Clinical anatomy. physiology and methods of larynx research. Acute diseases of the larynx. Laryngeal edema. Laryngeal stenosis. Diphtheria of the larynx.
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Clinical Anatomy, Physiology, and Research Methods of the Larynx — Acute Diseases, Edema, Stenosis, and Diphtheria
1. Clinical Anatomy of the Larynx
The larynx is a hollow musculoligamentous structure with a cartilaginous framework that caps the lower respiratory tract. It is continuous below with the trachea and opens above into the pharynx, posterior and inferior to the tongue. It serves two primary roles: a sphincter/valve protecting the lower airways, and a sound-producing instrument for phonation.
Cartilaginous Framework
Three unpaired cartilages:
- Thyroid cartilage — the largest; its anterior angle (laryngeal prominence/"Adam's apple") provides the anterior wall. The superior horns attach to the hyoid via the lateral thyrohyoid ligaments; the inferior horns articulate with the cricoid at the cricothyroid joints.
- Cricoid cartilage — the only complete cartilaginous ring in the airway, shaped like a signet ring with a broad posterior lamina and narrow anterior arch. It is the most inferior laryngeal cartilage and articulates with both the thyroid and arytenoid cartilages.
- Epiglottis — a leaf-shaped cartilage attached to the inner surface of the thyroid angle; during swallowing, the epiglottis swings down toward the arytenoids, closing the laryngeal inlet.
Three pairs of smaller cartilages:
- Arytenoid cartilages — sit on the posterosuperior surface of the cricoid lamina. Each has a vocal process (for attachment of the vocal ligament) and a muscular process (for attachment of the posterior and lateral crico-arytenoid muscles). Movement of the arytenoids (gliding and rotating on the cricoid) opens and closes the rima glottidis.
- Corniculate cartilages — small conical projections articulating with the apices of the arytenoids; their apices project posteromedially.
- Cuneiform cartilages — club-shaped, lying in the aryepiglottic folds anterior to the corniculates.
Ligaments and Membranes
| Structure | Connects | Function |
|---|---|---|
| Thyrohyoid membrane | Superior thyroid margin → hyoid | Suspends larynx; pierced by superior laryngeal artery, internal branch of superior laryngeal nerve |
| Hyo-epiglottic ligament | Epiglottis → hyoid body | Anchors epiglottis anteriorly |
| Cricotracheal ligament | Inferior cricoid → first tracheal ring | Joins larynx to trachea |
| Quadrangular membrane | Upper fibro-elastic membrane | Free inferior edge forms the vestibular (false vocal) fold |
| Conus elasticus (cricovocal membrane) | Lower fibro-elastic membrane | Free superior edge forms the vocal ligament (true vocal cord) |
| Median cricothyroid ligament | Midline portion of conus elasticus | Surgical access point for emergency cricothyrotomy |
Cavity of the Larynx
The laryngeal cavity is divided by the folds into three regions:
- Vestibule — above the vestibular (false) folds; the laryngeal inlet is its superior opening
- Ventricle (laryngeal sinus) — between the vestibular folds above and vocal folds below; extends laterally as the laryngeal appendix
- Infraglottic cavity — below the true vocal folds, continuous with the trachea
The rima glottidis is the gap between the two vocal folds; it widens during inspiration (posterior crico-arytenoid muscles — the only abductors of the vocal folds) and closes during phonation, swallowing, and effort closure.
Intrinsic Muscles and Their Functions
| Muscle | Action | Innervation |
|---|---|---|
| Posterior crico-arytenoid | Abducts vocal folds (opens rima glottidis) — sole abductor | Recurrent laryngeal n. |
| Lateral crico-arytenoid | Adducts vocal folds | Recurrent laryngeal n. |
| Transverse arytenoid | Adducts arytenoids | Recurrent laryngeal n. |
| Oblique arytenoid | Sphincter of laryngeal inlet | Recurrent laryngeal n. |
| Thyro-arytenoid (+ Vocalis) | Adducts and relaxes/tenses vocal folds | Recurrent laryngeal n. |
| Cricothyroid | Lengthens and tenses vocal folds (tilts thyroid forward on cricoid) | External branch of superior laryngeal n. |
The cricothyroid is the only intrinsic laryngeal muscle innervated by the superior laryngeal nerve (external branch); all others are supplied by the recurrent laryngeal nerve (branch of vagus [X]).
