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Larynx: Clinical Anatomy, Physiology, Research Methods, and Acute Diseases

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PART 1: CLINICAL ANATOMY OF THE LARYNX

1.1 Location and Overview

• The larynx is an organ of the conducting airway extending from the inferior laryngeal part of the pharynx to the trachea.
• Located at the level of C3–C6 in men; slightly higher in women and children.
• It lies in the anterior midline of the neck, embedded in the visceral space between the pretracheal and prevertebral layers of cervical fascia.
• Anteriorly: covered by cervical fascia and skin; posteriorly: laryngopharynx.
• The laryngeal prominence (Adam's apple) and cricothyroid ligament are palpable through the skin.
• The total range of up-and-down movement (during swallowing, vocalization, breathing) is up to 4 cm.
• During swallowing, the larynx elevates 2–3 cm.

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1.2 Functions

1. Airway patency — maintains patent passage for respiration
2. Airway protection — prevents aspiration via glottic closure reflex (mediated by bilateral superior laryngeal nerves)
3. Phonation — sound production via vocal fold vibration
4. Cough — forced expiration to clear the airway

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1.3 Laryngeal Skeleton (Cartilages)

Thyroid and cricoid are hyaline and undergo ossification with age. Epiglottis, corniculate, cuneiform are elastic and do not ossify.

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1.4 Joints and Ligaments

• Cricothyroid joint (synovial): between inferior horn of thyroid and lateral cricoid — allows rocking/rotation, changes vocal fold tension
• Cricoarytenoid joint (synovial): shallow ball-and-socket; arytenoid rocks inward (adduction) or outward (abduction)
• Thyrohyoid membrane: connects upper thyroid to hyoid; pierced by superior laryngeal vessels and internal laryngeal nerve
• Cricothyroid membrane (conus elasticus): connects thyroid to cricoid anteriorly — key surgical landmark for emergency cricothyrotomy
• Vocal ligament: upper free edge of conus elasticus, from thyroid to vocal process of arytenoid
• Quadrangular membrane: from epiglottis to arytenoid; free lower margin = vestibular ligament

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1.5 Laryngeal Cavity — Three Compartments

┌──────────────────────────────────────┐
│  SUPRAGLOTTIS (Vestibule)            │
│  Laryngeal inlet → vestibular folds  │
│  (False vocal cords)                 │
├──────────────────────────────────────┤
│  GLOTTIS                             │
│  True vocal folds + anterior         │
│  commissure + posterior arytenoid    │
│  area + ventricles (sinus of Morgagni)│
├──────────────────────────────────────┤
│  SUBGLOTTIS                          │
│  Below true cords → lower border     │
│  of cricoid                          │
│  (5 mm anterior / 10 mm posterior)   │
└──────────────────────────────────────┘

• Rima glottidis: opening between the true vocal folds
• Ventricle (sinus of Morgagni): lateral recess between vestibular and vocal folds
• Piriform recess: lateral to aryepiglottic folds — common site for foreign bodies and malignancy

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1.6 Laryngeal Muscles

Intrinsic Muscles (all within larynx; move vocal folds)

Complete glottic closure requires simultaneous action of all adductors (LCA + TA + transverse arytenoid). The PCA is the only muscle that actively opens the larynx.

Extrinsic Muscles

• Depressors (pull larynx down): sternohyoid, thyrohyoid, omohyoid
• Elevators (pull larynx up): geniohyoid, mylohyoid, anterior belly of digastric, stylohyoid

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1.7 Innervation (Branches of Vagus Nerve — CN X)

• Right RLN loops around right subclavian artery
• Left RLN loops around aortic arch (longer course — more vulnerable to mediastinal pathology)
• Clinical: Unilateral RLN damage → hoarseness (unilateral cord paresis); Bilateral damage → stridor, respiratory distress

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1.8 Blood Supply

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1.9 Lymphatic Drainage

• Supraglottis: rich lymphatic network → deep cervical nodes (levels II–IV) bilaterally
• Glottis (true cords): almost avascular and alymphatic — explains why early glottic cancer rarely metastasizes
• Subglottis: drains to pretracheal (Delphian), paratracheal, and inferior deep cervical nodes

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1.10 Histology / Mucosa

• Supraglottis and subglottis: pseudostratified ciliated columnar epithelium (respiratory type)
• True vocal folds: stratified squamous non-keratinizing epithelium (resists friction)
• Transition zone at free edge of vocal cord — clinically important (junction squamo-columnar)

