Clinical Anatomy and Physiology of the Larynx

Overview

Motor and sensory innervation is entirely via the vagus nerve [X].

Embryology (Clinically Relevant)

Cartilaginous Framework

Unpaired Cartilages

• The most inferior laryngeal cartilage and the only complete cartilaginous ring in the airway
• Shaped like a signet ring: broad posterior lamina + narrow anterior arch
• Sits at the level of C6
• Provides articular facets for the arytenoid cartilages (on the superolateral lamina) and the inferior horns of the thyroid cartilage (lateral lamina)
• The posterior lamina bears two oval depressions (for posterior cricoarytenoid muscles) separated by a vertical ridge (esophageal attachment)

• The largest laryngeal cartilage; supports most laryngeal soft tissues
• Two laminae fuse anteriorly to form the laryngeal prominence (Adam's apple) — more pronounced in males due to testosterone-driven growth
• The superior thyroid notch is a key landmark for percutaneous airway techniques and laryngeal nerve blocks
• Superior and inferior horns (cornua): inferior horns articulate with the cricoid at the cricothyroid joint
• The cricothyroid membrane (CTM) spans the gap between the thyroid and cricoid anteriorly — the target for emergency cricothyrotomy

• A leaf-shaped fibroelastic cartilage that forms the anterior border of the laryngeal inlet
• Anterior surface attached to the hyoid bone via the hyoepiglottic ligament and to the thyroid cartilage via the thyroepiglottic ligament
• Deflects food bolus away from the airway during swallowing (though this function is not essential for aspiration prevention)
• The vallecula is the space between the base of tongue and the anterior epiglottis — the target for placement of a Macintosh laryngoscope blade

Paired Cartilages

• Vocal process (anterior): attachment of the vocal ligament
• Muscular process (lateral): attachment of the intrinsic muscles that rotate and glide the arytenoid

Joints and Ligaments

• Thyrohyoid membrane: connects the thyroid cartilage to the hyoid bone; pierced by the internal branch of the superior laryngeal nerve and superior laryngeal vessels
• Cricothyroid membrane: connects thyroid to cricoid anteriorly — clinically vital for emergency airways
• Conus elasticus (cricovocal membrane): extends from the superior surface of the cricoid arch upward, thickening medially to form the vocal ligament — the free upper edge of the membrane
• Quadrangular membrane: extends from the lateral epiglottis to the arytenoid; its free lower edge is the vestibular ligament (false cord)

Laryngeal Cavity: Three Compartments

SUPRAGLOTTIS (Vestibule)
  ─ Laryngeal inlet
  ─ Aryepiglottic folds
  ─ False vocal cords (vestibular folds) ─ contain vestibular ligaments
      ↕ Laryngeal ventricles + saccules
GLOTTIS
  ─ True vocal cords (vocal folds) ─ contain vocal ligaments + vocalis muscle
  ─ Rima glottidis
      ↕ narrowest part of adult larynx (wider in children — subglottis is narrowest)
SUBGLOTTIS (Infraglottic cavity)
  ─ Inferior border of vocal folds → inferior border of cricoid

Intrinsic Muscles

The posterior cricoarytenoid is the only abductor of the vocal folds. Bilateral RLN palsy paralyzes all intrinsic muscles except the cricothyroid, leaving the cords in a median/paramedian position with the glottis closed — causing inspiratory stridor and potential asphyxia.

Extrinsic Muscles

Innervation

• Internal branch (iSLN): sensory to the laryngeal mucosa above the vocal folds; pierces the thyrohyoid membrane with the superior laryngeal artery; mediates the cough and laryngospasm reflexes from supraglottic stimulation
• External branch (eSLN): motor to the cricothyroid muscle only; at risk during thyroid surgery

• Motor to all intrinsic laryngeal muscles except cricothyroid
• Sensory to mucosa below the vocal folds
• Ascends in the tracheoesophageal groove; enters the larynx deep to the inferior pharyngeal constrictor
• Left RLN has a longer course (loops around the aortic arch) → more vulnerable to mediastinal pathology
• At risk in thyroid/parathyroid surgery, neck dissection, and thoracic procedures

• Unilateral RLN palsy → hoarse, breathy voice (paralyzed cord in paramedian position)
• Bilateral RLN palsy → airway obstruction, stridor
• eSLN palsy → loss of high-pitch phonation (cricothyroid paralysis)

Blood Supply

Lymphatic Drainage

Physiology

1. Airway Protection

1. Aryepiglottic folds (oblique arytenoids)
2. False vocal folds (thyroarytenoid + quadrangular membrane)
3. True vocal folds (lateral cricoarytenoids + transverse arytenoids)

