Anatomy Of The Larynx

Foundations and mechanisms

Structural organisation and clinically relevant dimensions

The larynx is a specialised sphincteric airway organ extending approximately from C3 to C6 in the adult, suspended from the hyoid and continuous inferiorly with the trachea at the lower border of the cricoid cartilage. In neonates and infants it lies higher, typically around C2–C3, with a relatively large tongue, omega-shaped epiglottis and more cephalad/anterior glottis; these features materially alter laryngoscopy, mask ventilation and supraglottic airway behaviour. The adult male vocal fold is approximately 17–23 mm long and the female 12–17 mm; the posterior cartilaginous glottis is proportionally important during quiet respiration, whereas the membranous anterior glottis dominates phonation.

The classical anaesthetic teaching that the infant airway is “funnel-shaped” with the cricoid as the narrowest point is an oversimplification: imaging and endoscopic studies show the paediatric larynx is more cylindrical/elliptical, and the narrowest functional point may be the glottis or subglottis depending on age, tone and instrumentation. Clinically, however, the cricoid remains the only complete cartilaginous ring and a critical site for fixed circumferential obstruction. A term neonate has a subglottic diameter of roughly 4.0–5.0 mm; 1 mm circumferential oedema may reduce cross-sectional area by more than 50%, with resistance increasing disproportionately according to Poiseuille principles.

Component	Key anatomy	Exam-relevant mechanism
Supraglottis	Epiglottis, aryepiglottic folds, false cords, vestibule	Protective closure; sensory afferents via internal laryngeal nerve; common site of oedema and obstruction
Glottis	True vocal folds and rima glottidis	Primary variable resistor; phonation; laryngospasm occurs by reflex adduction
Subglottis	Inferior to vocal folds to lower cricoid border	Fixed ring at cricoid; stenosis graded by percentage luminal obstruction

Cartilages, joints and intrinsic muscle mechanisms

The laryngeal framework comprises three unpaired cartilages—thyroid, cricoid and epiglottic—and three paired cartilages—arytenoid, corniculate and cuneiform. The cricoid forms a complete ring with a broad posterior lamina and narrow anterior arch; this explains why posteriorly directed pressure may compress the oesophagus variably but also distort laryngeal geometry. Cricoarytenoid joints permit rotation, sliding and rocking of the arytenoids, enabling abduction, adduction and tensioning of the vocal folds. Cricoarytenoid arthritis, fixation or posterior glottic scarring can mimic recurrent laryngeal nerve palsy.

Function	Main muscle	Action	Nerve
Abduction	Posterior cricoarytenoid	Only abductor of vocal folds	Recurrent laryngeal nerve
Adduction	Lateral cricoarytenoid, transverse/oblique arytenoids	Closes membranous and cartilaginous glottis	Recurrent laryngeal nerve
Tension	Cricothyroid	Tilts thyroid cartilage forwards; lengthens vocal folds	External laryngeal nerve
Relaxation/fine control	Thyroarytenoid and vocalis	Shortens and adjusts vocal fold stiffness	Recurrent laryngeal nerve

All intrinsic muscles are supplied by the recurrent laryngeal nerve except the cricothyroid, supplied by the external branch of the superior laryngeal nerve. This single exception is a high-yield Primary FRCA fact because cricothyroid integrity preserves pitch modulation despite recurrent laryngeal palsy. Bilateral recurrent laryngeal nerve palsy classically leaves cords near the paramedian position, causing inspiratory stridor with relatively preserved voice; bilateral external laryngeal nerve injury causes weak, monotonous voice with impaired high pitch and ineffective cough.

Neurophysiology, reflexes and airway obstruction

Sensation above the vocal cords is via the internal laryngeal nerve, a branch of the superior laryngeal nerve piercing the thyrohyoid membrane with the superior laryngeal vessels. Sensation below the cords is via the recurrent laryngeal nerve. The laryngeal adductor reflex is a vagally mediated protective reflex: supraglottic stimulation triggers glottic closure, apnoea, bradycardia and cough. During light anaesthesia, airway secretions, blood, volatile irritants, supraglottic airway malposition or extubation stimulation may produce laryngospasm, sustained predominantly by thyroarytenoid, lateral cricoarytenoid and interarytenoid contraction.

