Vocal Cord Nodules

Bilateral, symmetrical, benign lesions of the vocal fold epithelium and superficial lamina propria arising from repetitive phonotrauma. They are the archetypal benign phonotraumatic lesion and the clearest demonstration that voice disorders are often behavioural in origin and behavioural in treatment.

Why they occur where they do

Nodules form at the junction of the anterior and middle thirds of the membranous vocal fold. This is the point of maximum amplitude of vibration and therefore of maximum collision force during phonation. It is also the midpoint of the membranous fold, which extends from the anterior commissure to the vocal process, and it is a relative watershed for the vascular supply. The repeated impact at this point produces microtrauma, basement membrane injury, fibronectin deposition, oedema and eventually fibrosis and epithelial hyperplasia.

Pathophysiology and the vibratory consequence

Early lesions are oedematous and soft, with loose oedematous superficial lamina propria and an intact mucosal wave. With continued trauma they become firm and fibrotic, with thickened basement membrane, collagen deposition and epithelial hyperkeratosis. The lesion increases the mass of the vibrating cover and, once fibrotic, increases its stiffness, damping the mucosal wave. The bilateral lesions prevent complete glottic closure, producing a characteristic hourglass glottic configuration with an anterior and posterior gap, which causes air escape and breathiness. The patient compensates by increasing subglottic pressure and adductory force, which increases collision and perpetuates the lesion. Breaking this cycle is the treatment.

Epidemiology and risk

• Commonest benign vocal fold lesion.
• Adult women aged 20 to 50, and prepubertal boys, are the groups most affected. The female predominance in adults relates to a higher fundamental frequency with more vibratory cycles per unit time, a shorter membranous fold, a lower hyaluronic acid content in the superficial lamina propria which is less protective, and occupational factors.
• Occupational groups: teachers, singers, actors, call centre workers, clergy, coaches, market traders, aerobics instructors and nursery staff.
• Children: nodules occur in an estimated 15 to 20 percent of school aged children with dysphonia, associated with shouting and hard glottal attack. They frequently regress at puberty in boys as the larynx grows.

Contributing factors: vocal misuse and abuse, hard glottal attack, speaking at an inappropriate pitch or volume, poor breath support, dehydration, laryngopharyngeal reflux, smoking, allergic rhinitis with throat clearing, and psychological stress with laryngeal muscle tension.

• Hoarseness of gradual onset, typically described as rough and breathy.
• Reduced vocal range with loss of the upper register and difficulty with soft high notes, which singers notice long before speakers do.
• Vocal fatigue with the voice deteriorating through the day and through the week, and recovering with rest, which is a characteristic pattern.
• Increased effort required to phonate.
• Delayed voice onset and voice breaks.
• Frequent throat clearing and a sensation of a lump.
• Neck and laryngeal discomfort from compensatory muscle tension.
• Symptoms present for months to years.
• No pain, no dysphagia, no dyspnoea, no weight loss. Any of these should redirect the diagnosis.

Examination

• Perceptual voice assessment using GRBAS or the Consensus Auditory Perceptual Evaluation of Voice, and a patient reported measure such as the Voice Handicap Index.
• Reduced maximum phonation time.
• Flexible nasolaryngoscopy showing bilateral, symmetrical, whitish or greyish elevations at the junction of the anterior and middle thirds, with an hourglass glottic closure pattern.
• Signs of muscle tension dysphonia: supraglottic anteroposterior or lateral compression, which frequently coexists and which must be addressed.
• Assessment of the whole larynx for reflux changes, other lesions and mobility.

Red flags indicating a different diagnosis

• Unilateral lesion, which is not a nodule and requires a different differential including polyp, cyst, granuloma, papilloma and carcinoma.
• Progressive rather than fluctuating hoarseness.
• Sudden onset, suggesting haemorrhage or a polyp.
• Pain, dysphagia, otalgia, haemoptysis or weight loss.
• A neck mass.
• Smoking history with a persistent white lesion, requiring biopsy for dysplasia and carcinoma.
• Failure to improve with adequate voice therapy, which requires reassessment and often microlaryngoscopy.

• Flexible nasolaryngoscopy, which identifies the lesions but which cannot reliably distinguish a nodule from a cyst or a small polyp.
• Videostroboscopy, which is the key investigation and which should be regarded as necessary rather than optional in this condition. It assesses the mucosal wave, amplitude, symmetry, periodicity and glottic closure. A soft oedematous nodule preserves the mucosal wave; a fibrotic nodule reduces it; a subepithelial cyst produces a segmentally absent wave over the lesion with an associated contact reaction on the opposite fold which mimics a contralateral nodule. This distinction is central, because nodules respond to voice therapy while cysts do not, and operating on a nodule or persisting with therapy for a cyst are the two commonest errors in this area.
• Acoustic analysis with jitter, shimmer and harmonic to noise ratio, and aerodynamic measures including maximum phonation time and phonation threshold pressure, which quantify the disorder and track response.
• Direct microlaryngoscopy under general anaesthesia where the diagnosis is uncertain, where there is a suspicion of malignancy, and as part of planned surgery. Palpation of the lesion at microlaryngoscopy distinguishes a soft nodule from a firm cyst.
• Assessment for reflux, allergy and nasal disease.