2. Phonation

• The vocal folds (vocalis muscle + vocal ligament + overlying mucosa) vibrate due to aerodynamic forces — the Bernoulli effect draws adducted folds together as air passes between them
• Pitch (fundamental frequency): determined by length and tension of vocal folds
  • Cricothyroid elongates/tenses folds → higher pitch
  • Vocalis shortens/slackens folds → lower pitch
  • Males: vocal folds ~17–23 mm; pitch ~110 Hz
  • Females: vocal folds ~12–17 mm; pitch ~220 Hz
  • Testosterone increases vocal fold mass and length → lower pitch (relevant in transgender men on HRT)
• Loudness: determined by subglottic air pressure
• Quality/timbre: shaped by resonating chambers (pharynx, oral cavity, nasal cavity)

3. Cough Reflex

• Afferent: iSLN (above cords) and RLN (below cords) → vagus → nucleus tractus solitarius
• Deep inspiration → tight glottic closure (adduction) → buildup of intrathoracic pressure → sudden explosive glottic opening → airflow >12 L/s clears the airway

4. Valsalva Maneuver

5. Fixation of the Thorax

Anatomical Diagrams

Key Clinical Correlations

Acute and Chronic Tonsillitis

Anatomy — Brief Review

Classification

I. Acute Tonsillitis

1. Viral (majority of cases)
2. Bacterial
3. Membranous (e.g., diphtheria, EBV with pseudomembrane)

II. Chronic Tonsillitis

1. Recurrent acute tonsillitis — repeated discrete episodes with full recovery between attacks
2. Chronic follicular/crypt tonsillitis — deep crypts with retained debris (tonsilloliths), chronic bacterial colonisation, persistent symptoms
3. Chronic hypertrophic tonsillitis — enlarged tonsils causing obstructive symptoms (OSA, dysphagia)

Etiology

Acute Tonsillitis

• Adenovirus, rhinovirus, echovirus, coxsackievirus, RSV, influenza, parainfluenza
• Epstein-Barr virus (EBV, HHV-4) — causes infectious mononucleosis; the most important viral cause to distinguish clinically

• Group A β-hemolytic Streptococcus (GABHS / S. pyogenes) — most common bacterial pathogen; peak incidence ages 5–6 years
• Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus
• Diphtheria (Corynebacterium diphtheriae) — in unimmunized populations
• Mixed anaerobes — particularly in peritonsillar abscess
• Mycobacterium tuberculosis — rare, in immunocompromised patients

Chronic Tonsillitis

• Polymicrobial including anaerobes; Actinomyces species is a key organism — its presence in crypt debris indicates established chronic infection that is unlikely to resolve with antibiotics alone
• Biofilm formation within tonsillar crypts
• Predisposing factors: recurrent acute episodes, smoking, poor dental hygiene, gastroesophageal/laryngopharyngeal reflux, chronic mouth breathing

Pathogenesis

Acute Tonsillitis

1. Viral or bacterial pathogens colonise the tonsillar crypts
2. Acute inflammatory response: mucosal invasion → neutrophil infiltration → oedema, hyperaemia, and crypt exudate
3. GABHS produces multiple virulence factors: streptolysins (O and S), erythrogenic toxin (causing the rash of scarlet fever), streptokinase, hyaluronidase, and M-protein (antiphagocytic), enabling tissue invasion and immune evasion
4. M-protein shares structural similarity with cardiac sarcomeric proteins → molecular mimicry → rheumatic fever if untreated
5. Streptococcal antigens activate complement and form immune complexes → post-streptococcal glomerulonephritis

Chronic Tonsillitis

• Deep tonsillar crypts accumulate desquamated epithelial cells, food debris, and bacteria
• This provides an anaerobic microenvironment ideal for bacterial persistence and biofilm formation
• Repeated cycles of subclinical infection → progressive scarring and fibrosis of tonsillar tissue
• Crypts widen and become obstructed → tonsilloliths (calcified debris) → halitosis, foreign body sensation
• Persistent antigen stimulation → reactive cervical lymphadenopathy

Clinical Features

Acute Viral Tonsillitis

• Gradual onset of sore throat, low-grade or no fever
• Pharyngeal erythema without exudate
• Rhinorrhoea, nasal congestion, hoarseness, oral ulcers (features suggesting viral aetiology)
• Mild to moderate sore throat severity

Acute Bacterial (GABHS) Tonsillitis

• Sudden onset fever, severe sore throat, odynophagia
• Associated: malaise, dysphagia, otalgia, headache, nausea, abdominal pain
• Physical findings:
  • Oropharyngeal erythema with tonsillar enlargement ± creamy/yellow exudate
  • Palatal petechiae
  • Swollen uvula
  • Tender anterior cervical lymphadenopathy
  • Scarlatiniform rash (in scarlet fever) — descending erythematous rash from neck to trunk, fading in ~1 week
  • Strawberry tongue (enlarged papillae ± white membrane)

EBV Infectious Mononucleosis (key differential)

• High fever, severe malaise, headache
• Severe pharyngitis ± green/gray tonsillar exudate (indistinguishable from streptococcal on exam)
• Palatal petechiae at the hard-soft palate junction
• Large, tender cervical lymphadenopathy (may be bilateral)
• Hepatosplenomegaly
• Characteristic rash developing after amoxicillin/ampicillin exposure (morbilliform, mainly truncal)
• Risk of upper airway obstruction (tonsillar hypertrophy + oedema)
• Rare: splenic rupture, haematologic/neurologic/cardiac complications

