Complete ENT (Otorhinolaryngology) question bank — ear, nose, throat, larynx, airway & head-neck — in explanation-first exam-topper style, with 72 diagrams.
12chapters144questions77High-Yield
THE CONCEPT
Laryngeal carcinoma is a malignant tumour of the larynx, almost always squamous cell carcinoma, strongly related to smoking and alcohol. It is classified by site into supraglottic, glottic (commonest) and subglottic.
The larynx (coronal)
epiglottis
supraglottis
glottis
subglottis
false cord
TRUE cord
↓ trachea
The larynx is divided into three regions: the supraglottis (above the true cords, including the epiglottis and false cords), the glottis (the true vocal cords), and the subglottis (below the cords down to the lower border of the cricoid). This division underlies both cancer staging and the localisation of stridor.
RISK FACTORS & SUBSITES
Risk factors are smoking (major), alcohol (synergistic), HPV, reflux and occupational exposures, mainly in older men. The behaviour differs by site:
Glottic (vocal cords) — the commonest: presents early with persistent hoarseness (any hoarseness >2–3 weeks needs laryngoscopy) and, having poor lymphatic drainage, spreads to nodes late → better prognosis.
Supraglottic: throat discomfort, dysphagia, referred otalgia and later hoarseness; rich lymphatics → early nodal spread → worse prognosis; presents later.
Laryngeal cancer subsites
Supraglottic
rich lymphatics →early nodes, presents late
worse prognosis
Glottic (cords)
COMMONEST; earlyHOARSENESS; poor lymphatics
→ good prognosis
Subglottic
rare; stridor/airwayobstruction, presents late
Almost always squamouscell carcinoma (SCC).
Risk: SMOKING (major) +alcohol (synergistic),HPV, reflux.
Any hoarseness > 3 weeks
→ laryngoscopy.
Early → radiotherapy/laser(voice-sparing).
Advanced → laryngectomy +neck dissection ± chemoRT.
Laryngeal cancer (almost always squamous cell carcinoma, driven by smoking and alcohol) behaves differently by subsite: glottic tumours are commonest and present early with hoarseness and, having poor lymphatic drainage, carry a good prognosis; supraglottic tumours have rich lymphatics and spread early to nodes; subglottic tumours are rare and present late.
DIAGNOSIS & MANAGEMENT
Diagnosis is by laryngoscopy (indirect/flexible plus direct laryngoscopy under GA) and biopsy, with CT/MRI of the neck and chest for staging (TNM) and assessment of cord mobility. Management is stage-dependent: early tumours (T1/T2) are treated with radiotherapy or transoral laser/partial laryngectomy (voice-preserving, with good cure rates); advanced tumours (T3/T4) need total/partial laryngectomy with neck dissection and radiotherapy/chemoradiation (or organ-preservation chemoradiation), followed by voice rehabilitation (oesophageal speech, electrolarynx, or a tracheo-oesophageal voice prosthesis).
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CLINICAL PEARL: Laryngeal carcinoma = squamous cell carcinoma; smoking + alcohol. Glottic (cords) = commonest, presents early with persistent hoarseness, poor lymphatics → good prognosis. Supraglottic = rich lymphatics → early nodes, worse prognosis, presents late (throat pain, referred otalgia, dysphagia). Any hoarseness >3 weeks → laryngoscopy. Diagnose with laryngoscopy + biopsy, CT/MRI. Treat: early → radiotherapy/laser (voice-sparing); advanced → laryngectomy + neck dissection + chemoradiation; voice rehab after.
WHY GLOTTIC CANCER HAS THE BEST PROGNOSIS
A central concept in laryngeal cancer is why glottic (vocal-cord) tumours, though the commonest, carry the best prognosis, and the answer lies in two features of the vocal cords. First, the true vocal cords have a very sparse lymphatic supply, so a glottic cancer tends to stay local for a long time and spreads to the lymph nodes only late — nodal metastasis being the main determinant of poor outcome in head-and-neck cancer. Second, the cords are exquisitely sensitive to any disturbance of vibration, so even a small tumour causes persistent hoarseness early, bringing the patient to attention while the disease is still confined and curable. The combination of early symptoms and late spread means glottic cancers are typically caught at an early stage and cured with voice-preserving treatment. This is the mirror image of supraglottic cancer, whose rich lymphatics and silent early course produce the opposite, worse, outcome.
WHY PERSISTENT HOARSENESS IS A RED FLAG
The single most important public-health and clinical message of laryngeal cancer is that persistent hoarseness must never be ignored, because it is often the only early sign of a curable glottic tumour. Since the earliest glottic cancers announce themselves through a change in the voice, the rule that any hoarseness lasting more than about three weeks — particularly in a smoker over 40 — warrants laryngoscopy to visualise the cords is a simple, powerful way to catch the disease early. Dismissing prolonged hoarseness as 'just laryngitis', or treating it repeatedly with antibiotics without ever looking at the larynx, risks missing a cancer until it has advanced and voice-preserving cure is no longer possible. This is why the symptom of hoarseness sits at the heart of laryngeal-cancer teaching, and why prompt referral for laryngoscopy is emphasised so strongly — the difference between an early, curable tumour and an advanced one can hinge on it.
SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
Vocal cord palsy is paralysis of a vocal cord from interruption of its motor nerve supply — the recurrent laryngeal nerve (RLN), a branch of the vagus (the external branch of the superior laryngeal nerve supplies only cricothyroid). It may be unilateral (common) or bilateral, and the cord adopts a characteristic position.