Blood Supply and Innervation
- Superior laryngeal artery (from superior thyroid artery of external carotid) — enters with the internal branch of the superior laryngeal nerve through the thyrohyoid membrane
- Inferior laryngeal artery (from inferior thyroid artery of thyrocervical trunk) — ascends with the recurrent laryngeal nerve in the tracheo-esophageal groove
- Sensory innervation: above the vocal folds — internal branch of superior laryngeal nerve; below — recurrent laryngeal nerve
- Motor innervation: all intrinsic muscles via recurrent laryngeal nerve (except cricothyroid via external branch of superior laryngeal nerve)
2. Physiology of the Larynx
The larynx performs three key physiological functions:
2.1 Respiration
During quiet breathing, the rima glottidis is open in a triangular configuration with abducted arytenoids. During forced inspiration, the posterior crico-arytenoid muscles rotate the arytenoids laterally, widening the rima to a rhomboid shape and maximizing airway diameter. During effort closure (e.g., heavy lifting, raising intra-abdominal pressure for defecation/parturition), the rima glottidis is completely sealed at both the level of the vocal folds (rima glottidis) and vestibular folds (rima vestibuli).
2.2 Phonation
The vocal folds are adducted and air from the lungs is forced through the closed rima glottidis. This causes the folds to vibrate, producing sound. Pitch is controlled by tension in the vocal ligaments, regulated by the cricothyroid muscle (increased tension = higher pitch) and vocalis muscle. Volume depends on the force of expiratory airflow.
2.3 Swallowing (Airway Protection)
During deglutition, the larynx moves up and forward, the rima glottidis and vestibule close, the laryngeal inlet narrows, and the epiglottis swings posteroinferiorly to cover the inlet. Simultaneously, the forward movement opens the esophageal entrance. Food passes through the piriform fossae into the esophagus.
3. Methods of Laryngeal Research / Examination
3.1 Indirect Mirror Laryngoscopy
The simplest, fastest, and least expensive method. A small rod-mounted mirror is introduced into the oropharynx, and the larynx is illuminated via a head mirror or headlight. It allows visualization of the epiglottis, aryepiglottic folds, arytenoids, vestibular folds, true vocal cords, and upper tracheal rings. The glare-free view permits observation of subtle color variations. Note that the image is mirror-reversed. It requires patient cooperation and may be impossible in patients with a strong gag reflex. — Pfenninger and Fowler's Procedures for Primary Care
3.2 Direct Laryngoscopy
Performed with a rigid laryngoscope introduced directly into the larynx. Provides excellent visualization for biopsy, foreign body removal, and surgical procedures. Usually performed under general anesthesia.
3.3 Flexible Nasolaryngoscopy (Fiberoptic/Video)
A flexible fiberoptic or video nasendoscope is passed transnasally into the hypopharynx, permitting direct visualization in the awake patient. Allows dynamic assessment of vocal cord movement, laryngeal inlet, and detection of mucosal lesions. It is complementary to rigid telescopy — both methods together are recommended in the professional voice patient. — Cummings Otolaryngology
3.4 Rigid Telescopy (70° or 90° telescope)
Provides high-resolution, magnified images of the larynx. Particularly useful for stroboscopy (synchronized strobe light to analyze vocal fold mucosal wave, revealing early lesions not apparent under continuous light).
3.5 Stroboscopy
Combines rigid or flexible laryngoscopy with a strobe light to visualize vocal fold vibration in apparent slow motion. Detects subtle mucosal lesions, scarring, and vocalis muscle pathology.
3.6 Imaging
- CT scan with contrast (CECT): Best for assessing deep tissue invasion in laryngeal tumors, cartilage destruction, subglottic extension, and nodal disease. Also detects hematoma, laryngoceles, and fractures (bone windows for ossified cartilage).
- MRI: Particularly useful for coronal assessment of craniocaudal tumor extent in the glottic/supraglottic larynx, and for evaluating the preepiglottic and paraglottic fat spaces.
- Fat planes in the preepiglottic space and paralaryngeal fat are major landmarks easily identified on CT and MRI. — Cummings Otolaryngology / Grainger & Allison's Diagnostic Radiology
3.7 Microlaryngoscopy
Laryngoscopy under general anesthesia using a laryngoscope and operating microscope, for diagnosis and surgical treatment of vocal cord lesions.
4. Acute Diseases of the Larynx
4.1 Acute Laryngitis
Etiology: Allergic, viral, bacterial, or chemical insult; often associated with upper respiratory tract infection, heavy tobacco smoke exposure, or gastroesophageal reflux.
Pathophysiology: Mucosal congestion, exudation, and edema. Most infections are self-limited. In infants and young children, the small airway dimensions mean that even mild mucosal swelling can produce critical airway obstruction — a medical emergency.
Clinical features: Hoarseness, dysphonia, dry cough, sore throat, odynophagia.
Treatment: Voice rest, humidification, hydration; antibiotics if bacterial superinfection; treat underlying GERD. — Robbins, Cotran & Kumar Pathologic Basis of Disease
4.2 Acute Epiglottitis (Supraglottitis)
Etiology: Historically caused by Haemophilus influenzae type b (Hib); now rare in vaccinated populations. Also caused by β-hemolytic streptococci. Can occur at any age; historically predominantly in children aged 2–5.