From a mechanics perspective, the glottis behaves as a dynamic Starling resistor. Negative inspiratory pressure increases transmural collapse in the presence of supraglottic obstruction, explaining paradoxical worsening when an inadequately anaesthetised patient inspires forcefully against a closed glottis. Management relies on removing the stimulus, jaw thrust/continuous positive airway pressure, deepening anaesthesia, and when necessary neuromuscular blockade; commonly cited emergency dosing is suxamethonium 0.1–0.5 mg kg^-1 IV for partial laryngospasm or 1 mg kg^-1 IV for complete obstruction, with atropine considered in children with severe bradycardia.

Classifications relevant to anaesthesia

Direct laryngoscopic view is commonly described using the Cormack–Lehane system, modified to subdivide grade 2. Although it is not a pure anatomical classification, it links laryngeal anatomy to intubation difficulty and is therefore central to airway examination.

Grade	View	Implication
1	Full glottic aperture visible	Usually straightforward intubation
2a	Partial glottis visible	Often intubatable with optimisation
2b	Only arytenoids/posterior cords visible	Increased need for bougie or videolaryngoscopy
3	Epiglottis only	Difficult direct intubation
4	No glottic structure visible	High-risk failed intubation scenario

Subglottic stenosis is often described by the Myer–Cotton grading system: grade I 0–50%, grade II 51–70%, grade III 71–99%, and grade IV no detectable lumen. For airway instrumentation, tracheal tube cuff pressure should generally be maintained at 20–30 cmH₂O; pressures above capillary perfusion pressure, often approximated at 30–35 cmH₂O, increase risk of mucosal ischaemia, ulceration, posterior glottic injury and subsequent stenosis.

Clinical assessment and investigations

Clinical presentation and bedside interpretation

Assessment of the larynx is primarily an assessment of airway patency, glottic competence and recurrent/superior laryngeal nerve function. Symptoms localise anatomically: supraglottic disease commonly produces muffled voice, dysphagia, odynophagia and drooling; glottic disease causes early dysphonia; subglottic disease produces exertional dyspnoea and biphasic stridor. Hoarseness persisting beyond 3–4 weeks, especially in smokers, mandates laryngeal visualisation; NICE recommends urgent suspected cancer referral for adults aged ≥45 years with persistent unexplained hoarseness or an unexplained neck lump.

Stridor is a late sign. Because resistance varies inversely with radius to the fourth power, small reductions in glottic or subglottic radius produce large increases in work of breathing. Inspiratory stridor suggests extrathoracic variable obstruction, expiratory wheeze intrathoracic obstruction, and biphasic stridor fixed obstruction at or just below the glottis. In adults, exertional dyspnoea may occur when the tracheal/subglottic lumen is <8 mm; rest stridor is typical at <5 mm. Do not repeatedly examine an agitated patient with suspected epiglottitis or laryngeal trauma: deterioration may be abrupt.

Clinical feature	Likely anatomical level	Important differential diagnoses
Hoarseness, weak cough, aspiration	Glottis/recurrent laryngeal nerve	Vocal cord palsy, malignancy, post-intubation injury, thyroid/mediastinal disease, brainstem lesion
Muffled “hot potato” voice, drooling, odynophagia	Supraglottis	Epiglottitis, supraglottitis, deep neck space infection, angio-oedema
Biphasic stridor, previous intubation/tracheostomy	Subglottis/proximal trachea	Post-intubation stenosis, cricoarytenoid fixation, granuloma, tumour
Acute pain, surgical emphysema, haemoptysis	Laryngeal framework	Blunt/penetrating laryngeal trauma, thyroid cartilage fracture, cricotracheal separation
Intermittent inspiratory obstruction, normal oxygenation	Functional glottic closure	Paradoxical vocal fold motion, inducible laryngeal obstruction, anxiety, reflux-associated laryngospasm

Airway examination relevant to anaesthesia

General airway assessment must be integrated with laryngeal pathology rather than replacing it. Mallampati class, mouth opening, mandibular protrusion, thyromental distance and neck movement predict difficulty with direct laryngoscopy, but not necessarily difficulty with mask ventilation or front-of-neck access. Red flags for loss of airway after induction include orthopnoea, stridor at rest, inability to lie flat, rapidly progressive swelling, previous radiotherapy, distorted neck anatomy and a lesion seen to obstruct the glottic inlet. In such cases, awake intubation, awake tracheostomy or inhalational maintenance of spontaneous ventilation may be safer than intravenous induction and neuromuscular blockade.