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PART 2: PHYSIOLOGY OF THE LARYNX

2.1 Respiratory Function

• Maintains patent airway; regulates airflow resistance
• Abduction of vocal folds during inspiration (PCA activated)
• Partial adduction during expiration (increases resistance → helps maintain FRC/alveolar stability)
• The cricoid is the only complete rigid ring — prevents collapse

2.2 Protective Function (Glottic Closure Reflex)

• Stimuli (food, water, secretions, irritants) activate superior laryngeal nerve sensory endings
• Reflex arc: SLN afferents → nucleus tractus solitarius → motor output via RLN → forceful adduction of all intrinsic muscles
• Laryngospasm: sustained spasm of the glottic muscles — causes stridor; can cause complete airway obstruction
  • Triggers: blood, secretions on vocal cords, light anesthesia
  • Treatment: positive pressure oxygen, IV succinylcholine if severe

2.3 Phonation (Voice Production)

• Bernoulli effect / myoelastic-aerodynamic theory:
  1. Respiratory muscles generate subglottic pressure via lung recoil
  2. Adductors close the glottis (vocal folds together)
  3. Subglottic pressure increases → forces vocal folds open
  4. Bernoulli effect + elastic recoil → folds snap closed again
  5. Rapid opening-closing cycle = acoustic vibration → sound
• Pitch: controlled by cricothyroid (lengthens/tenses folds) — higher tension = higher frequency
• Volume: controlled by subglottic pressure
• Quality (timbre): shaped by vocal tract resonance (pharynx, oral/nasal cavity)

2.4 Deglutition (Swallowing)

1. Soft palate closes nasopharynx
2. Larynx elevates 2–3 cm under hyoid
3. Epiglottis deflects over laryngeal inlet
4. Glottis closes (true and false cords adduct)
5. Cricopharyngeus relaxes → food enters esophagus

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PART 3: METHODS OF LARYNX RESEARCH (EXAMINATION)

3.1 Indirect Laryngoscopy

• Method: laryngeal mirror + light source (headlight or fibroptic)
• Position: patient leans forward, tongue protruded, mouth open; angled mirror placed against soft palate
• Reveals: vocal folds, epiglottis, arytenoids, piriform sinuses
• Limitations: patient discomfort, strong gag reflex, limited in obese/short neck patients

3.2 Direct Laryngoscopy

• Rigid laryngoscope under general or topical anesthesia
• Used for: diagnostic examination, biopsy, foreign body removal, surgical procedures
• Types: Macintosh, Miller, Lindholm, Kleinsasser microlaryngoscopy
• Suspension laryngoscopy: laryngoscope suspended on chest support; allows bimanual surgical technique under operating microscope

3.3 Flexible Fiberoptic Nasolaryngoscopy (FFNL)

• Flexible endoscope passed transnasally under topical anesthesia
• Gold standard for office-based dynamic laryngeal examination
• Assesses: vocal fold mobility, mucosal lesions, laryngeal inlet, supraglottic structures
• Can be combined with stroboscopy for mucosal wave analysis

3.4 Video Laryngostroboscopy

• Uses stroboscopic light synchronized near vocal fold vibration frequency (~100 Hz)
• Creates apparent slow-motion image of vocal fold mucosal wave
• Evaluates: mucosal wave amplitude, symmetry, glottic closure, vibratory phase
• Detects early submucosal pathology (polyps, scarring, early carcinoma) not visible on standard endoscopy

3.5 High-Speed Videoendoscopy (HSV)

• Records at 2,000–10,000 frames/second
• Captures true real-time vocal fold vibration (not stroboscopic inference)
• Research gold standard; expensive

3.6 Electromyography (EMG)

• Laryngeal EMG: needle electrodes placed into intrinsic laryngeal muscles (cricothyroid, thyroarytenoid, PCA via posterior approach)
• Differentiates neurogenic from mechanical vocal fold fixation
• Determines prognosis in RLN paralysis (presence of fibrillations vs. reinnervation potentials)
• Guides Botulinum toxin injections in spasmodic dysphonia

3.7 Acoustic Analysis (Voice Analysis)

• Microphone recordings analyzed for: fundamental frequency (F0), jitter (pitch perturbation), shimmer (amplitude perturbation), harmonic-to-noise ratio (HNR)
• Objective voice quality assessment

3.8 Aerodynamic Testing

• Measures: subglottic pressure, mean airflow rate, glottal resistance
• Phonation threshold pressure (PTP): minimum pressure to initiate vibration
• Diagnoses glottic insufficiency, spasmodic dysphonia

