Larynx
A valve of cartilage and muscle at the top of the trachea: it seals the airway shut when you swallow, and vibrates to make your voice.
What it normally does
The larynx is the narrowest part of the upper airway, and in a small child it is the least forgiving. On imaging in both children and adults the glottis and immediate subglottis are the narrowest points, but the subglottis is ringed by the cricoid — the only complete ring of cartilage in the airway — so it is the narrowest part that cannot stretch. Poiseuille: for laminar flow, resistance is inversely proportional to the fourth power of the radius (halve the radius, sixteen times the resistance), and once flow turns turbulent it worsens faster still.
a millimetre of circumferential swelling an adult would barely notice halves the radius of a 4 mm infant subglottis — about a 75% loss of cross-sectional area and roughly a sixteen-fold rise in resistance — and that is stridor and visible work of breathing.
Contact with the laryngeal inlet reflexly closes the cords (the laryngeal adductor reflex, exaggerated as laryngospasm), and the reflex is blunted by sleep, sedation and anaesthesia. Sensation comes from the internal branch of the superior laryngeal nerve above the cords and from the recurrent laryngeal nerve below. A cough uses the same machinery — close the cords, build pressure, release it explosively.
lose that sensation or that closure and food and saliva go straight into the trachea, with no effective cough available to clear them.
One nerve moves almost everything. The recurrent laryngeal nerve supplies every intrinsic muscle of the larynx except cricothyroid (external branch of the superior laryngeal nerve), and only one of those muscles opens the cords — posterior cricoarytenoid.
one nerve out leaves a cord that will not move and a breathy voice, usually with an adequate airway; both nerves out leaves nothing that can abduct the cords at all.
The recurrent laryngeal nerves take a long detour before they reach the larynx — the left hooks under the arch of the aorta at the ligamentum arteriosum, the right under the right subclavian artery — and both then ascend towards the larynx in or near the tracheo-oesophageal groove, closely related to the thyroid gland and its inferior thyroid artery.
hoarseness can be the first sign of disease in the chest (the left nerve has far more thorax to be caught in), and surgery — thyroidectomy above all — is the commonest way these nerves are injured.
What goes wrong
- Croup (laryngotracheobronchitis)← from “The larynx is the narrowest part of the upper …”
Parainfluenza virus (most often type 1) inflames the lining of the larynx and trachea. The mucosa just below the cords swells, and because the cricoid is a rigid complete ring it can only swell inwards. A millimetre of oedema takes a large fraction of a toddler's subglottic radius, and since resistance is inversely proportional to the fourth power of the radius, the work of breathing rises steeply and flow through the narrowed segment turns turbulent and audible.
Subglottic oedema inside a rigid cricoid ring. Barking cough, hoarse voice, inspiratory stridor. A single dose of oral corticosteroid is recommended at all severities, including the mild child going home; nebulised adrenaline is added when there is stridor at rest. Keeping the child calm matters — distress worsens the obstruction.
You would find: A barking, seal-like cough with a hoarse voice and inspiratory stridor in a child, typically 6 months to 6 years with a peak in the second year, worse at night. Stridor only when upset is mild; stridor at rest with chest recession is not. A toxic-looking child who drools, sits forward and will not cough is a different disease — epiglottitis (now rare since Hib vaccination, though invasive Hib disease still falls disproportionately on under-vaccinated Aboriginal and Torres Strait Islander children) or bacterial tracheitis, which is not Hib-related and is not prevented by that vaccine.
- Unilateral recurrent laryngeal nerve palsy← from “The recurrent laryngeal nerves take a long det…”
The nerve is injured out along its detour, not at the larynx — caught during thyroidectomy, invaded by a left hilar or aortopulmonary-window lung tumour, or stretched by an aortic arch aneurysm. Every intrinsic muscle on that side except cricothyroid is denervated, so that cord stops moving and usually comes to rest in the paramedian position (close to, but not at, the midline; a complete vagal lesion, which also takes out cricothyroid, tends to leave it further out in the intermediate or cadaveric position). The working cord cannot quite close against it, so the glottis does not seal: air leaks during speech and pressure cannot be built for a cough.
One cord fixed in the paramedian position → breathy voice, bovine cough, aspiration risk. New persistent hoarseness means visualising the cords, and a left-sided palsy with no neck operation means looking in the chest.
You would find: A breathy, weak voice and a soft bovine cough with no explosive start, sometimes with coughing on thin fluids. Many patients compensate over weeks as the mobile cord crosses the midline, so the voice can improve without the nerve recovering. Hoarseness persisting beyond about three weeks in an adult — particularly a smoker — warrants laryngoscopy: the cause may be lung cancer pressing on the left nerve, or cancer of the larynx itself. Head and neck cancer is diagnosed later and kills more often in Aboriginal and Torres Strait Islander people, largely on the back of higher smoking rates.