Pathophysiology: Acute bacterial infection causing massive inflammatory edema of the epiglottis and aryepiglottic folds, potentially causing complete airway obstruction. Onset is rapid and severe.
Clinical features: Sudden high fever, severe sore throat, dysphagia, drooling, inspiratory stridor, the "tripod" or "sniffing" position. The "thumbprint sign" on lateral neck X-ray (swollen epiglottis).
Differentiation from diphtheria: Acute epiglottitis has a more rapid onset and laryngoscopy reveals an erythematous, edematous epiglottis without membrane formation — in contrast to diphtheria. — Rosen's Emergency Medicine
Management: Secure the airway immediately (intubation or tracheostomy); IV antibiotics (3rd-generation cephalosporin); corticosteroids; ICU monitoring.
4.3 Croup (Laryngotracheobronchitis)
Etiology: Parainfluenza virus (most common), RSV, adenovirus. Children aged 6 months – 3 years.
Pathophysiology: Subglottic mucosal edema (the narrowest part of the pediatric airway) causes the characteristic bark-like cough and inspiratory stridor.
Clinical features: Preceded by 1–2 days of URTI; then barking cough, hoarseness, low-grade fever, inspiratory stridor. The "steeple sign" on AP neck X-ray (subglottic narrowing).
Management: Nebulized epinephrine for acute distress; corticosteroids (dexamethasone); humidified oxygen. Most cases are mild and self-limited. — Robbins, Cotran & Kumar
4.4 Laryngotracheitis / Laryngotracheobronchitis
Croup extending below into the trachea and bronchi; same viral etiology with more diffuse respiratory involvement.
5. Laryngeal Edema
Definition
Abnormal accumulation of fluid in the submucosal tissues of the larynx. The supraglottic larynx (especially epiglottis, aryepiglottic folds, and arytenoids) is most susceptible due to its loose submucosal connective tissue. The true vocal folds contain little submucosa and are rarely edematous in isolation.
Etiology and Classification
| Category | Causes |
|---|---|
| Inflammatory/Infectious | Acute epiglottitis, croup, diphtheria, peritonsillar/retropharyngeal abscess, Ludwig's angina |
| Allergic / Angioedema | Anaphylaxis (type I hypersensitivity to foods, drugs, insect venom), hereditary angioedema (C1-inhibitor deficiency), ACE inhibitor–induced |
| Traumatic | Inhalation burns, caustic ingestion, prolonged endotracheal intubation, post-extubation |
| Iatrogenic/Post-intubation | Post-extubation edema; especially children (no cricoid ring accommodation) |
| Neoplastic/Compressive | Lymphoma, thyroid mass, tumor |
| Systemic | Severe hypothyroidism (myxedema), cardiac failure, hypoalbuminemia |
Pathophysiology
Inflammatory or allergic mediators (histamine, bradykinin, prostaglandins, cytokines) increase vascular permeability in the laryngeal submucosa, causing rapid accumulation of protein-rich fluid. In allergic angioedema, bradykinin-mediated increase in vascular permeability (NOT histamine-mediated) is the key mechanism — this explains why antihistamines alone are insufficient and why ACE inhibitor–induced angioedema (which prevents bradykinin breakdown) may not respond to epinephrine.
Clinical Features
- Hoarseness, muffled ("hot potato") voice or aphonia
- Inspiratory stridor (high-pitched; indicates supra- or glottic obstruction)
- Dysphagia, drooling
- Respiratory distress: tachypnea, use of accessory muscles, intercostal retraction
- Cyanosis in severe cases (pre-terminal sign)
- In anaphylaxis: associated urticaria, flushing, hypotension, bronchospasm
Degrees of Severity / Grading of Dyspnea (Laryngeal Obstruction)
| Grade | Features |
|---|---|
| I (compensated) | Stridor at rest absent or mild; SpO2 normal; minor use of accessory muscles |
| II | Moderate stridor at rest; mild tachypnea; some accessory muscle use |
| III | Severe stridor; marked dyspnea; cyanosis; anxiety/agitation |
| IV | Severe cyanosis; gasping; altered consciousness; impending respiratory arrest |
Management
- Assess airway urgency — the priority is securing the airway before it closes completely
- Anaphylactic/allergic edema: IM epinephrine (0.3–0.5 mg, 1:1000) — first-line; IV/IM corticosteroids; IV antihistamines (H1 + H2 blockers); nebulized racemic epinephrine
- Infectious: appropriate antimicrobials; IV corticosteroids to reduce swelling; nebulized epinephrine
- Airway intervention: endotracheal intubation (performed in OR when possible); if intubation fails — emergency cricothyrotomy or tracheostomy
- Position: sit upright; avoid any intervention that may cause patient to close airway (do not examine throat forcefully if epiglottitis suspected in child)
6. Laryngeal Stenosis
Definition
Narrowing of the laryngeal lumen, which may be acute (dynamic/functional) or chronic (structural/fibrotic). May involve the supraglottic, glottic, or subglottic regions.