Differential diagnosis and the discriminating feature

• Vocal fold polyp: usually unilateral, often pedunculated, frequently with a history of a single episode of vocal strain or of a haemorrhage.
• Intracordal cyst: unilateral, subepithelial, with a segmentally absent mucosal wave and a contralateral reactive lesion. Does not respond to voice therapy and requires microsurgical excision.
• Pseudocyst and fibrous mass.
• Reinke oedema: diffuse bilateral polypoid swelling of the whole membranous fold in a smoker, with a very low pitched voice.
• Sulcus vocalis and vocal fold scar: a linear depression with an adherent epithelium and an absent mucosal wave.
• Contact granuloma: posterior, on the vocal process, associated with reflux and intubation.
• Papillomatosis: exophytic verrucous lesions.
• Dysplasia and carcinoma: usually unilateral, irregular, with leukoplakia and reduced mucosal wave in a smoker.
• Muscle tension dysphonia without a lesion.

Voice therapy is the primary treatment, and surgery is reserved for failure. The order matters: operating first and offering therapy afterwards produces recurrence, because the behaviour that created the lesion is unchanged.

Voice therapy, which is first line in essentially every case

• Referral to a speech and language therapist with experience in voice disorders.
• Vocal hygiene: adequate hydration with the aim of pale urine, avoidance of throat clearing with substitution of a hard swallow or a sip of water, avoidance of whispering, avoidance of shouting and of speaking over background noise, avoidance of caffeine, alcohol and smoking, and adequate sleep.
• Direct therapy techniques: resonant voice therapy, semi occluded vocal tract exercises including straw phonation, lip trills and humming, which reduce vocal fold collision force while maintaining vibration; confidential voice; and the Lessac Madsen resonant voice therapy or vocal function exercise programmes.
• Elimination of hard glottal attack, using easy onset and breathy onset techniques.
• Optimisation of breath support and reduction of laryngeal muscle tension, with manual circumlaryngeal therapy where there is palpable tension.
• Adjustment of habitual pitch and loudness.
• Occupational modification: amplification for teachers, scheduled voice rest periods, reduced speaking hours, and workplace acoustic improvements.
• A course of therapy is typically 6 to 12 sessions over 3 to 6 months, and adherence determines outcome. Explain at the outset that this is a behavioural treatment requiring sustained practice, not a passive intervention.
• Around 70 to 90 percent of true nodules resolve or improve sufficiently with adequate therapy, which is why surgery should not be offered first.

Treat coexisting conditions

• Laryngopharyngeal reflux with lifestyle modification and a proton pump inhibitor taken 30 to 60 minutes before meals for 8 to 12 weeks.
• Allergic rhinitis and chronic rhinosinusitis, which drive throat clearing and cough.
• Chronic cough.
• Smoking cessation.
• Psychological factors and stress, with referral where anxiety is driving muscle tension.

Surgery

Indications:

• Failure of an adequate trial of voice therapy, meaning a properly delivered course with documented adherence over at least 3 to 6 months.
• Fibrotic, mature nodules that are unlikely to resolve with therapy alone, though these should still have therapy first and afterwards.
• Diagnostic uncertainty requiring tissue.
• Suspicion of malignancy.
• A professional voice user whose livelihood is at stake and in whom therapy has failed, after full discussion of the risks.

Technique:

• Microlaryngoscopy under general anaesthesia with suspension, using microlaryngeal instruments and an operating microscope.
• Microflap technique with a cordotomy incision lateral to the lesion and elevation of the epithelium, allowing removal of the lesion from within the superficial lamina propria with preservation of the overlying epithelium and the deeper layers.
• Preserve the superficial lamina propria absolutely. This layer cannot be reconstructed, and its loss produces permanent scarring with an absent mucosal wave and a voice that is worse than before surgery. Overzealous excision is the principal complication and it is irreversible.
• Avoid stripping the vocal fold, which is an obsolete technique that produces scarring.
• Cold steel instruments are preferred to laser for these lesions, given the thermal injury to adjacent lamina propria with laser.
• Address both folds where both are involved, but avoid dissecting both anterior commissure regions in the same operation where the lesions are close to the commissure, given the risk of anterior glottic web formation.

Perioperative and postoperative care

• Absolute voice rest for 3 to 7 days, followed by graduated return to voice use under therapist supervision over 2 to 4 weeks.
• Hydration and humidification.
• Antireflux therapy.
• Avoid nonsteroidal anti inflammatory drugs and aspirin perioperatively given bleeding into the fold.
• Mandatory postoperative voice therapy. Surgery without behavioural change guarantees recurrence, and this must be stated before the patient consents.
• Return to professional voice use at around 4 to 6 weeks, guided by stroboscopy.

Children

• Voice therapy is the treatment. Surgery is very rarely indicated in a child with nodules.
• Many resolve spontaneously at puberty, particularly in boys, as the larynx enlarges.
• Therapy must be age appropriate and involve parents and teachers, addressing shouting behaviour and the environment. In a child who shouts because of a hearing loss, treat the hearing loss.
• Assess for adenotonsillar obstruction, allergy and reflux, which contribute.

Follow up

Review with videostroboscopy at 3 and 6 months, and again after any surgery. Continue therapy support for professional voice users indefinitely. Recurrence indicates that the phonotraumatic behaviour has resumed and calls for renewed behavioural intervention rather than repeat surgery.