- Bilateral recurrent laryngeal nerve palsy← from “One nerve moves almost everything. The recurre…”
Both recurrent nerves are out — classically after total thyroidectomy, where they run right beside the gland. Posterior cricoarytenoid, the only abductor, is denervated on both sides, so nothing is left to open the cords. Both cords sit near the midline with only a narrow chink between them, and that chink is now the entire airway.
Both posterior cricoarytenoids denervated → cords stuck near midline → stridor with a surprisingly good voice. Post-thyroidectomy stridor is bilateral palsy (or an expanding neck haematoma) until proven otherwise.
You would find: Stridor and rising work of breathing on extubation or in the hours after thyroid surgery. The trap is the voice, which can sound near normal — cords that sit together still phonate while blocking the airway. This is an airway emergency: senior airway help, reintubation, sometimes tracheostomy.
- Aspiration through an unprotected larynx← from “Contact with the laryngeal inlet reflexly clos…”
After a stroke, with a reduced conscious state, or in bulbar disease such as motor neurone disease, laryngeal sensation and the closure reflex it drives are lost. Food, fluid or saliva crosses the cords without provoking closure or a cough — silent aspiration. Aspirate most often follows gravity down the right main bronchus, which is wider, shorter and more vertical: towards the basal segments of the right lower lobe in an upright patient, and towards the posterior segment of the right upper lobe or the superior segment of the right lower lobe in someone lying flat.
No laryngeal sensation → no cough → silent aspiration → right-sided (gravity-dependent) pneumonia. Swallow screen before anything by mouth.
You would find: A wet, gurgly voice after swallowing, coughing on thin fluids, or recurrent right-sided pneumonia in someone who has had a stroke. This is why nothing goes in the mouth after a stroke — not food, not fluids, not tablets — until a validated swallow screen has been passed.
- Laryngeal oedema in anaphylaxis (and ACE inhibitor angioedema)← from “The larynx is the narrowest part of the upper …”
In anaphylaxis, mast cells and basophils degranulate and histamine and other mediators make mucosal capillaries leak. Fluid collects in the loose submucosal tissue of the larynx and pushes into the narrowest part of the airway, where there is no spare room. ACE inhibitors produce similar swelling by a different route: ACE (kininase II) normally degrades bradykinin, so blocking it lets bradykinin accumulate and make the same mucosa leak — this is not an IgE- or mast-cell-driven allergic reaction. That difference matters, because the two do not respond to the same drugs.
Swelling at the narrowest point of the airway. Voice change plus stridor means the airway, not the skin. In anaphylaxis, intramuscular adrenaline is the immediate treatment. In ACE inhibitor angioedema the swelling is bradykinin-mediated, so adrenaline, antihistamines and steroids should not be relied on: the priorities are airway assessment and protection and permanently stopping the ACE inhibitor.
You would find: A change in the voice, a tight throat, swelling of lips or tongue, and stridor — with urticaria, wheeze and hypotension if it is anaphylaxis. ACE inhibitor angioedema looks similar but typically has no rash, no itch and no hypotension, often favours lips, tongue and floor of mouth, and can start months or years after the drug was begun; it is more common in people of African ancestry.
What we give, and how it works
Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.
- Binds
- The cytoplasmic glucocorticoid receptor in mucosal, endothelial and inflammatory cells
- Which does
- The drug–receptor complex moves into the nucleus, represses transcription of inflammatory genes (largely NF-kB driven cytokines) and induces anti-inflammatory ones. Capillary leak and inflammatory cell recruitment fall, and the subglottic oedema resolves.
- So you see
- Croup scores improve measurably by about one to two hours and keep improving over the following several hours as swelling inside the rigid cricoid ring subsides, the radius recovers and stridor and recession settle. A single oral dose of dexamethasone acts for well over a day (biological half-life roughly 36–54 hours, far longer than its plasma half-life of a few hours), and trials show fewer return visits, fewer admissions and shorter stays.
- And the same mechanism causes
- The same receptor sits in liver, muscle, bone, immune cells and the hypothalamic–pituitary axis, so the same signal that quietens inflammation also raises blood glucose, and with repeated or prolonged courses suppresses the child's own cortisol production and slows growth. A single dose does not do that; transient behavioural change or a rise in glucose is the most a one-off dose produces.
- Handling
- Oral dexamethasone is well absorbed and long-acting, so a single dose covers the illness; oral prednisolone is an accepted alternative in Australia. Doses are in the local paediatric guideline — do not prescribe from a revision page.
Catches people out: It is not fast enough to be the only treatment in a child obstructing now. In practice the steroid is given early in every child, with nebulised adrenaline alongside it when there is stridor at rest, to hold the airway open until the steroid takes effect.
- Binds
- Alpha-1 adrenoceptors on the arterioles of the subglottic mucosa (beta-2 receptors on airway smooth muscle are also stimulated, but the useful action here is vascular, not bronchodilator)
- Which does
- Alpha-1 is a Gq-coupled receptor: stimulation raises intracellular calcium in vascular smooth muscle and the arterioles constrict. Mucosal blood volume and capillary hydrostatic pressure fall, so less fluid is filtered into the swollen tissue and the oedema already present is reabsorbed.