Laryngoscopic view is commonly documented using Cormack–Lehane grading: grade 1, full glottis; grade 2a, partial glottis; grade 2b, arytenoids/posterior cords only; grade 3, epiglottis only; grade 4, neither epiglottis nor glottis. A POGO score quantifies percentage of glottic opening visualised from 0–100%. These scores describe view, not intubation success; external laryngeal manipulation, videolaryngoscopy and bougie use may change success without changing underlying anatomy.

Endoscopic assessment

Flexible nasendoscopy is the key investigation in awake patients. It assesses epiglottis, aryepiglottic folds, arytenoids, vocal fold mobility, pooling of secretions, tumour bulk and dynamic collapse. Topicalisation commonly uses lidocaine 2–4%; total lidocaine dose should generally remain ≤9 mg kg^-1 for airway topicalisation in adults, with caution in hepatic impairment, low cardiac output and pregnancy. Co-phenylcaine or xylometazoline may improve nasal passage but systemic vasoconstrictor effects are relevant in ischaemic heart disease and uncontrolled hypertension.

Findings should distinguish unilateral vocal fold paralysis from fixation. Paralysis produces immobility with preserved passive movement at direct laryngoscopy; fixation may follow cricoarytenoid arthritis, malignancy or posterior glottic stenosis. Left recurrent laryngeal nerve palsy requires imaging from skull base to aortic arch; right-sided palsy from skull base to thoracic inlet, extended if clinically indicated.

Imaging and physiological investigations

CT neck with intravenous contrast is preferred for laryngeal trauma, abscess, cartilage invasion and tumour mapping; thin-slice CT with multiplanar reconstruction defines minimal airway diameter and length of stenosis. MRI better assesses soft tissue, perineural spread and pre-epiglottic/paraglottic space involvement but is slower and less suitable for unstable airways. Plain lateral neck radiographs are now adjunctive: epiglottitis may show the “thumb sign”, but a normal film does not exclude dangerous supraglottitis.

Flow-volume loops can support diagnosis of fixed upper airway obstruction: both inspiratory and expiratory limbs are flattened, with reduced peak inspiratory and expiratory flows. However, sensitivity is limited and normal spirometry does not exclude clinically important laryngeal obstruction, particularly intermittent vocal cord dysfunction. Arterial blood gas analysis is a late marker; normocapnia or hypercapnia in a distressed patient suggests impending ventilatory failure.

Stenosis, trauma and severity classifications

Classification	Grade	Interpretation
Cotton–Myer subglottic stenosis	I	0–50% obstruction
	II	51–70% obstruction
	III	71–99% obstruction with detectable lumen
	IV	No detectable lumen
Schaefer–Fuhrman laryngeal trauma	I	Minor endolaryngeal haematoma/laceration, no fracture
	II	Oedema, mucosal disruption, non-displaced fracture
	III	Massive oedema, exposed cartilage, displaced fracture or cord immobility
	IV	Unstable fractures, severe mucosal injury, anterior commissure disruption
	V	Complete laryngotracheal separation

Clinically significant post-intubation injury is associated with high cuff pressure, prolonged intubation, large tubes and movement. Tracheal tube cuff pressure should be maintained at 20–30 cmH₂O: below this aspiration risk rises, above this mucosal capillary perfusion is impaired, predisposing to ulceration, granuloma and stenosis.

Management, pharmacology and procedures

Airway relevance of laryngeal anatomy

The larynx is both a conduit and a sphincter; anaesthetic management must account for its narrowest functional segments, reflex innervation and vascularity. In adults the narrowest portion is usually the glottic aperture, whereas in infants it is the non-distensible cricoid ring. The vocal cords lie approximately at C4–C5; the cricothyroid membrane lies between the thyroid and cricoid cartilages and is the key landmark for emergency front-of-neck access. Sensation above the cords is via the internal branch of the superior laryngeal nerve, below the cords via the recurrent laryngeal nerve; motor supply is recurrent laryngeal except cricothyroid, supplied by external superior laryngeal nerve.