Recurrent laryngeal nerve course
larynx
trachea
aortic arch
R subclavian a.
L vagus
R vagus
Left RLN: longer, intrathoracic (loops under aortic arch)
→ more often affected (e.g. lung/mediastinal disease)
The recurrent laryngeal nerves supply all the intrinsic laryngeal muscles except cricothyroid. The left nerve has a much longer, intrathoracic course, looping under the aortic arch, which makes it more vulnerable — for example to lung and mediastinal disease — than the right, which loops under the right subclavian artery.
ANATOMY & CAUSES
The RLN supplies all the intrinsic laryngeal muscles except cricothyroid; the left RLN has a longer, intrathoracic course (looping under the aortic arch), so it is more commonly affected. Causes include:
Surgical/iatrogenic — thyroid surgery is the commonest cause (also oesophageal, cardiac, cervical surgery).
Neurological (stroke, vagal/skull-base lesions), idiopathic (viral), trauma and aortic aneurysm.
CORD POSITION & FEATURES
By Semon's law, in progressive lesions the abductors (posterior cricoarytenoid) are affected before the adductors, so an RLN palsy leaves the cord in the paramedian position; a complete (combined vagal) palsy gives the cadaveric (intermediate) position.
Vocal cord positions
median(phonation)
paramedianRLN palsy
cadaveric(intermediate)
gentleabduction
fullabduction
Semon's law: abductors fail first → RLN palsy leaves the cord in the paramedian position
Vocal-cord positions: from the midline (median, for phonation) through paramedian and the cadaveric (intermediate) position to full abduction. By Semon's law the abductors fail first, so a recurrent laryngeal nerve palsy characteristically leaves the cord in the paramedian position.
Unilateral: a hoarse, breathy voice and weak cough initially, often improving as the other cord compensates by crossing the midline; risk of aspiration.
Bilateral (abductor) palsy: both cords paramedian → a narrow airway → stridor and dyspnoea (an airway emergency), though the voice may be near normal.
INVESTIGATION & MANAGEMENT
WHY THE LEFT NERVE IS MORE OFTEN AFFECTED
A frequently-examined anatomical point is why the left recurrent laryngeal nerve is more often paralysed than the right, and it follows directly from their different courses. The right nerve loops under the right subclavian artery high in the root of the neck and then ascends, whereas the left nerve descends into the chest to loop under the arch of the aorta before ascending back to the larynx. This gives the left nerve a much longer, intrathoracic course, exposing it to a far wider range of pathology — lung and mediastinal tumours, an enlarged left atrium, an aortic aneurysm and mediastinal lymphadenopathy — in addition to the neck causes that affect both sides. Consequently, a left vocal-cord palsy, especially in a smoker, should prompt a careful search of the chest and mediastinum for a cause such as bronchial carcinoma. Understanding the anatomy therefore directly guides the investigation of the palsy.
WHY BILATERAL PALSY THREATENS THE AIRWAY BUT SPARES THE VOICE
One of the most useful and counter-intuitive points about vocal-cord palsy is that a bilateral palsy endangers the airway while often preserving the voice, whereas a unilateral palsy spoils the voice but leaves the airway safe — and the explanation lies in cord position. In an abductor (recurrent laryngeal nerve) palsy, the affected cord(s) lie in the paramedian position, close to the midline. With both cords sitting near the midline, they can still meet for phonation (so the voice is reasonably good), but they cannot open the airway on inspiration, leaving only a narrow chink — hence stridor and potentially life-threatening obstruction. In a unilateral palsy, by contrast, the single paralysed paramedian cord leaves an adequate airway, but the gap between it and the mobile cord during phonation produces a breathy, hoarse voice until the healthy cord compensates. Grasping this trade-off explains why bilateral palsy is an airway emergency often needing tracheostomy, while unilateral palsy is primarily a voice problem.
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DANGER / REMEMBER: Investigation is laryngoscopy (cord position/mobility) plus a search for the cause (CT from skull base to mediastinum, thyroid/chest imaging). Management is to treat the cause; for unilateral palsy — voice therapy, and if persistent, medialization (type-I thyroplasty or injection medialization) to improve the voice and reduce aspiration; for bilateral palsy — secure the airway (often tracheostomy), with later cordotomy/arytenoidectomy/lateralization to widen the airway (at the cost of voice).
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CLINICAL PEARL: Vocal cord palsy = RLN interruption (the RLN supplies all intrinsic muscles except cricothyroid). The left RLN is longer (loops under the aortic arch) → more affected. Commonest cause = thyroid surgery; also lung/thyroid/oesophageal malignancy. By Semon's law the abductors fail first → cord in the paramedian position; complete → cadaveric. Unilateral → hoarse/breathy voice (may compensate); bilateral → stridor/airway obstruction (voice preserved). Treat the cause; unilateral → medialization thyroplasty; bilateral → airway (tracheostomy) ± cordotomy.
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KEY POINTS / NUMBERS (viva)
Vocal cord palsy = RLN palsy; RLN supplies ALL intrinsic laryngeal muscles except cricothyroid (external branch of SLN). Left RLN longer/intrathoracic (loops under aortic arch) → more often affected.
Causes: thyroid surgery (commonest), other neck/thoracic surgery; malignancy (lung — esp left, thyroid, oesophageal, mediastinal); neurological, idiopathic/viral, trauma, aortic aneurysm.
SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
Laryngitis is inflammation of the larynx (especially the vocal cords), producing hoarseness. It is acute (usually viral, self-limiting) or chronic (persistent, from ongoing irritation).
ACUTE LARYNGITIS
It is usually caused by a viral upper respiratory infection (commonest), voice abuse, secondary bacterial infection or irritants, giving hoarseness/aphonia, a dry cough, a sore/irritated throat and mild systemic symptoms with URI features, and red swollen cords. Management is voice rest (the key), steam/humidification, hydration, avoiding irritants/smoking and analgesia — antibiotics only if bacterial; it is self-limiting over a few days. (The airway emergencies of acute epiglottitis and croup are covered separately.)
CHRONIC LARYNGITIS
This results from ongoing irritation — smoking (major), voice abuse/misuse, gastro-oesophageal (laryngopharyngeal) reflux, chronic sinusitis/postnasal drip, alcohol, occupational irritants/dust and chronic cough — giving persistent hoarseness, throat clearing, cough and globus, with thickened/red cords (and sometimes Reinke's oedema). Specific chronic laryngitis includes tuberculosis (posterior larynx, with pulmonary TB), fungal and syphilitic forms.
WHY ACUTE LARYNGITIS IS MANAGED WITH VOICE REST
It is worth understanding why voice rest, rather than medication, is the mainstay of acute laryngitis, since this is often misunderstood. Acute laryngitis is usually a self-limiting viral inflammation of the cords, and antibiotics are of no benefit unless there is a genuine bacterial infection. The inflamed, swollen cords vibrate abnormally, producing the hoarseness; continuing to use — and especially to strain — the voice traumatises the already inflamed cords further, prolonging recovery and risking submucosal haemorrhage or the development of nodules. Resting the voice, keeping the cords moist with steam and hydration, and avoiding irritants such as smoke allows the inflammation to settle naturally. This is why the advice centres on voice rest and supportive measures rather than drugs, and why patients — particularly professional voice users — are warned against the temptation to force their voice through an episode of acute laryngitis.
WHY PERSISTENT HOARSENESS DEMANDS LARYNGOSCOPY
The most important safety principle across all laryngitis is that chronic or persistent hoarseness must be investigated by laryngoscopy to exclude cancer, and understanding why prevents a dangerous error. Chronic laryngitis and early laryngeal carcinoma share the same major risk factor — smoking — and can produce identical symptoms of persistent hoarseness, so it is impossible to distinguish a benign inflamed larynx from an early cancer on the history alone. Treating a smoker's persistent hoarseness as 'chronic laryngitis' without looking at the cords risks missing a curable glottic tumour. This is why the rule is absolute: hoarseness persisting beyond about three weeks requires visualisation of the larynx, with biopsy of any suspicious lesion. Chronic laryngitis is, in effect, a diagnosis made only after malignancy has been excluded by direct inspection of the cords — a point that underlies the whole approach to the hoarse patient.
A NOTE ON LARYNGOPHARYNGEAL REFLUX
An increasingly recognised cause of chronic laryngeal symptoms is laryngopharyngeal reflux — the backflow of gastric contents up to the larynx — which deserves specific mention because it is common and easily overlooked. Unlike classic gastro-oesophageal reflux, it often causes little or no heartburn; instead the acid and pepsin irritate the sensitive posterior larynx, producing hoarseness, chronic throat clearing, a sensation of a lump in the throat (globus), a chronic cough and posterior laryngeal redness/oedema on examination. Because the throat symptoms dominate and heartburn may be absent, the reflux basis is frequently missed and the patient treated repeatedly for 'infection'. Recognising the pattern allows effective treatment with lifestyle measures, dietary changes and acid suppression (a proton-pump inhibitor), together with voice hygiene. This is a practically important, treatable contributor to chronic laryngitis and hoarseness that is worth actively considering.
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DANGER / REMEMBER: Management is to remove the cause (stop smoking, voice hygiene/therapy, treat reflux with a PPI, treat sinusitis) and, crucially, to exclude malignancy — persistent hoarseness (>3 weeks) needs laryngoscopy and biopsy if suspicious.
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Hoarseness (dysphonia) is a change in the quality of the voice (rough, breathy, strained or weak) from disorders affecting vocal-cord vibration or closure. It is a common symptom with a wide differential — the key clinical task is to exclude malignancy.
Benign vocal-cord lesions (endoscopic)
nodulesbilateral, ant⅓–post⅔
polypunilateral
Reinke's oedemadiffuse, bilateral
The common benign vocal-cord lesions on endoscopy: vocal nodules are bilateral and symmetrical at the junction of the anterior third and posterior two-thirds; a polyp is usually unilateral; and Reinke's oedema is a diffuse, bilateral boggy swelling of the cords, strongly linked to smoking.
The entire clinical approach to hoarseness is organised around one priority: excluding laryngeal cancer. Although the great majority of hoarse voices have a benign cause — laryngitis, reflux, nodules, a polyp — the differential includes a curable malignancy whose early sign is precisely this symptom, and the cost of missing it is high. This is why the assessment is built not around treating the commonest cause but around identifying the red flags that mark out the dangerous minority: a persistent hoarseness beyond three weeks, a neck lump, difficulty or pain on swallowing, referred ear pain, stridor, coughing blood or weight loss — especially in a smoker over 40. Any of these mandates prompt laryngoscopy to look directly at the cords. Structuring the approach this way ensures that, whatever the eventual diagnosis, a cancer is not overlooked while a benign explanation is assumed — which is the crux of managing hoarseness safely.