3.9 Imaging

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PART 4: ACUTE DISEASES OF THE LARYNX

4.1 Acute Laryngitis

• Viral (most common): rhinovirus, influenza, parainfluenza, adenovirus
• Bacterial: Haemophilus influenzae, Streptococcus, Staphylococcus (secondary)
• Non-infectious: voice overuse, acid reflux, inhalation injury

• Hoarseness / dysphonia (cardinal symptom)
• Sore throat, dry cough
• Mild dysphagia
• Low-grade fever
• Symptoms worsen with voice use

• Voice rest (most important)
• Adequate hydration, humidification
• Analgesics/NSAIDs
• Avoid irritants (smoking, alcohol)
• Antibiotics only if bacterial cause confirmed
• Corticosteroids in professional voice users (short-term)
• Resolution in 1–2 weeks; persistent hoarseness >3 weeks → laryngoscopy to exclude malignancy

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4.2 Acute Epiglottitis

• Children: classically Haemophilus influenzae type b (Hib) — now rare due to Hib vaccination
• Adults: Streptococcus pyogenes, Streptococcus pneumoniae, Staphylococcus aureus, H. influenzae

1. Dysphagia (severe, drooling)
2. Dysphonia (muffled/"hot potato" voice)
3. Dyspnoea (progressive stridor, tripod position)
4. High fever (38.5–40°C), toxic appearance
5. Minimal cough (distinguishes from croup)
6. "Thumb sign" on lateral neck X-ray (swollen epiglottis)

• Airway is priority — do not disturb child; no oropharyngeal examination in emergency department
• Immediate intubation or tracheostomy in controlled setting (OR with ENT + anesthesia)
• IV antibiotics: Cefotaxime or Ceftriaxone
• Corticosteroids (adjunctive)
• Hib vaccination is key prevention

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4.3 Acute Subglottic Laryngitis (Croup / Laryngotracheobronchitis)

• Prodromal URTI (1–2 days)
• Seal-bark cough (hallmark)
• Inspiratory stridor
• Hoarseness
• Worse at night; better with cool humidified air
• Low/moderate fever; not toxic-appearing
• "Steeple sign" on AP neck X-ray (subglottic narrowing)

• Mild: cool mist, oral corticosteroids (dexamethasone 0.15–0.6 mg/kg single dose)
• Moderate/severe: nebulized adrenaline (epinephrine) (1:1000, 0.5 mL/kg up to 5 mL) + dexamethasone
• Oxygen if SpO₂ <92%
• Intubation/tracheostomy if refractory

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4.4 Spasmodic Croup

• Sudden nocturnal onset of barking cough and stridor in a child who was well during the day
• No fever, no prodromal URTI
• Likely allergic/reflex etiology
• Self-resolves with steam inhalation / cool air; tends to recur

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4.5 Laryngeal Abscess

• Collection of pus in the supraglottic or periglottic tissues
• Complication of acute epiglottitis, perichondritis, or deep neck space infection
• Clinical: severe odynophagia, muffled voice, neck swelling, trismus
• Treatment: airway control, IV antibiotics, surgical drainage

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PART 5: LARYNGEAL EDEMA

5.1 Definition

5.2 Classification

5.3 Pathophysiology

• Allergic/Anaphylactic: IgE binds to mast cells on re-exposure to allergen → degranulation → histamine, leukotrienes, prostaglandins → increased vascular permeability → rapid supraglottic edema
• Hereditary Angioedema (HAE): C1-inhibitor deficiency → uncontrolled complement and bradykinin activation → non-histamine-mediated edema (antihistamines/adrenaline may be ineffective)
• Inflammatory: cytokine-mediated capillary leakage into submucosal tissue

5.4 Clinical Features

• Rapidly progressive — can evolve over minutes (anaphylaxis) to hours
• Inspiratory stridor (laryngeal obstruction > 50% of airway)
• Dysphagia (supraglottic edema)
• Muffled/"hot potato" voice or hoarseness
• Dyspnoea and use of accessory muscles
• Cyanosis — late sign (pre-terminal)
• Associated signs: urticaria, angioedema of face/lips/tongue (anaphylaxis)

5.5 Laryngoscopic Findings

• Pale, waterlogged, gelatinous appearance of epiglottis and aryepiglottic folds
• Arytenoid edema ("jug-handle" appearance)
• Narrowed laryngeal inlet
• In anaphylaxis: glottis may be completely obscured