Chronic Tonsillitis

• Recurrent sore throats, persistent low-grade throat discomfort
• Halitosis (foul odour from crypt debris)
• Tonsilloliths — white/yellow semisolid debris extruding from crypts; foul taste
• Foreign body sensation in the throat
• Chronic cough, irritability
• Tonsillar asymmetry (may suggest malignancy — requires evaluation)
• Recurrent febrile episodes

• Each episode lasts ~3 days
• ≥3 episodes recurring every ~3 weeks
• Symptom-free intervals
• Must exclude cyclical neutropenia

Diagnostics

Clinical Scoring — Centor/McIsaac Score for GABHS

Laboratory Investigations

• Detects GABHS group-A carbohydrate antigen
• Highly specific; if negative, confirm with throat culture (gold standard for GABHS)
• Culture on blood agar; ASO titres not recommended for diagnosis — they only indicate prior infection, not active disease

• Bacterial: leukocytosis with neutrophilia
• EBV: lymphocytosis (>50% lymphocytes), >10% atypical lymphocytes; ESR more likely elevated in EBV than bacterial infection

• Sensitivity: 85% overall; less sensitive in the first two weeks; 100% specific
• Repeat weekly for 6 weeks if initial negative and EBV suspected
• Commercial tests: sensitivity 81–95%, positive predictive value >95%

• IgM anti-VCA: acute infection
• IgG anti-VCA + IgG anti-EBNA: past infection
• PCR for EBV DNA: used in suspected EBV encephalitis

Differential Diagnosis

Treatment

Acute Viral Tonsillitis

• Supportive care: analgesia (NSAIDs preferred — ibuprofen), hydration, rest
• Antibiotics not indicated
• EBV mononucleosis: NSAIDs for pain; avoid β-lactams (amoxicillin/ampicillin → morbilliform rash in ~30%); oral/parenteral corticosteroids for moderate-to-severe tonsillopharyngitis and mild airway obstruction
• Severe airway obstruction: nasopharyngeal airway; rarely tonsillectomy, intubation, or tracheotomy

Acute Bacterial (GABHS) Tonsillitis

• Penicillin V (oral, 10 days) or amoxicillin — drug of choice; targets GABHS to prevent rheumatic fever
• Full 10-day course is essential to eradicate GABHS and prevent complications

• Azithromycin (5 days) or clarithromycin
• Clindamycin (for recurrent/penicillin-tolerant strains)
• Cephalosporins if allergy is not anaphylactic

• NSAIDs/paracetamol for analgesia and antipyresis
• Single dose of dexamethasone — reduces symptom severity and duration in severe cases

Chronic Tonsillitis

• Frequent gargling with hydrogen peroxide mouthwash
• Manual expression of tonsillar debris
• Prolonged antibiotics: amoxicillin 500 mg TDS × 21 days, or clindamycin 300 mg TDS × 21 days
• Note: Presence of Actinomyces indicates long-term antibiotics will likely fail → surgery required

• ≥7 episodes in 1 year
• ≥5 episodes per year for 2 consecutive years
• ≥3 episodes per year for 3 consecutive years

• 2 weeks of school/work lost per year

• Peritonsillar abscess (on same side)
• Tonsillar hypertrophy causing upper airway obstruction (OSA) or swallowing difficulty
• Recurrent tonsillitis causing febrile seizures
• Suspicion of malignancy (unilateral enlargement; unknown primary)
• Diphtheria carrier state
• PFAPA unresponsive to medical treatment

• Post-operative haemorrhage: 2–4% (primary within 24 h; secondary at days 5–10)
• Mortality: ~1 in 25,000 (haemorrhage, airway obstruction, anaesthesia)

Complications

Local/Regional Complications

Systemic (Non-Suppurative) Complications of GABHS

Prevention

Primary Prevention

• Prompt treatment of GABHS tonsillitis with a full 10-day course of penicillin (eradicates GABHS, preventing ARF)
• Avoiding close contact during acute illness (droplet precautions)
• Hand hygiene; avoid sharing utensils
• Vaccination: diphtheria toxoid (DPT/Td) — prevents membranous tonsillitis
• H. influenzae type b (Hib) vaccination — prevents epiglottitis, reduces one complication pathway
• Smoking cessation (reduces chronic tonsillar irritation)
• Treatment of gastro-oesophageal/laryngopharyngeal reflux

Secondary Prevention

• Benzathine penicillin G IM monthly (for patients with documented rheumatic fever or ARF risk) — long-term secondary prophylaxis to prevent recurrent GABHS and further cardiac damage
• Duration: at least 5 years after last episode or until age 21 (longer if carditis present)

Tertiary Prevention

• Tonsillectomy in patients meeting criteria — removes the nidus of recurrent infection

Summary Table: Acute vs. Chronic Tonsillitis