WHY LARYNGOSCOPY IS THE KEY INVESTIGATION
A defining principle in evaluating hoarseness is that the voice cannot be properly assessed without looking at the cords — laryngoscopy is the key investigation. Because so many different conditions (inflammation, benign lesions, cancer, cord palsy, functional disorders) produce a similar-sounding hoarse voice, the history and listening alone cannot reliably distinguish them. Direct visualisation of the vocal cords — by indirect mirror examination or, better, flexible fibreoptic laryngoscopy — shows whether the cords are inflamed, bear a nodule or polyp, harbour a suspicious lesion, or fail to move (a palsy), and often makes the diagnosis at a glance. It also allows biopsy of anything suspicious. This is why no assessment of persistent hoarseness is complete until the cords have been seen, and why access to laryngoscopy is central to ENT practice. The dictum is simple: a persistently hoarse patient needs their larynx looked at, not just listened to.
A NOTE ON THE VALUE OF VOICE THERAPY
An important and sometimes underappreciated point is that many causes of hoarseness are best treated not by drugs or surgery but by voice therapy delivered by a speech-and-language therapist. A large proportion of dysphonia arises from how the voice is used — vocal abuse producing nodules, or excessive muscular tension producing muscle-tension dysphonia — and these respond to retraining rather than to any medication. Even where there is a structural lesion or a cord palsy, voice therapy plays a valuable role in optimising vocal technique, reducing strain, and helping the patient compensate. Recognising this steers management away from the reflex of prescribing antibiotics or rushing to operate, toward addressing the behaviour that underlies so much hoarseness. It also explains why the assessment of the hoarse voice is often multidisciplinary, involving the ENT surgeon and the voice therapist together, and why conservative, behaviour-focused treatment is frequently the first and most effective step.
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DANGER / REMEMBER:Red flags requiring urgent laryngoscopy: hoarseness >3 weeks (especially a smoker/>40), a neck lump, dysphagia, odynophagia, otalgia, stridor, haemoptysis or weight loss. Assessment is by history (duration, voice use, smoking, reflux, surgery) and laryngoscopy (indirect/flexible — the key investigation to visualise the cords), with biopsy/imaging as needed. Management is directed at the cause — voice therapy/hygiene (nodules, muscle-tension dysphonia), stopping smoking, a PPI (reflux), surgery (polyp, carcinoma) or medialization (palsy).
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CLINICAL PEARL: Hoarseness (dysphonia) = a change in voice quality with a wide differential: inflammatory (laryngitis, reflux), benign lesions (nodules, polyp, Reinke's), malignant (laryngeal cancer), neurological (cord palsy) and functional. The key rule: hoarseness >3 weeks (especially a smoker >40) → laryngoscopy to exclude carcinoma. Red flags: neck lump, dysphagia, otalgia, stridor, weight loss. Treat the cause (voice therapy, stop smoking, PPI, surgery).
Key investigation = laryngoscopy (indirect/flexible) to visualise the cords ± biopsy.
Treat the cause: voice therapy, stop smoking, PPI (reflux), surgery (polyp/carcinoma), medialization (palsy).
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Stridor is a harsh, noisy sound from turbulent airflow through a partially obstructed airway (larynx/trachea/large bronchi). It is a sign of upper-airway obstruction — a potential emergency — not a diagnosis.
Stridor: phase localises the level
supraglottis/glottis
subglottis/trachea
bronchi
INSPIRATORYsupraglottic/glottic
BIPHASICsubglottic/tracheal
EXPIRATORYlower airway
Infants: laryngomalacia · children: croup/epiglottitis/FB · adults: tumour/cord palsy
A sign of airway obstruction — a potential emergency
Stridor localises by its phase: inspiratory stridor points to a supraglottic/glottic obstruction, biphasic stridor to a fixed subglottic/tracheal lesion, and expiratory noise to the lower airway. The likely cause varies with age — laryngomalacia in infants, croup/epiglottitis/foreign body in children, and tumour or bilateral cord palsy in adults.
TYPES (localise by phase)
Inspiratory stridor → obstruction at/above the glottis (supraglottic/glottic) — e.g. laryngomalacia, epiglottitis.
Biphasic (inspiratory + expiratory) → a fixed subglottic/tracheal lesion — e.g. subglottic stenosis, croup.
WHY THE PHASE OF STRIDOR LOCALISES THE OBSTRUCTION
A clinically invaluable concept is that the phase of the respiratory cycle in which stridor occurs localises the level of the obstruction, allowing the site to be inferred at the bedside before any investigation. The principle rests on airway dynamics. An obstruction above or at the glottis (supraglottic/glottic) produces inspiratory stridor, because the extrathoracic airway tends to collapse inward as air is drawn in past the narrowing. A fixed lesion in the subglottis or trachea produces biphasic stridor (heard in both inspiration and expiration), since a rigid narrowing obstructs flow in both directions. An obstruction in the lower, intrathoracic airway produces expiratory noise (wheeze), as those airways narrow on expiration. So simply noting when the noise occurs — breathing in, both, or breathing out — points to the level and helps narrow the likely cause, which is why this is such a useful and frequently-tested piece of clinical reasoning.
