Laryngeal cancer and airway compromise

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Most laryngeal cancers are squamous carcinomas related to tobacco, with alcohol contributing. Anatomy predicts presentation: even a small true-vocal-cord lesion alters vibration and produces hoarseness, whereas the more capacious supraglottis permits silent growth until pain, aspiration or nodal disease appears. Subglottic cancer is uncommon and may present late with stridor. A normal chest radiograph or temporary response to reflux treatment does not exclude a visible laryngeal lesion.

Airway severity is a clinical diagnosis. Stridor marks substantial narrowing, and decreasing noise may mean exhaustion rather than improvement. Keep the patient upright, preserve spontaneous breathing and summon senior ENT and anaesthetic expertise. Flexible nasendoscopy can define the level if performed calmly by someone able to act on the result, but repeated scopes, CT transfer or sedating medication can precipitate obstruction. A deliberately secured airway in theatre is safer than a crash front-of-neck procedure after complete closure.

After the airway is stable, endoscopic biopsy provides histology and CT or MRI defines local and nodal extent. Treatment depends on subsite, T and N stage, cartilage or extralaryngeal invasion, pulmonary reserve, aspiration, baseline voice and swallow, comorbidity and preference. Early tumours usually receive transoral surgery or radiotherapy. For selected advanced tumours, chemoradiotherapy may preserve the anatomical larynx; extensive cartilage destruction, poor baseline function or aspiration may make total laryngectomy more reliable.

Recovery requires functional expertise. A total laryngectomy creates a permanent end stoma: inhaled oxygen, suction, humidification and emergency ventilation must be delivered at the neck, while speech may use a tracheoesophageal prosthesis, electrolarynx or oesophageal voice. Non-laryngectomy chemoradiotherapy can still cause chronic oedema, stenosis and aspiration, so swallowing, nutrition, thyroid, dental, pulmonary and voice surveillance remains important regardless of the chosen modality.

Key points

Glottic cancer classically causes persistent progressive hoarseness early; supraglottic cancer more often causes sore throat, dysphagia, odynophagia, referred otalgia, aspiration or a neck node.
First-line diagnostic assessment is flexible nasendoscopy by a trained clinician, but a severely compromised patient needs a controlled airway plan before repeated examination or transfer.
The diagnostic reference standard is direct laryngoscopy with biopsy and histology once the airway is secure; do not biopsy a precarious obstructing lesion in an uncontrolled setting.
Contrast CT neck and chest stages cartilage, spaces, nodes, airway and thoracic disease; MRI adds selected cartilage, soft-tissue, tongue-base or prevertebral detail.
Early glottic disease is commonly treated with one modality, such as transoral laser microsurgery or radiotherapy, with broadly high local control and different voice trade-offs.
Locally advanced disease may need total laryngectomy with neck and risk-adapted adjuvant therapy or organ-preserving chemoradiotherapy after realistic functional assessment.
Dexamethasone and nebulised adrenaline may temporarily reduce oedema in selected acute cases, but neither removes tumour and neither should delay definitive airway control.
Avoid sedatives, opioids and neuromuscular blockade before a shared difficult-airway plan when spontaneous ventilation is maintaining a critically narrow airway.
A tracheostomy may retain an upper-airway connection; a total-laryngectomy stoma does not. In laryngectomy, apply oxygen and ventilate through the stoma only.
Smoking cessation, nutrition, dental preparation, swallowing therapy, voice rehabilitation and emergency stoma education are integral to treatment.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Tobacco exposure

Cigarette and other inhaled tobacco causes cumulative carcinogen injury and is the dominant risk factor for laryngeal squamous cell carcinoma and synchronous aerodigestive cancer.

Alcohol and combined exposure

Heavy alcohol use independently increases risk and acts synergistically with tobacco, particularly for supraglottic and adjacent hypopharyngeal mucosa.

Prior mucosal injury and cancer

Previous head-and-neck cancer, radiotherapy and continued field exposure raise recurrence and second-primary risk; occupational agents contribute less commonly.

