Laryngeal Pathology
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Direct answer
Hoarseness persisting beyond three weeks in an adult is laryngeal carcinoma until laryngoscopy proves otherwise — the rule that organises all laryngeal pathology. The benign lesions are vocal cord nodules (singer's nodes, matrix oedema and fibrosis at the junction of the anterior and middle thirds, from voice abuse), polyps (haemorrhagic, single), Reinke's oedema (bilateral gelatinous swelling of the Reinke space in smokers), and squamous papilloma (human papillomavirus types 6 and 11). Squamous cell carcinoma causes over 95% of laryngeal malignancy, dividing into glottic (true cord, earliest hoarseness, late spread, best prognosis), supraglottic and subglottic subsites; in India, tobacco chewing, bidi smoking and areca nut push hypopharyngeal extension and advanced disease, making the pyriform fossa a close companion diagnosis.
What you must remember
- Site-specific behaviour: glottic carcinoma hoarsens early (vocal cord has no lymphatics beyond the cord margins), so it is diagnosed small and is highly curable; supraglottic tumours have rich lymphatics and present with neck nodes and dysphagia; subglottic tumours are rare, silent and worst.
- Premalignant spectrum: squamous hyperplasia, keratosis, mild-moderate-severe dysplasia, carcinoma in situ, invasive carcinoma; leucoplakia and erythroplasia are clinical descriptors, not histological ones — erythroplasia carries the higher malignant potential.
- Vocal cord nodule versus polyp: the nodule is bilateral, symmetrical, at the vibratory midpoint, fibre-free matrix oedema in voice-abusers (treat with speech therapy); the polyp is unilateral, haemorrhagic-stromal and pedunculated, in smokers; the papilloma is a vascular, exophytic, koilocyte-bearing lesion.
- Recurrent respiratory papillomatosis: juvenile-onset, HPV 6/11, multiple recurring papillomas demanding repeated laser de-bulking; malignant transformation is rare but rises after irradiation and with HPV 16; distal spread to tracheobronchial tree is the feared complication.
- Indian aetiology: bidi smoking and smokeless tobacco with areca nut (gutkha) drive laryngeal and especially hypopharyngeal carcinoma; the submucous fibrosis field predisposes the upper aerodigestive tract broadly.
- Croup versus epiglottitis: paediatric inflammation in the larynx — viral laryngotracheobronchitis (parainfluenza, barking cough, subglottic oedema) versus bacterial acute epiglottitis (Haemophilus influenzae type b, drooling, thumb sign, do not examine the throat); diphtheritic laryngitis with membrane still appears in under-immunised Indian pockets.
- Vocal cord immobility: recurrent laryngeal nerve palsy (thyroid surgery, mediastinal tumours) presents with a bovine cough; bilateral palsy stridors and sits near the airway.
A hoarse voice, walked from symptom to biopsy
A 58-year-old bidi smoker has had hoarseness for four months. Step one: laryngoscopy, because any adult hoarseness beyond three weeks needs a view of the cords. Step two: localise — a whitish, irregular, exophytic lesion on the right true cord is glottic carcinoma until biopsy says otherwise; a smooth bilaterally swollen cord with a baggy, amber look in a female smoker is Reinke's oedema; paired nodules at the anterior third in a teacher who shouts are singer's nodes needing speech therapy, not a blade. Step three: biopsy the suspicious lesion — severe dysplasia and carcinoma in situ are treated by stripping or radiotherapy; invasive glottic T1 lesions receive radiotherapy or transoral laser excision with voice preservation. Step four: stage the neck — a clinically negative neck in early glottic disease can be observed, while supraglottic disease demands nodal treatment because its lymphatics betray it early. The reasoning chain — duration, site, appearance, biopsy, spread — is exactly what the viva wants, and the contrast case is the 45-year-old gutkha chewer whose "laryngeal" pain on swallowing turns out to be a pyriform fossa tumour with a node.
Where students slip
Candidates quote "hoarseness more than two weeks" and then fail to explain why: the vocal cord's mucous membrane is tautly fixed with virtually no lymphatics, so a glottic tumour announces itself early and spreads late — that anatomical fact, not a convention, drives the three-week rule. Second, students biopsy every laryngeal lesion without respecting the papilloma's vascularity and recurrence biology, and forget that juvenile papillomatosis is managed by airway maintenance and serial excision rather than a single curative procedure. Third, the Indian slip: treating hypopharyngeal carcinoma as laryngeal cancer with a different name — pyriform fossa tumours present with referred otalgia and dysphagia, are diagnosed late, and carry a far worse prognosis than their glottic neighbours.
Frequently asked questions
Why does glottic carcinoma present earliest?
The true vocal cord lacks lymphatics and any lesion splays the stiff vibratory epithelium, so even a small tumour alters voice long before it can metastasise.
What is the histology of a singer's nodule?
Fibrous or oedematous stroma with dilated vessels and thickened basement membrane at the anteriormiddle-third junction, always bilateral and symmetrical from voice abuse.
Which HPV types cause recurrent respiratory papillomatosis?
Types 6 and 11, producing multiple recurring squamous papillomas with koilocytes in children and adults, requiring serial endoscopic excision.
What distinguishes Reinke oedema from a polyp?
Reinke oedema is a bilateral, diffuse, gelatinous filling of the Reinke space giving a husky voice, typically in smokers, whereas a polyp is a unilateral haemorrhagic pedunculated lesion.
Which laryngeal subsite has the worst outlook?
Subglottic carcinoma — silent, diagnosed late, with cartilage invasion and spread beyond the larynx by the time hoarseness or stridor appears.