5.6 Management

Anaphylactic/Allergic:

1. Position: upright (reduces edema)
2. Adrenaline (Epinephrine) IM 0.3–0.5 mg (1:1000) — first-line — repeat every 5 min PRN
   • Nebulized adrenaline as adjunct (1:1000, 5 mL)
3. Airway: 100% O₂; early intubation before complete obstruction; tracheostomy if failed intubation
4. IV corticosteroids: hydrocortisone 200 mg IV (reduce biphasic reaction)
5. IV antihistamines: chlorphenamine 10 mg IV
6. IV fluids for hemodynamic support

HAE:

• Adrenaline/antihistamines have limited effect
• Specific treatments: C1-inhibitor concentrate, icatibant (bradykinin B2 receptor antagonist), or fresh frozen plasma (FFP)

Inflammatory:

• Treat underlying cause (antibiotics for infection)
• Corticosteroids (dexamethasone IV)
• Nebulized adrenaline for acute relief

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PART 6: LARYNGEAL STENOSIS

6.1 Definition

6.2 Classification

By Level:

• Supraglottic (rare)
• Glottic (posterior glottic — bilateral vocal fold immobility; anterior — web)
• Subglottic (most common acquired form)

By Etiology:

Prolonged intubation is the leading cause of acquired subglottic stenosis in adults — endotracheal tube cuff pressure >25 cmH₂O → mucosal ischemia → ulceration → cicatricial fibrosis

6.3 Pathophysiology of Acquired Stenosis

1. Mucosal trauma/ischemia (e.g., cuff pressure, intubation injury)
2. Mucosal ulceration → bacterial colonization
3. Perichondritis → chondritis → cartilage necrosis
4. Granulation tissue formation → fibroblast proliferation
5. Collagen deposition → circumferential cicatricial scar
6. Progressive luminal narrowing

6.4 Grading — Cotton-Myer Classification (Subglottic)

6.5 Clinical Features

• Biphasic stridor (both inspiratory and expiratory — fixed obstruction)
• Progressive dyspnoea on exertion → at rest
• Recurrent "croup-like" symptoms in children
• Impaired secretion clearance → recurrent pulmonary infections
• Hoarseness if glottic involvement
• Patients often tolerate significant stenosis asymptomatically until >50–70% obstruction

6.6 Diagnosis

1. History (previous intubation, trauma, systemic disease)
2. Flexible nasolaryngoscopy: assesses supraglottis, glottis, vocal fold mobility
3. Rigid endoscopy under anesthesia: gold standard — defines extent, type, severity of stenosis
4. CT scan: 3D reconstruction; measures cross-sectional area; evaluates cartilaginous framework
5. Flow-volume loop: fixed extrathoracic obstruction → plateau on both inspiratory and expiratory limbs (box-shaped pattern)
6. Spirometry: reduced peak flow, FEV1/FVC may be preserved

6.7 Management

Endoscopic (Mild–Moderate, Soft Stenosis):

• Endoscopic laser division (CO₂ laser): radial incisions to dilate scar
• Balloon dilation: pneumatic dilation of stenotic segment
• Intralesional corticosteroids: triamcinolone injection post-dilation reduces re-stenosis
• Mitomycin C application: antifibrotic agent applied topically post-dilation
• Repeated procedures often needed

Open Surgery (Severe/Complex Stenosis):

• Laryngotracheal reconstruction (LTR): cartilage grafts (typically costal cartilage) to expand subglottis
• Cricotracheal resection (CTR): resection of stenotic segment with primary anastomosis — best results for isolated subglottic stenosis
• Tracheostomy: bypass stenosis pending definitive repair; sometimes permanent in severe bilateral cord immobility
• Glottis: anterior commissure web → endoscopic keel placement; posterior stenosis → arytenoidectomy or vocal fold lateralization

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PART 7: DIPHTHERIA OF THE LARYNX

7.1 Definition

7.2 Pathogen

• Corynebacterium diphtheriae — biotypes: gravis, mitis, intermedius
• Toxin production requires lysogeny by bacteriophage β (tox+ gene)
• Diphtheria toxin: ADP-ribosylates elongation factor EF-2 → inhibits protein synthesis → cell death
• Local effect: epithelial necrosis with pseudomembrane formation
• Systemic effects: myocarditis, polyneuropathy (via toxin absorption)

7.3 Epidemiology

• Rare in vaccinated populations (DTP/DPT immunization)
• Still endemic in parts of Africa, Asia, Eastern Europe
• Unvaccinated children most susceptible; adults with waning immunity
• Transmission: respiratory droplets, direct contact with skin lesions