Papillomavirus context

High-risk HPV has a clear causal role in oropharyngeal cancer but a less consistent role in laryngeal SCC, so p16 is not used as an automatic laryngeal surrogate.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Mucosal dysplasia becomes invasive
Repeated carcinogen damage produces epithelial dysplasia and carcinoma that breaches the basement membrane and invades intrinsic laryngeal muscles, cartilage and adjacent spaces.
2
Subsite determines early symptom
Small glottic lesions disturb vocal-cord vibration and cause early hoarseness; supraglottic lesions may remain hidden until swallowing pain, nodal spread or airway narrowing.
3
Airway resistance rises steeply
Tumour, oedema, secretions and impaired cord movement reduce laryngeal radius, causing disproportionate turbulent-flow resistance and rapid decompensation after small additional narrowing.
4
Lymphatic behaviour differs
True vocal cords have sparse lymphatics, whereas supraglottic structures drain richly to bilateral cervical nodes; nodal risk therefore varies by subsite and extent.
5
Treatment changes airway separation
Total laryngectomy permanently separates pharynx from trachea, creating an end stoma and eliminating aspiration but requiring lifelong neck breathing and alternative speech rehabilitation.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Glottic cancer

Persistent progressive dysphonia, reduced cord movement, a focal irregular vocal-fold lesion or haemoptysis suggests a glottic primary.

Supraglottic cancer

Throat pain, dysphagia, aspiration, referred ear pain, muffled voice and early upper-neck nodes can occur before obvious hoarseness.

Subglottic or transglottic disease

Progressive breathlessness, biphasic stridor, fixed cord or circumferential narrowing may reflect tumour extending below or across the glottis.

Threatened airwayRed flag

Stridor at rest, inability to speak normally, secretion intolerance, recession, orthopnoea, cyanosis or exhaustion requires immediate airway action.

Laryngectomy anatomyRed flag

A mature end stoma without upper-airway airflow, loss of normal voice and a neck-breather alert identifies total laryngectomy rather than simple tracheostomy.

Advanced local invasion

Neck mass, cartilage tenderness, skin involvement, vocal-cord fixation, severe pain or aspiration indicates more extensive disease and affects preservation options.

Red flags requiring action

Stridor at rest, drooling, severe recession, silent airflow, fatigue, cyanosis or reduced consciousness requires an immediate controlled airway response.
Progressive or persistent unexplained hoarseness, especially with tobacco exposure, warrants urgent laryngeal visualisation rather than repeated reflux treatment.
Odynophagia, dysphagia, referred otalgia, haemoptysis, weight loss, neck mass or aspiration suggests invasive or supraglottic disease.
A patient after total laryngectomy breathes only through the neck stoma; oral or nasal oxygen and intubation cannot ventilate the lungs.
Fresh tracheostomy or stoma bleeding, especially a pulsatile sentinel bleed, can precede major vessel haemorrhage and needs immediate surgical and major-haemorrhage support.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line flexible nasendoscopyFirst stepFirst line
Why
Visualise supraglottis, glottis, subglottic inlet, pooling, tumour and vocal-cord movement and assess airway calibre.
Interpretation and limitations
Record site, surface, mobility and obstruction; in critical stridor perform only within a resourced airway strategy and do not mistake a limited view for a reassuring examination.
02
Reference-standard direct laryngoscopy and biopsy
Why
Map the lesion under controlled conditions and obtain adequate tissue for invasive histology.
Interpretation and limitations
Plan airway and biopsy together when obstruction is significant; avoid debulking that obscures margins unless it is a deliberate therapeutic airway procedure.
03
First-line contrast CT neck and chest for stagingFirst line
Why
Assess laryngeal spaces, cartilage, extralaryngeal spread, cervical nodes, airway, lung metastasis and synchronous lung cancer.
Interpretation and limitations
Correlate radiology with endoscopy because inflammation can mimic cartilage invasion and superficial mucosal extent may be underestimated.
04
MRI for selected local staging
Why
Clarify equivocal cartilage, pre-epiglottic, paraglottic, tongue-base, prevertebral and perineural involvement.
Interpretation and limitations
Use when the answer could change resection or radiotherapy; motion and post-biopsy inflammation can reduce specificity.
05
Ultrasound-guided node FNA or core
Why
Confirm nodal metastasis and obtain additional tissue without open-neck disruption.
Interpretation and limitations
Sample a radiologically suspicious node even when the laryngeal primary is small because nodal stage changes treatment fields and prognosis.
06
Functional and treatment-fitness assessment
Why
Quantify voice, swallowing, aspiration, pulmonary reserve, nutrition and suitability for surgery or cisplatin-based radiotherapy.
Interpretation and limitations
Include speech and language therapy, dietetics, dental review, renal function, magnesium, audiometry and performance; an anatomically preservable larynx may be functionally unsafe.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Benign vocal-fold disease

Nodules, polyps, cysts and haemorrhage cause dysphonia, often with voice overuse, but persistent or atypical lesions still require endoscopic assessment.