- So you see
- The mucosa shrinks back off the airway wall within about 10 to 30 minutes. Because resistance is inversely proportional to the fourth power of the radius, a small gain in radius makes a large difference — stridor and recession visibly improve.
- And the same mechanism causes
- The vasoconstriction lasts only as long as drug is at the receptor, so as it wears off over roughly two hours the mucosa refills and the stridor can return to where it started. That is the drug wearing off, not a paradoxical worsening — but it is why the child is observed for several hours rather than discharged on the improvement. Enough is absorbed systemically to cause tachycardia, tremor and pallor from the same alpha and beta actions.
Catches people out: It shrinks swelling; it does not treat the infection or shorten the illness. It is used alongside a corticosteroid rather than instead of one, and the child is observed until the adrenaline has worn off and they remain stable.
- Binds
- Alpha-1, beta-1 and beta-2 adrenoceptors
- Which does
- Alpha-1 constricts arterioles, including in the laryngeal mucosa, reducing the leak and the swelling and restoring blood pressure. Beta-1 raises heart rate and contractility. Beta-2 relaxes bronchial smooth muscle and, by raising cAMP in mast cells, damps further mediator release.
- So you see
- The airway swelling settles, wheeze eases and blood pressure comes back up, usually within minutes. Thigh muscle is well perfused, so absorption from the anterolateral thigh is faster and more reliable than from the deltoid or from subcutaneous tissue. Doses are repeated at intervals if there is no response — follow the ASCIA action plan, not a revision page.
- And the same mechanism causes
- The receptors are not confined to the airway: beta-1 stimulation gives palpitations and a pounding chest, beta-2 stimulation of skeletal muscle gives tremor, central and systemic sympathetic effects give anxiety and a sense of dread, and alpha-1 vasoconstriction gives pallor and a rise in blood pressure. Given intravenously by mistake, or as an undiluted bolus, the same actions become arrhythmia, myocardial ischaemia or hypertensive crisis — which is exactly why intramuscular is the standard route and IV adrenaline is reserved for infusion by experienced clinicians.
Catches people out: Antihistamines and steroids do not open a swollen larynx: antihistamines block H1 receptors and do nothing about mediators already acting or about the airway, and steroids take hours and have not been shown to prevent biphasic reactions. Adrenaline is the drug that reverses the obstruction, and delay is what kills. Note that this reasoning applies to mast-cell anaphylaxis — ACE inhibitor angioedema is bradykinin-mediated and typically does not respond to adrenaline, so there the priority is airway assessment and protection and stopping the drug.
- Binds
- Penicillin-binding proteins, the bacterial transpeptidases that cross-link peptidoglycan; clavulanate binds and inactivates many bacterial beta-lactamases
- Which does
- Cross-linking of the cell wall stops, so the wall fails under the organism's own osmotic pressure and dividing bacteria lyse. Clavulanate has negligible antibacterial activity of its own — it protects amoxicillin from beta-lactamases produced by many oral and gut organisms.
- So you see
- The pneumonia clears: fever settles, oxygen requirement falls, and the consolidation resolves on imaging over subsequent weeks.
- And the same mechanism causes
- The drug cannot tell inhaled mouth bacteria from the ones living in the colon. The same wall-directed killing strips out gut commensals, which is why diarrhoea is common and why Clostridioides difficile can take over the space that is left. (Clavulanate also carries a distinctive risk of cholestatic hepatitis, which is idiosyncratic rather than a consequence of the wall-killing mechanism.)
- Handling
- Choice and duration follow the current Therapeutic Guidelines and local antimicrobial stewardship advice, which vary with severity and setting.
Catches people out: Two traps. First, many aspiration events cause a chemical pneumonitis, which produces fever and an infiltrate within hours and often settles without antibiotics — antibiotics are for aspiration that goes on to bacterial pneumonia, not for every witnessed aspiration. Second, this treats the consequence, not the cause: the larynx is still unprotected. What changes the outcome is a speech pathology swallow assessment, texture-modified diet and fluids, upright positioning and mouth care — not another course of antibiotics.
Hoarseness and stridor both come from the larynx but they mean different things. Hoarseness means the cords cannot vibrate or meet properly — a nerve, or a lesion on the cord. Stridor means the airway is critically narrowed, and the phase of the noise localises it: supraglottic and glottic narrowing gives inspiratory stridor; subglottic and extrathoracic tracheal narrowing (croup) also starts as inspiratory stridor and becomes biphasic as it tightens; narrowing inside the thorax gives expiratory noise. Trace each one back: hoarse and breathy after a thyroidectomy is one recurrent laryngeal nerve; stridor with a surprisingly good voice after the same operation is both. And notice that no drug on this page fixes a nerve — steroids and adrenaline shrink swelling; a paralysed cord needs laryngoscopy, a search for the cause along the nerve's course, and often speech pathology or surgery.
Now test whether it stuck
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