Acute management of laryngeal airway compromise

Problem	Anatomical basis	Immediate management	Definitive considerations
Laryngospasm	Reflex glottic closure mediated by superior laryngeal afferents and recurrent laryngeal efferents	100% oxygen, remove stimulus, jaw thrust/CPAP 10–20 cmH2O, deepen anaesthesia with propofol 0.5–1 mg kg-1	If persistent: suxamethonium 0.1–0.5 mg kg-1 IV; if no IV, 4 mg kg-1 IM. Treat negative-pressure pulmonary oedema
Post-extubation stridor	Glottic/subglottic oedema; cricoid ring limits expansion	High-flow oxygen, nebulised adrenaline 5 mg of 1:1000, dexamethasone 0.15–0.6 mg kg-1 IV	Reintubate early if fatigue, hypoxaemia, hypercapnia, or silent chest. Consider cuff leak test in high-risk ICU patients
Epiglottitis/supraglottitis	Supraglottic oedema with risk of complete obstruction	Minimal handling, senior anaesthetist/ENT, maintain spontaneous ventilation, prepare difficult airway and FONA	IV ceftriaxone 2 g daily or cefotaxime; add vancomycin if MRSA risk. Steroids often used though evidence limited
Laryngeal trauma	Disruption of cartilaginous framework, mucosal oedema, vocal cord immobility	Humidified oxygen, avoid blind instrumentation, CT neck if stable	Awake tracheostomy may be safer than oral intubation in major disruption

Awake tracheal intubation and topical airway anaesthesia

Awake tracheal intubation is indicated when difficult laryngoscopy, difficult facemask ventilation, aspiration risk or failed rescue oxygenation is anticipated. The Difficult Airway Society awake tracheal intubation guideline emphasises preparation, topicalisation, cautious sedation and oxygenation throughout. Local anaesthetic systemic toxicity is a major examination theme: maximum lidocaine dose is commonly 3 mg kg^-1 plain and up to 7 mg kg^-1 with adrenaline, though many airway guidelines recommend keeping total lidocaine <9 mg kg^-1 and preferably <500 mg in adults.

Technique	Target anatomy	Key details
Topicalisation	Nasopharynx, oropharynx, supraglottis, glottis	Lidocaine 2–4% via atomiser, gargle, spray-as-you-go. Onset 2–5 min; duration 20–40 min
Superior laryngeal nerve block	Internal branch piercing thyrohyoid membrane with superior laryngeal artery	2 ml lidocaine 2% per side after aspiration; risk intravascular injection/haematoma
Transtracheal block	Recurrent laryngeal sensory territory below cords; cough disperses LA upward	3–4 ml lidocaine 4% via cricothyroid membrane; avoid in coagulopathy, infection, distorted anatomy
Sedation	Preserve airway tone and ventilatory drive	Remifentanil target-controlled infusion 1–3 ng ml-1 or dexmedetomidine 0.2–0.7 microgram kg-1 h-1; avoid oversedation

Emergency front-of-neck access

In a “can’t intubate, can’t oxygenate” situation, the cricothyroid membrane is the preferred access site in adults because it is superficial, relatively avascular and below the cords but above the first tracheal ring. DAS 2015 recommends a scalpel-bougie-tube technique: identify membrane, transverse stab incision through membrane, rotate blade, pass bougie caudally, railroad a cuffed 6.0 mm tracheal tube, inflate cuff and confirm with waveform capnography. Needle cricothyroidotomy with high-pressure jet ventilation is less favoured because of barotrauma, failure of egress, catheter kinking and displacement.