Inflammatory or neurological dysfunction

Laryngitis, reflux-associated irritation and unilateral recurrent-laryngeal palsy cause hoarseness; palsy itself may result from neck, thyroid, mediastinal or lung cancer.

Infective supraglottitis or abscess

Rapid fever, severe odynophagia, drooling and toxic appearance suggests infection, but airway precautions are the same and tumour can coexist or obstruct drainage.

Non-laryngeal obstruction

Thyroid mass, tracheal tumour, bilateral vocal-cord paralysis, angioedema and foreign body can produce stridor and require anatomy-specific airway treatment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Critical airwaySecure oxygenation without losing spontaneous ventilationFirst stepThe patient has rest stridor, severe work of breathing, secretion intolerance, hypoxaemia or exhaustion.

1Call senior ENT, anaesthesia and critical care, keep upright and calm, give oxygen, attach monitoring and prepare suction and difficult-airway equipment while identifying prior tracheostomy or laryngectomy anatomy.
2Agree the planned and rescue airway before drugs or transfer; a controlled awake approach, rigid endoscopic debulking, tracheostomy or front-of-neck access may be selected according to level and anatomy.
3DefinitiveTreat oedema or infection concurrently when suspected, but regard steroid, adrenaline or antibiotics as bridges and proceed to definitive airway control if clinical obstruction persists or progresses.

02Stable suspected cancerVisualise, image and biopsyPersistent hoarseness or another suspicious laryngeal symptom is present without immediate compromise.

1Arrange urgent specialist head-and-neck examination and flexible nasendoscopy, documenting cord mobility, neck nodes, swallowing and airway symptoms.
2Obtain contrast CT neck and chest and selected MRI, then perform direct laryngoscopy and biopsy in a setting matched to anticipated airway difficulty.
3Complete pathological and nodal stage and baseline dental, nutritional, voice, swallow, pulmonary, renal and hearing assessment before the MDT treatment decision.

03Curative treatmentBalance tumour control with usable functionHistology and staging show potentially curable laryngeal squamous cancer.

1For suitable early disease, compare transoral laser surgery and radiotherapy, explaining local control, voice, logistics, salvage and patient preference.
2For advanced disease, compare total laryngectomy-based treatment with organ-preserving chemoradiotherapy using cartilage invasion, aspiration, cord fixation, comorbidity and likelihood of a functional larynx.
3Deliver speech, swallowing, nutrition, dental, smoking and alcohol support from before treatment through rehabilitation, and monitor actively for recurrence, stenosis and aspiration.

04Neck-breather emergencyTreat the stoma as the airwayA patient with a tracheostomy or total laryngectomy has respiratory distress or cannot be ventilated normally.

1Call for airway help, expose the neck, remove stoma covers or speaking attachments, apply high-flow oxygen to the stoma and use suction if a catheter passes safely.
2Establish whether this is a tracheostomy with possible upper-airway continuity or a total laryngectomy with none; remove a blocked inner tube or displaced tracheostomy component according to the emergency algorithm.
3EscalationFor total laryngectomy, ventilate and if required intubate through the stoma with a cuffed tube; do not persist with oral intubation, and escalate bleeding or obstruction to ENT urgently.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reduces inflammatory oedema around a tumour or recent treatment but does not remove fixed malignant narrowing.

Dexamethasone as an airway bridge

For significant tumour-associated upper-airway oedema, a specialist may give dexamethasone 8 mg intravenously initially and continue 4 to 8 mg every 6 to 12 hours for the shortest effective period while definitive airway treatment proceeds; follow the local airway protocol.

Do not delay airway control for response. Monitor glucose, delirium, infection and gastrointestinal risk, document duration and taper after more prolonged use; infection or haemorrhage may need different concurrent treatment.

Produces short-lived mucosal vasoconstriction where oedema contributes to obstruction while personnel and definitive airway control are prepared.

Nebulised adrenaline as a temporary bridge

In a monitored resuscitation area, use the locally approved nebulised adrenaline regimen for acute upper-airway oedema only after senior airway review; repeat dosing and concentration must follow that protocol.

