NICE NG12 mandates 2WW head and neck referral for unexplained hoarseness lasting more than 3 weeks in any adult — the PPV for laryngeal pathology (including cancer) is sufficient to justify urgent investigation. Laryngeal cancer detected at stage I has a 90% 5-year survival; stage IV drops to 30%. Recurrent laryngeal nerve palsy from a mediastinal mass is a critical presentation — a CXR showing an apical lung mass (Pancoast tumour) in a hoarse smoker is a cancer emergency. Epiglottitis in children (H. influenzae type b — now rare due to Hib vaccine) and adults (Streptococcus, Staph) can progress to complete airway obstruction within minutes — do NOT examine the oropharynx, keep patient calm, and call 999.

Laryngopharyngeal reflux (LPR) is the most common benign cause of chronic hoarseness in non-smokers — it differs from classic GORD in that patients often have minimal heartburn but have throat clearing, morning hoarseness, globus, and chronic cough. LPR is caused by microaspiration of gastric acid onto the laryngeal mucosa, causing posterior commissure inflammation. Hypophonia (abnormally quiet, monotone voice) is a specific feature of Parkinson's disease — it results from reduced respiratory drive and vocal fold hypomobility. Lee Silverman Voice Treatment (LSVT LOUD) is a specific speech therapy programme with good evidence for Parkinson's-related dysphonia.

Vocal cord palsy from a mediastinal mass (particularly left-sided, as the left recurrent laryngeal nerve loops under the aortic arch) is a critical diagnosis — causes include lung cancer, lymphoma, aortic aneurysm, and mediastinal fibrosis. A CXR is mandatory in all unilateral vocal cord palsy of unclear cause. Hypothyroidism-related voice change (due to myxoedematous infiltration of the laryngeal mucosa and TA muscle weakness) is completely reversible with levothyroxine replacement — TFTs are a cheap and simple investigation that should not be missed. Functional dysphonia (muscle tension dysphonia) is frequently over-referred to ENT — it responds excellently to voice therapy with a speech and language therapist and rarely requires laryngoscopy if the clinical picture is clear.

Thyroid cancer presenting as hoarseness (RLN invasion) is one of the most important diagnoses not to miss — it indicates a locally advanced tumour. Thyroid gland examination (palpation) is mandatory in all hoarseness presentations. A hard, irregular, non-tender thyroid mass in a hoarse patient is a 2WW thyroid cancer referral. Inspection of the posterior pharyngeal wall and post-cricoid region through a tongue depressor + torch examination, while limited in primary care, can sometimes identify significant pathology — pooling of saliva in the piriform fossa (pyriform fossa sign) suggests a hypopharyngeal tumour with obstruction at that level.

The NICE 2WW threshold for hoarseness (≥3 weeks) should be applied strictly — there is no evidence that treating empirically (with PPIs, antibiotics, or voice rest) and reviewing is safer than immediate referral. The risk of delayed laryngeal cancer diagnosis far outweighs the risk of "unnecessary" endoscopy. Professional voice users (singers, actors, teachers) should have a lower threshold for ENT referral — even 2 weeks of hoarseness may warrant referral because vocal cord nodules are career-threatening conditions for voice professionals that require early specialist management.

CXR has high yield in unexplained hoarseness — it identifies lung cancer (including Pancoast), mediastinal lymphadenopathy (lymphoma), and aortic aneurysm (RLN stretch). A normal CXR does not exclude these conditions — CT chest is required if clinical suspicion remains high. TFTs are inexpensive and frequently diagnostic for a completely reversible cause of hoarseness (hypothyroidism) — they should be checked at every hoarseness presentation. Calcium abnormalities cause laryngospasm (hypocalcaemia) and rarely vocal cord oedema in hypercalcaemia — an unusual but important association in sarcoidosis and hyperparathyroidism.

LPR requires twice-daily PPI dosing for adequate acid suppression — once-daily dosing controls GORD (single acid peak) but not LPR, which requires suppression of both the morning and evening acid production peaks. The minimum treatment trial is 8–12 weeks (longer than for GORD) as laryngeal mucosal healing is slower. Whispering during acute laryngitis is counterintuitive but harmful — it places more tension on the vocal folds than relaxed quiet speaking and should be specifically advised against. Steroid inhaler dysphonia affects 30–50% of patients using MDI beclometasone — switching to a spacer device reduces oropharyngeal deposition by 80% and largely resolves the dysphonia without compromising asthma control.

Vocal hygiene measures have strong evidence for preventing and treating benign voice disorders — they are the cornerstone of voice therapy programmes. Throat clearing causes direct vocal fold trauma with each event (the cords adduct forcefully) — it is a maintaining factor in LPR and functional dysphonia. Training patients to substitute a hard swallow (which clears the throat without direct cord contact) can dramatically reduce symptoms. Studies show that each 10% reduction in cigarette consumption reduces laryngeal cancer risk proportionally — smoking cessation at any stage reduces risk, although it never fully returns to non-smoker levels.

The absolute rule in persistent hoarseness is: no more empirical treatment after 3 weeks without ENT assessment. Studies of delayed laryngeal cancer diagnosis consistently identify repeated GP prescribing of antibiotics, PPIs, or voice rest as the primary cause of delay — patients present at a later stage with worse outcomes. Vocal cord medialization for permanent unilateral palsy not only improves voice quality but also prevents aspiration — the paralysed cord sits in an abducted position and cannot protect the airway during swallowing. Injection augmentation (Restylane, fat, hydroxyapatite) produces immediate improvement and is an important quality-of-life intervention.