Airway devices, cuff pressures and laryngeal complications

Endotracheal tube cuff pressure should be maintained at 20–30 cmH₂O to reduce microaspiration while preserving mucosal perfusion; tracheal mucosal capillary pressure is approximately 25–35 mmHg. Excessive cuff pressure may cause mucosal ischaemia, ulceration, granuloma, subglottic stenosis and recurrent laryngeal nerve palsy. Laryngeal mask airways sit with the cuff tip at the upper oesophageal sphincter and aperture facing the glottis; malposition may compress the lingual, hypoglossal or recurrent laryngeal nerves. Persistent hoarseness beyond 48–72 h, dysphagia, aspiration, stridor or weak cough mandates laryngoscopy.

Long-term management and follow-up

Vocal cord palsy requires localisation: recurrent laryngeal nerve lesions affect all ipsilateral intrinsic muscles except cricothyroid, whereas external superior laryngeal nerve injury impairs pitch and cough strength. Bilateral abductor palsy causes inspiratory stridor and may require tracheostomy, posterior cordotomy or arytenoidectomy. Unilateral palsy is managed initially with voice therapy and aspiration precautions; medialisation injection or thyroplasty is considered if dysphonia or aspiration persists. Post-intubation granulomas are treated with voice rest, proton-pump inhibitor therapy, inhaled steroids in selected cases and microlaryngoscopic excision if refractory.

Follow-up after laryngeal injury or difficult airway should include clear documentation, patient notification, difficult-airway alert systems and communication to primary care. For exam purposes, always link management to anatomy: supraglottic sensation determines topical block choice, cricothyroid membrane anatomy determines emergency access, and the fixed cricoid ring explains paediatric obstruction and subglottic stenosis.

Exam controversies and advanced synthesis

Viva-level integration: anatomy as a risk-management tool

In the Primary FRCA, laryngeal anatomy is rarely examined as pure morphology; it is tested as applied airway decision-making. Candidates should be able to move seamlessly from the hyoid–thyroid–cricoid framework, through the glottic aperture and recurrent laryngeal nerve, to practical consequences: laryngoscopy, aspiration prevention, cricothyroidotomy, tube sizing, cuff injury, and post-extubation obstruction. A common pitfall is to describe the larynx as a static tube. Functionally, it is a sphincteric, innervated, dynamically mobile structure in which small changes in oedema, neuromuscular tone or external pressure can critically alter airway resistance; by Poiseuille’s relationship, resistance varies inversely with the fourth power of radius.

Cricoid pressure: anatomical rationale versus clinical controversy

Sellick’s manoeuvre was proposed to occlude the upper oesophagus against the cricoid cartilage, exploiting the cricoid as the only complete cartilaginous ring in the airway. The traditional force is 10 N while awake, increasing to 30 N after loss of consciousness. However, modern imaging demonstrates that the oesophagus is frequently lateral to the midline, and cricoid pressure may distort the laryngeal inlet, worsen the view at laryngoscopy, impede mask ventilation or supraglottic airway insertion, and reduce lower oesophageal sphincter tone.

The large IRIS randomised non-inferiority trial compared rapid sequence induction with and without cricoid pressure. Pulmonary aspiration was rare in both groups, with a difference that did not conclusively demonstrate non-inferiority, but the study reinforced that aspiration is an uncommon endpoint requiring very large numbers. Contemporary practice is therefore pragmatic: cricoid pressure remains recommended in many rapid sequence induction protocols for patients at high aspiration risk, but it should be reduced or released immediately if it impairs ventilation, laryngoscopy or intubation. In an examination, an absolutist answer is unsafe; the defensible answer is anatomically informed, risk-stratified, and consistent with Difficult Airway Society principles.

Issue	Anatomical principle	Exam-safe synthesis
Cricoid pressure	Complete cricoid ring may compress hypopharynx/oesophagus	Use 10 N awake, 30 N unconscious; release if airway management is compromised
Post-extubation stridor	Narrowest adult functional segment is glottic/subglottic; oedema markedly increases resistance	Suspect laryngeal oedema, bilateral vocal cord dysfunction, haematoma or laryngospasm
CICO rescue	Cricothyroid membrane lies between thyroid and cricoid cartilages	Use scalpel cricothyroidotomy in adults per DAS 2015; avoid delay from repeated attempts

Front-of-neck access: anatomy, guidelines and pitfalls

The cricothyroid membrane is the critical emergency airway landmark. It is bounded superiorly by the thyroid cartilage, inferiorly by the cricoid cartilage, and laterally by the cricothyroid muscles. In adults it is approximately 9 mm high and 22–30 mm wide, though obesity, neck pathology and female sex reduce palpability. The cricothyroid artery may cross its upper portion; hence the recommended incision is through the lower central membrane when feasible.