WHY YOU MUST NOT DISTRESS A CHILD WITH STRIDOR
A crucial safety rule in managing a child with stridor is that the child must not be upset or examined invasively, because distress can precipitate complete airway obstruction — and understanding why is vital, particularly with suspected acute epiglottitis. A child with a critically narrowed airway is maintaining a fragile equilibrium; crying, struggling or an attempt to examine the throat with a spatula can increase airflow turbulence, provoke laryngospasm, or dislodge a swollen epiglottis, tipping partial obstruction into complete obstruction and respiratory arrest. This is why such a child is kept calm on the parent's lap, given oxygen non-threateningly, and taken to a controlled environment (theatre/anaesthetic room) where the airway can be secured by experts before any examination. The instinct to look in the throat or to lie the child down must be resisted. Recognising stridor as a sign of a precarious airway, to be handled gently and urgently rather than probed, can be the difference between a safe outcome and a catastrophe.
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DANGER / REMEMBER: Do not distress a child (especially with suspected epiglottitis — it may precipitate complete obstruction); assess severity (recession, cyanosis, exhaustion, saturation) and take a careful history/examination, with radiology/endoscopy when safe. Management is to secure/support the airway first (oxygen; possibly intubation/tracheostomy) and treat the cause (nebulised adrenaline + steroids for croup, antibiotics + airway care for epiglottitis, remove a foreign body, manage a tumour), with an emergency airway (tracheostomy/cricothyroidotomy) for impending obstruction.
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CLINICAL PEARL: Stridor = noisy breathing from turbulent flow through a partially obstructed upper airway — a sign (potential emergency), not a diagnosis. Phase localises: inspiratory = supraglottic/glottic; biphasic = subglottic/tracheal; expiratory = lower airway. Causes by age: infants — laryngomalacia (commonest congenital); children — croup, epiglottitis, foreign body; adults — tumour, bilateral cord palsy. Don't distress a child. Manage: secure the airway first + treat the cause (adrenaline/steroids for croup, antibiotics for epiglottitis, remove FB); emergency tracheostomy if obstructing.
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KEY POINTS / NUMBERS (viva)
Stridor = turbulent flow through a partially obstructed upper airway; a SIGN of obstruction (potential emergency), not a diagnosis.
Manage: secure airway first + treat cause (adrenaline/steroids — croup; antibiotics — epiglottitis; remove FB); emergency tracheostomy if obstructing.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Vocal nodules are small, bilateral, symmetrical swellings of the vocal cords at the junction of the anterior third and posterior two-thirds (the point of maximum contact/vibration), caused by chronic vocal abuse/misuse.
Benign vocal-cord lesions (endoscopic)
nodulesbilateral, ant⅓–post⅔
polypunilateral
Reinke's oedemadiffuse, bilateral
The common benign vocal-cord lesions on endoscopy: vocal nodules are bilateral and symmetrical at the junction of the anterior third and posterior two-thirds; a polyp is usually unilateral; and Reinke's oedema is a diffuse, bilateral boggy swelling of the cords, strongly linked to smoking.
FEATURES & MANAGEMENT
They are common in singers, teachers and children who scream ('screamer's nodules'), giving hoarseness, vocal fatigue and a breathy voice, with bilateral symmetrical whitish nodules on laryngoscopy. Management is voice therapy/hygiene (the mainstay — most resolve) and treatment of contributing factors (reflux), with surgical excision (microlaryngoscopy) only for persistent/mature nodules failing conservative therapy.
A NOTE ON WHY VOICE THERAPY COMES FIRST
The most important management principle for vocal nodules is that voice therapy, not surgery, is the first-line treatment, and understanding why is essential. Because nodules are caused by the mechanical trauma of vocal abuse or misuse, correcting the underlying vocal behaviour allows most nodules to resolve without any operation. A speech-and-language therapist teaches the patient to use the voice more efficiently and to avoid the shouting, throat-clearing or poor technique that produced the nodules in the first place. Operating without addressing the behaviour is illogical — the nodules would simply recur, and surgery on the delicate vibrating edge of the cord risks scarring that can permanently worsen the voice. This is why surgical excision is reserved for the minority of mature, fibrotic nodules that persist despite adequate voice therapy, and why the contrast with a polyp (which usually does need excision) is such a common teaching point.
THE BOTTOM LINE
Vocal nodules are bilateral cord swellings from vocal abuse that usually resolve with voice therapy, surgery being reserved for persistent mature nodules.
It is also worth noting that vocal nodules are especially common in certain occupational and behavioural groups — professional singers, teachers, telephone workers and habitually loud or screaming children — so identifying and modifying the vocal demands of the patient's work or lifestyle is an integral part of both treating existing nodules and preventing their recurrence after any treatment.
A useful final point is that the diagnosis is usually straightforward once the cords are seen, the bilateral symmetrical swellings at the characteristic junction being fairly distinctive, so the emphasis quickly shifts from diagnosis to the behavioural treatment that will actually resolve them and prevent their return.
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KEY POINTS TO REMEMBER
Vocal nodules = bilateral, symmetrical cord swellings at the junction of the anterior 1/3 and posterior 2/3, from chronic vocal abuse.
Common in singers, teachers, and screaming children ('screamer's nodules').
Hoarseness, vocal fatigue, breathy voice; bilateral symmetrical nodules on laryngoscopy.