Effect may wear off and tumour bulk remains. Monitor heart rate, rhythm and blood pressure and never send the patient away or to unmonitored imaging because stridor briefly improves.

Radiosensitises appropriately selected locally advanced laryngeal squamous cancers in an organ-preservation strategy.

Cisplatin with definitive radiotherapy

A common specialist schedule gives cisplatin 100 mg/m² intravenously every 3 weeks during radiotherapy, while some protocols use 40 mg/m² weekly; the MDT must prescribe the exact regimen and hydration.

Assess renal function, magnesium, hearing, neuropathy, marrow and performance before and during treatment; severe baseline aspiration or a non-functional larynx is a treatment-selection problem not corrected by changing dose.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute airway obstruction

Progressive tumour, treatment oedema, bleeding, secretions or bilateral cord immobility can convert a marginal airway into complete obstruction with little warning.

Aspiration and pneumonia

Impaired sensation and closure, tumour-related fistula or post-treatment dysfunction allows saliva and food into the airway, causing recurrent infection and malnutrition.

Voice and swallowing loss

Tumour and treatment can cause aphonia, dysphagia, stenosis and feeding dependence, requiring speech-and-language rehabilitation and sometimes surgical voice restoration.

Stomal and post-laryngectomy emergencies

Mucus plugging, crusting, displaced voice prosthesis, stenosis or bleeding can threaten a neck breather and must be managed through the stoma.

Recurrence and late effects

Local or nodal relapse, hypothyroidism, chondronecrosis, fibrosis, lymphoedema and second primary lung or oesophageal cancer require prolonged surveillance.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

In any marginal airway, trend stridor at rest, voice, secretion handling, respiratory rate, work, oxygenation, carbon dioxide, fatigue and ability to lie flat; do not rely on oxygen saturation alone.
During radiotherapy or chemoradiotherapy, review airway oedema, aspiration, intake, weight, mucositis, skin, pain, hydration, kidney function, magnesium, hearing and infection at least weekly.
After endoscopic surgery, examine healing, anterior commissure or subglottic stenosis, voice and swallow and investigate recurrent hoarseness rather than attributing it to scar automatically.
After total laryngectomy, review stoma calibre and crusting, humidification, pulmonary rehabilitation, voice prosthesis, swallowing, fistula, shoulder and psychosocial needs.
After neck irradiation, monitor thyroid function, carotid and vascular risk, lymphoedema, dental disease, fibrosis, chondronecrosis and aspiration over years.
Provide a written emergency plan identifying tracheostomy versus laryngectomy anatomy and ensure the patient and carers know where oxygen and ventilation must be applied.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Quiet stridor can be worse

Falling stridor volume with increasing fatigue may reflect critically low airflow, so judge work, consciousness and gas exchange rather than sound alone.

Hoarseness localises early

Millimetres of glottic mucosal change can disrupt vibration, which is why glottic cancer often presents earlier than a similarly sized supraglottic lesion.

Do not anaesthetise away the airway

Sedation or paralysis can remove muscle tone and spontaneous ventilation, converting a partially patent malignant airway into an impossible ventilation and intubation scenario.

An intact larynx may not function

Severe pretreatment aspiration, fixation and pulmonary frailty can make anatomical organ preservation less safe than laryngectomy followed by rehabilitation.

Laryngectomy means no oral route

After total laryngectomy the mouth and nose end in the pharynx, not the lungs; oxygenation, capnography, ventilation and intubation belong at the stoma.

Steroids buy time, not space

Dexamethasone may reduce oedema around cancer but cannot widen a lumen occupied by fixed tumour, and apparent improvement can be transient.

11Common pitfallsFrequent interpretation and management errors.

01
Treating progressive hoarseness repeatedly as reflux or infection without visualising the larynx.
02
Sending a stridulous patient to CT before senior airway assessment and a rescue plan.
03
Giving sedative premedication to a patient whose spontaneous effort is maintaining a narrow airway.
04
Allowing transient improvement after dexamethasone or nebulised adrenaline to cancel definitive airway control.
05
Biopsying an obstructing lesion in a setting that cannot rescue bleeding or complete obstruction.
06
Choosing organ preservation based on anatomy while ignoring baseline aspiration and expected functional outcome.
07
Attempting prolonged oral intubation or applying oxygen only to the face of a total-laryngectomy patient.
08
Failing to give the patient and ward a clear neck-breather emergency plan.