mass) and metastasize early because the supraglottic region is richly supplied with lymphatics. This anatomic logic dictates both the clinical presentation and the staging workup, and it is tested repeatedly.

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