Rx: voice therapy/hygiene (mainstay — most resolve), treat reflux; surgical excision only if persistent/mature.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
A vocal cord polyp is a benign, usually unilateral, pedunculated or sessile swelling of the vocal cord, arising from vocal abuse, smoking, or a single episode of vocal strain (it may be haemorrhagic/angiomatous).
FEATURES & MANAGEMENT
It causes hoarseness, sometimes a 'ball-valve' effect (intermittent voice change) and, if large, airway obstruction, appearing as a unilateral polyp on laryngoscopy. Management is usually surgical excision (microlaryngeal surgery — unlike nodules) plus voice therapy and removal of the cause (stop smoking/voice abuse). It is distinguished from nodules (which are bilateral and managed conservatively).
A NOTE ON WHY A POLYP DIFFERS FROM A NODULE
The key learning point is the practical distinction between a vocal polyp and vocal nodules, because it determines treatment. Both arise from vocal trauma and both cause hoarseness, but they differ in important ways: nodules are bilateral, symmetrical and callus-like, resulting from chronic repetitive abuse, and usually respond to voice therapy; a polyp is typically unilateral, often pedunculated, and may follow a single episode of vocal strain or be haemorrhagic, and it generally requires surgical removal because it does not resolve with conservative measures alone. Recognising which lesion is present — bilateral symmetrical swellings versus a single unilateral polyp on laryngoscopy — thus points to the correct management, conservative for nodules and surgical (with voice therapy and removal of the cause) for a polyp. This clean contrast is exactly the sort of distinction examiners like to test.
THE BOTTOM LINE
A vocal polyp is usually a unilateral cord swelling from vocal trauma that generally requires surgical excision with voice therapy, unlike the conservatively-managed bilateral nodules.
It is also worth noting that, because a polyp can occasionally act like a ball-valve at the glottis, it may cause an intermittent change in the voice or, if large, a degree of airway compromise, so a large or awkwardly-placed polyp warrants prompt removal both to restore the voice and to secure the airway, after which the tissue is examined histologically to confirm its benign nature.
A useful final point is that any cord lesion excised at surgery should be sent for histological examination, since occasionally what appears to be a benign polyp harbours unexpected pathology, and confirming the benign diagnosis provides reassurance and completes the management.
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KEY POINTS TO REMEMBER
Vocal cord polyp = benign, usually unilateral, pedunculated/sessile cord swelling; from vocal abuse, smoking, or a single strain (may be haemorrhagic).
Hoarseness, 'ball-valve' intermittent voice change, obstruction if large; unilateral polyp on laryngoscopy.
Distinguish from nodules (bilateral, conservative).
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Reinke's oedema (polypoid corditis) is a diffuse, bilateral oedema of the superficial lamina propria (Reinke's space) of the vocal cords, producing floppy, polypoid, boggy cords.
CAUSE, FEATURES & MANAGEMENT
It is caused by chronic irritation, especially smoking (the major factor), and also voice abuse, reflux and hypothyroidism. It characteristically gives a low-pitched, gruff/hoarse voice (especially in women — a 'smoker's voice'), with bilateral diffuse cord swelling on laryngoscopy. Management is to stop smoking (essential), voice therapy and treatment of reflux/hypothyroidism, with surgery (microlaryngeal incision and reduction of the oedema) for persistent/large disease.
A NOTE ON ITS STRONG LINK WITH SMOKING
The most important association to remember with Reinke's oedema is its strong link with smoking, which dominates both its cause and its treatment. The chronic irritation of tobacco smoke produces the diffuse fluid accumulation in Reinke's space that makes the cords floppy and boggy, giving the characteristic deep, gruff voice — classically noticed as an unusually low-pitched voice in a middle-aged female smoker. Because smoking is the driving factor, stopping smoking is the essential first step, without which the oedema will persist or recur even after surgery. This is why counselling on smoking cessation is central to management, alongside voice therapy and treatment of any reflux, with surgical reduction of the oedema reserved for cases that remain troublesome or cause airway concern. Reinke's oedema thus serves as a visible reminder of the laryngeal effects of smoking.
THE BOTTOM LINE
Reinke's oedema is a diffuse bilateral cord oedema strongly linked to smoking, giving a low gruff voice, whose treatment centres on stopping smoking with surgery for persistent cases.
It is also worth noting that, because Reinke's oedema chiefly affects middle-aged smokers and produces a strikingly deep voice, it is one of the causes of a woman being repeatedly mistaken for a man on the telephone — a clinical clue that, together with the smoking history, should bring the diagnosis to mind and prompt laryngoscopy to confirm the characteristic diffuse boggy cords.
A useful final point is that Reinke's oedema, being firmly associated with smoking, also serves as an opportunity to counsel the patient more broadly about the harms of tobacco, including the risk of laryngeal and other cancers, so its management dovetails with general smoking-cessation advice.
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KEY POINTS TO REMEMBER
Reinke's oedema (polypoid corditis) = diffuse bilateral oedema of the superficial lamina propria (Reinke's space) of the cords.
Cause: chronic irritation — especially smoking (major); also voice abuse, reflux, hypothyroidism.
Rx: STOP smoking (essential), voice therapy, treat reflux/hypothyroidism; microlaryngeal surgery for persistent/large.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Laryngeal papillomatosis is benign epithelial tumours (papillomas) of the larynx caused by human papillomavirus (HPV types 6 & 11) — the commonest benign laryngeal neoplasm in children.