The Difficult Airway Society 2015 unanticipated difficult intubation guidelines emphasise declaration of “can’t intubate, can’t oxygenate” and immediate progression to emergency front-of-neck access. In adults, the recommended technique is a scalpel-bougie-tube cricothyroidotomy: transverse stab incision through the membrane, rotate the blade 90°, insert bougie, railroad a cuffed tracheal tube, commonly 6.0 mm internal diameter. Needle cricothyroidotomy with high-pressure oxygenation is less favoured in adults because of barotrauma, kinking, posterior wall injury and failure of egress, particularly when upper airway obstruction is complete.

Laryngeal innervation controversies: lesions and examination traps

The recurrent laryngeal nerve supplies all intrinsic muscles except cricothyroid, which is supplied by the external branch of the superior laryngeal nerve. Sensory supply is via the internal laryngeal nerve above the cords and recurrent laryngeal nerve below them. A recurrent trap is to state that recurrent laryngeal nerve injury simply produces a “hoarse voice”. The clinical effect depends on unilateral versus bilateral injury and the position of the cords. Bilateral recurrent laryngeal nerve palsy may present with life-threatening inspiratory stridor if cords lie near the midline, whereas bilateral superior laryngeal nerve injury impairs pitch control and cough protection.

Lesion	Key anatomical deficit	Clinical implication for anaesthesia
Internal laryngeal nerve block/injury	Loss of supraglottic sensation	Aspiration risk; facilitates awake airway topicalisation
External laryngeal nerve injury	Cricothyroid weakness	Loss of high pitch; subtle voice fatigue, important in professional voice users
Unilateral recurrent laryngeal nerve palsy	Vocal cord immobility	Hoarseness, weak cough; risk if contralateral nerve subsequently injured
Bilateral recurrent laryngeal nerve palsy	Loss of abductors/adductors	Stridor or aphonia; may require urgent airway intervention

Cuffs, tubes and pressure injury

Although tracheal cuff injury is anatomically below the larynx, exam questions often link it with glottic trauma. Cuff pressure should generally be maintained at 20–30 cmH₂O; pressures exceeding mucosal capillary perfusion pressure, approximately 25–30 mmHg, increase risk of ischaemia. Nitrous oxide diffuses into air-filled cuffs, increasing pressure unless monitored. At the laryngeal level, excessive tube size, repeated attempts, stylet protrusion and arytenoid impingement cause ulceration, granuloma, arytenoid dislocation or vocal cord immobility. After extubation, the presence of a cuff leak is imperfect: it has relatively high specificity but limited sensitivity for clinically significant laryngeal oedema, so absence of a leak should prompt caution rather than automatic cancellation of extubation.

Paediatric and obstetric synthesis

The paediatric larynx is more cephalad and anterior, with a relatively large tongue and floppy epiglottis; the narrowest functional region is traditionally taught as the cricoid, although modern imaging suggests the glottis may be narrowest in relaxed children. For the Primary FRCA, the safe synthesis is that a small reduction in subglottic diameter has disproportionate effects, explaining rapid obstruction with croup or oedema. Obstetric airway risk reflects mucosal oedema, breast enlargement, reduced functional residual capacity, increased oxygen consumption, and aspiration risk; anatomy and physiology together justify early help, optimal positioning, videolaryngoscopy availability and strict limitation of attempts.

High-yield examination pitfalls

• Do not confuse the vestibular folds with true vocal cords; only the latter attach to vocal processes of arytenoids and form the rima glottidis.
• Do not say the cricoid cartilage is “C-shaped”; it is a complete ring, broader posteriorly.
• In emergency front-of-neck access, do not choose tracheostomy as the immediate adult CICO rescue unless a specialist surgical context exists.
• Always relate laryngeal sensory innervation to airway reflexes: superior laryngeal nerve stimulation may cause laryngospasm, bradycardia and apnoea, particularly in children.