7.4 Pathology

• Pseudomembrane: grayish-white, tough, fibrin-rich membrane composed of:
  • Fibrin, necrotic epithelium, leukocytes, erythrocytes, bacteria
  • Adheres firmly to underlying mucosa — bleeding occurs on attempted removal (distinguishes from other white membranes)
  • Can form in pharynx, tonsils, larynx, trachea, bronchi ("descending croup")

7.5 Clinical Features — Laryngeal Diphtheria

Stage 1 — Catarrhal (1–2 days):

• Mild sore throat, hoarseness, low-grade fever
• Malaise, anorexia
• Indistinguishable from viral URTI at this stage

Stage 2 — Membranous:

• Appearance of characteristic grayish-white pseudomembrane on tonsils/pharynx
• Membrane extends to larynx → hoarseness → aphonia
• Barking cough, stridor (inspiratory)
• "Bull neck" appearance: due to cervical lymphadenopathy and soft tissue swelling
• Nasal discharge (serosanguineous — "bloody snot" from nasal diphtheria)

Stage 3 — Obstructive:

• Progressive extension to subglottis/trachea
• Inspiratory → biphasic stridor
• Severe dyspnoea, suprasternal/intercostal retractions
• Cyanosis (pre-terminal)
• Respiratory failure → death if untreated

Systemic Complications (Toxin-Mediated):

1. Myocarditis (2nd–3rd week): arrhythmias (heart block, VF), cardiac failure → leading cause of death
2. Neuropathy: palatal palsy (nasal regurgitation), oculomotor palsy (diplopia), peripheral motor neuropathy, phrenic nerve palsy (respiratory paralysis)
3. Renal tubular necrosis
4. Thrombocytopenia

7.6 Diagnosis

1. Clinical: characteristic membrane + hoarseness + stridor + toxic child
2. Swab culture: tonsillar/pharyngeal swab on Loeffler's serum or Hoyle's tellurite medium (colonies appear black)
3. Gram stain: gram-positive rods with Chinese letter/palisade arrangement; metachromatic granules (volutin/Babes-Ernst granules) on Albert's or Neisser's stain
4. Elek test: gel immunodiffusion — confirms toxin production
5. PCR: detects tox gene
6. Laryngoscopy: confirms laryngeal involvement; membrane can be seen
7. Throat swab must not trigger gagging/airway emergency

7.7 Differential Diagnosis of Laryngeal Membrane

7.8 Management

Airway:

• Immediate assessment — do not disturb airway
• Tracheostomy or intubation if severe obstructive symptoms (membranous croup)
• O₂ supplementation

Antitoxin:

• Diphtheria Antitoxin (DAT) — the most critical treatment
• Must be given as early as possible (neutralizes free toxin only; cannot reverse bound toxin)
• Dose: 20,000–100,000 units IV (depending on site and severity) after skin/conjunctival sensitivity test
• IV route preferred for severe disease

Antibiotics (Eliminate Organism):

• Penicillin G IV: 100,000–150,000 U/kg/day for 10–14 days; OR
• Erythromycin 40 mg/kg/day (penicillin allergy)
• Antibiotics do NOT replace antitoxin
• Culture negative after 2 consecutive swabs before discharge

Supportive Care:

• Strict bed rest (cardiac monitoring for 3–4 weeks)
• Cardiac monitoring: ECG for heart block; pacemaker if needed
• Isolate patient; contact tracing
• Ventilatory support if phrenic palsy

Immunization:

• Diphtheria does not confer lasting immunity — vaccinate after recovery
• Contacts: booster dose + prophylactic erythromycin
• Active immunization: DTP (diphtheria toxoid + tetanus toxoid + pertussis) at 6 weeks, 10 weeks, 14 weeks, booster at 18 months, 5 years, 10 years

7.9 Prognosis

• Untreated laryngeal diphtheria: mortality 20–50%
• With prompt antitoxin + airway management: mortality <5%
• Death most commonly from myocarditis or airway obstruction
• Late deaths from phrenic nerve palsy causing respiratory paralysis

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SUMMARY TABLE: Key Differentiating Features of Acute Laryngeal Diseases

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• Color Atlas of Human Anatomy, Vol. 2 — Internal Organs (Thieme)
• Cummings Otolaryngology Head and Neck Surgery
• Miller's Anesthesia, 10e
• Gray's Anatomy for Students