FORMS & FEATURES
The juvenile form is acquired at birth from maternal genital warts and is multiple, recurrent and aggressive; the adult form is usually solitary and less aggressive. It causes hoarseness and, especially in children, progressive airway obstruction/stridor.
MANAGEMENT
A NOTE ON WHY RECURRENCE AND TRACHEOSTOMY MATTER
Two features make recurrent respiratory papillomatosis particularly challenging and worth understanding: its relentless recurrence and the special hazard of tracheostomy. Because the papillomas are driven by a persistent HPV infection of the airway lining, they regrow after removal, so children often need repeated surgical procedures over years simply to keep the airway and voice adequate — a considerable burden. The disease also has a tendency to seed to sites of mucosal injury, which is why tracheostomy is avoided whenever possible: creating a tracheostomy can spread the papillomas down into the trachea and lower airway, converting a laryngeal problem into a more dangerous distal one. These two points — expect recurrence, and avoid tracheostomy unless truly unavoidable — capture the essence of managing this frustrating condition, and explain the interest in adjuvant medical therapies and HPV vaccination to reduce the disease burden.
THE BOTTOM LINE
Recurrent respiratory papillomatosis is an HPV-driven benign laryngeal tumour of childhood that relentlessly recurs, is managed by repeated conservative excision, and in which tracheostomy is avoided to prevent distal spread.
It is also worth noting that the two forms behave differently: the juvenile-onset form, acquired from maternal genital warts at delivery, tends to be more extensive and aggressive with frequent recurrences through childhood, whereas the adult-onset form is often more limited — a distinction that influences how intensively and how often intervention is needed.
A useful final point is that, given the burden of repeated surgery and the risk of distal spread, there is considerable interest in prevention and in adjuvant medical treatments, and the wider adoption of HPV vaccination offers the prospect of reducing the incidence of this difficult disease in the future.
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DANGER / REMEMBER: Management is repeated surgical excision (microdebrider/CO2 laser) to maintain the airway and voice — recurrence is the rule (multiple procedures) — with adjuvants (cidofovir, interferon, bevacizumab); tracheostomy is avoided (it spreads disease) unless essential, and HPV vaccination may prevent it. Rare malignant transformation can occur.
Rx: repeated excision (microdebrider/CO2 laser) — recurrence is the rule; adjuvants (cidofovir/interferon/bevacizumab); avoid tracheostomy (spreads); HPV vaccine may prevent.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Laryngomalacia is the commonest congenital cause of stridor in infants, due to floppy, immature laryngeal/supraglottic structures that collapse inward on inspiration → inspiratory stridor.
FEATURES, DIAGNOSIS & MANAGEMENT
There is inspiratory stridor from birth/the first weeks, worse on feeding/crying/lying supine/exertion and better prone, usually mild and self-limiting. Diagnosis is by flexible laryngoscopy (an omega-shaped epiglottis, with collapse of the aryepiglottic folds/arytenoids on inspiration). Management is usually conservative (reassurance — it resolves by about 18–24 months as the cartilage stiffens), with treatment of reflux; surgery (supraglottoplasty) is reserved for severe disease (failure to thrive, apnoea, severe obstruction).
A NOTE ON WHY IT USUALLY NEEDS ONLY REASSURANCE
The most important management point in laryngomalacia is that the great majority of cases need only reassurance and observation, not surgery, and understanding why relieves a great deal of parental anxiety. The stridor arises because the infant's laryngeal cartilage is soft and immature, allowing the supraglottic structures to be sucked inward on inspiration; as the child grows over the first year or so, the cartilage naturally stiffens and the stridor resolves spontaneously, typically by 18–24 months. Provided the infant is feeding well, gaining weight and not having significant apnoeas or severe obstruction, the correct course is to explain the natural history and simply monitor, treating any coexisting reflux. Surgery (supraglottoplasty) is reserved for the small minority with severe disease — failure to thrive, apnoea or serious obstruction. Recognising laryngomalacia as a benign, self-resolving condition in most infants prevents both unnecessary intervention and undue alarm.
THE BOTTOM LINE
Laryngomalacia is the commonest congenital infant stridor, arising from a floppy immature larynx, that resolves spontaneously in most infants and needs surgery only when severe.
It is also worth noting that laryngomalacia is frequently associated with gastro-oesophageal reflux, which can aggravate the supraglottic oedema and worsen the stridor, so treating reflux is a useful adjunct in symptomatic infants and may reduce the severity of the obstruction while awaiting natural resolution.
A useful final point is that parents can be reassured with the characteristic history alone — stridor that is worse when the baby is upset, feeding or lying on its back and better when prone — which, in a thriving infant, is so typical of laryngomalacia that it strongly supports the benign diagnosis pending confirmation by laryngoscopy.
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KEY POINTS TO REMEMBER
Laryngomalacia = commonest congenital cause of infant stridor; floppy supraglottic structures collapse on inspiration.
Inspiratory stridor from birth/first weeks, worse on feeding/crying/supine/exertion, better prone; usually mild.
Dx: flexible laryngoscopy (omega-shaped epiglottis, aryepiglottic-fold/arytenoid collapse on inspiration).
Rx: conservative (resolves by ~18–24 months); treat reflux; supraglottoplasty only for severe (failure to thrive/apnoea).
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
A laryngocele is an abnormal air-filled dilatation/herniation of the laryngeal saccule (of the ventricle), communicating with the laryngeal lumen.
TYPES, CAUSE & FEATURES
Types are internal (within the larynx, in the false cord/aryepiglottic fold), external (herniating through the thyrohyoid membrane to give a neck swelling) or mixed. It results from raised intralaryngeal pressure (trumpeters, glassblowers) or from a laryngeal (ventricular) carcinoma obstructing the saccule — which must be excluded. Features are: internal — hoarseness/airway obstruction; external — a soft neck swelling that enlarges on Valsalva/blowing (reducible, resonant, may gurgle); it can become infected (laryngopyocele).
DIAGNOSIS & MANAGEMENT
Diagnosis is by CT (an air-filled sac); management is to exclude an underlying carcinoma and excise it surgically if symptomatic.
A NOTE ON EXCLUDING AN UNDERLYING CANCER
The crucial clinical caveat with a laryngocele is that it can be the outward sign of an underlying laryngeal cancer, which must always be excluded. Although many laryngoceles arise simply from chronically raised pressure in the larynx (as in wind-instrument players or glassblowers), a tumour of the laryngeal ventricle can obstruct the neck of the saccule and cause air to become trapped, producing a laryngocele. For this reason, a laryngocele is not dismissed as a benign curiosity: the larynx must be carefully examined and imaged to ensure there is no obstructing carcinoma at the ventricle before attributing it to benign causes. This principle — that an apparently innocent air-filled sac may be a signpost to a hidden malignancy — is the key teaching point, and it parallels the general ENT rule of always considering and excluding cancer behind unexplained laryngeal findings, especially in smokers.
THE BOTTOM LINE
A laryngocele is an air-filled saccular herniation that may signal an obstructing ventricular carcinoma, so an underlying cancer must be excluded before it is treated as benign.
It is also worth noting that an external laryngocele presents as a soft, reducible neck swelling that classically enlarges when the patient blows against resistance and empties again — a characteristic sign that, together with its resonance to percussion, helps distinguish it from other, solid neck lumps and points to its air-filled nature.
A useful final point is that an infected laryngocele (a laryngopyocele) can present acutely with a tender, enlarging neck swelling and features of infection, and may compromise the airway, so a previously asymptomatic laryngocele that suddenly becomes painful and swollen warrants prompt assessment.
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KEY POINTS TO REMEMBER
Laryngocele = air-filled dilatation/herniation of the laryngeal saccule, communicating with the lumen.
Internal (in the false cord/aryepiglottic fold), external (through the thyrohyoid membrane → neck swelling), or mixed.
Cause: raised intralaryngeal pressure (trumpeters/glassblowers) or a ventricular carcinoma obstructing the saccule (exclude!).
External swelling enlarges on Valsalva (reducible, resonant); Dx by CT; exclude carcinoma; excise if symptomatic.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Laryngeal tuberculosis is TB of the larynx, usually secondary to (and a marker of) active pulmonary TB (via infected sputum), rarely primary, affecting especially the posterior larynx (interarytenoid region, posterior cords).
FEATURES & DIAGNOSIS
It gives hoarseness (commonest), odynophagia (painful swallowing, which may be severe, with referred otalgia), a weak voice and cough, with laryngoscopy showing mucosal hyperaemia, oedema, ulceration and granulations in the posterior larynx ('mouse-nibbled' cords, 'turban' epiglottis).
A NOTE ON WHY IT MUST BE DISTINGUISHED FROM CANCER
The most important practical point about laryngeal tuberculosis is that it closely mimics laryngeal carcinoma and must be distinguished from it by biopsy. Both occur in similar patients, both cause persistent hoarseness, and both can produce ulcerated, granular lesions of the larynx on examination — so they cannot be told apart by appearance alone. Mistaking one for the other has serious consequences in either direction: treating a cancer as TB delays life-saving oncological treatment, while misdiagnosing TB as cancer could lead to unnecessary radical surgery and miss a highly infectious, readily treatable disease. This is why any suspicious laryngeal lesion is biopsied, with the tuberculous picture confirmed by caseating granulomas and by evidence of pulmonary TB (chest X-ray, sputum for acid-fast bacilli). The reassuring counterpoint is that, once correctly identified, laryngeal TB responds well to standard anti-tuberculous therapy — making the correct diagnosis all the more important.
THE BOTTOM LINE
Laryngeal tuberculosis, usually secondary to pulmonary TB, mimics laryngeal carcinoma and must be distinguished by biopsy, responding well to anti-tuberculous therapy once diagnosed.
It is also worth noting that laryngeal tuberculosis is important from an infection-control standpoint, since it usually accompanies open pulmonary tuberculosis and the patient is therefore highly infectious, so recognising it prompts not only anti-tuberculous treatment but also appropriate isolation and contact tracing to limit spread.
A useful final point is that the severe pain on swallowing that often accompanies laryngeal tuberculosis — sometimes out of proportion to the visible disease — is a helpful clinical clue, and that this symptom, together with a known history of pulmonary tuberculosis, should raise the suspicion and prompt the appropriate investigations.
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DANGER / REMEMBER: Importantly, it mimics carcinoma (biopsy is needed to differentiate) and is highly infectious. Diagnosis is by chest X-ray (pulmonary TB), sputum for AFB and biopsy (caseating granuloma). Management is anti-tuberculous therapy (to which it responds well), with voice rest and analgesia.
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KEY POINTS TO REMEMBER
Laryngeal TB = usually secondary to active pulmonary TB (via sputum); affects the posterior larynx (interarytenoid, posterior cords).