Etiology
| Type | Causes |
|---|---|
| Post-intubation / Post-tracheostomy | Most common cause; prolonged intubation causes mucosal ulceration → chondritis → fibrous cicatricial stenosis; subglottic level most commonly affected |
| Inflammatory / Autoimmune | Wegener's granulomatosis (GPA) — subglottic stenosis in ~15–23%; relapsing polychondritis; sarcoidosis; amyloidosis |
| Infectious | Diphtheria, tuberculosis, histoplasmosis, scleroma |
| External trauma | Blunt or penetrating neck trauma; fracture/dislocation of laryngeal cartilages |
| Thermal / Chemical | Inhalation injury; caustic ingestion; radiation therapy |
| Neoplastic | Primary or secondary laryngeal tumors |
| Congenital | Subglottic stenosis (congenital narrowing of the cricoid ring) |
Clinically important: Post-intubation glottic/subglottic stenosis follows mucosal inflammation and ulceration → exposed cartilage → perichondritis → granulation tissue → cicatricial (fibrotic) narrowing. Risk factors include intubation duration >72 hours, large ETT relative to larynx, excessive cuff pressure (>30 mmHg), patient agitation, GERD. — Morgan and Mikhail's Clinical Anesthesiology
Classification (Cotton-Myer Grading for Subglottic Stenosis)
| Grade | Lumen Obstruction |
|---|---|
| I | ≤50% |
| II | 51–70% |
| III | 71–99% |
| IV | Complete obstruction (atresia) |
Clinical Features
- Acute: stridor (biphasic in severe cases), dyspnea, respiratory distress
- Chronic: progressive dyspnea on exertion advancing to dyspnea at rest; dysphonia (if glottic involvement); recurrent pneumonias; stridor
- Patient often presents with exertional dyspnea years after a precipitating event (e.g., intubation), frequently misdiagnosed as asthma
Investigations
- Flexible laryngoscopy/nasendoscopy — visualize stenosis and assess vocal fold mobility
- CT of larynx and trachea — define level, length, and degree of stenosis
- Pulmonary function tests — flow-volume loop shows characteristic fixed upper airway obstruction pattern (flat inspiratory and expiratory plateaus)
- Bronchoscopy under general anesthesia — definitive assessment
Management
| Approach | Indication |
|---|---|
| Laser (CO2) endoscopic resection + dilation | Thin web-like stenosis, Grade I–II |
| Endoscopic balloon dilation | Post-intubation soft/immature stenosis |
| Open laryngotracheal reconstruction | Grade III–IV, complex long-segment stenosis; involves cricoid cartilage with rib/costal cartilage graft |
| Cricotracheal resection and anastomosis | Mature subglottic stenosis; excellent outcomes |
| Tracheostomy | Temporizing measure; bypasses obstruction |
Tracheostomy itself may later contribute to tracheal stenosis and should be decannulated as soon as possible. Post-tracheostomy complications include tracheomalacia, tracheo-innominate fistula, and tracheal stenosis. — Fishman's Pulmonary Diseases
7. Diphtheria of the Larynx
Etiology
Caused by Corynebacterium diphtheriae, a gram-positive, pleomorphic bacillus that produces a potent A-B exotoxin (diphtheria toxin) encoded by a bacteriophage gene. The toxin inhibits protein synthesis by ADP-ribosylation of elongation factor EF-2 (EF-Tu in prokaryotes), causing cell death in heart, nerves, and kidneys.
Epidemiology and Pathogenesis
Transmission is via respiratory droplets. The incubation period is 2–4 days (range 1–8 days). The organism colonizes the upper respiratory mucosa, producing a local inflammatory reaction and the characteristic pseudomembrane. The membrane starts as a thin exudate and thickens into a tough, grayish, leathery membrane that is tightly adherent to the underlying mucosa and bleeds when removed. Systemic toxin absorption causes myocarditis, polyneuropathy, and tubular necrosis.
Forms of Diphtheria
| Form | Features |
|---|---|
| Faucial (tonsillo-pharyngeal) | Most common (70%); gray pseudomembrane on tonsils/posterior pharynx; "bull-neck" from cervical adenopathy + soft tissue edema |
| Nasal | Serous or serosanguineous nasal discharge; membrane visible; usually mild |
| Laryngeal | May arise primarily or by downward spread from pharynx; most dangerous airway complication |
| Tracheobronchial | Extension of membrane; rapid airway compromise |
| Cutaneous | Chronic ulcer with grayish membrane; no systemic toxicity |
Laryngeal Diphtheria — Specific Features
- Presents as progressive hoarseness, barking cough, then inspiratory stridor
- The pseudomembrane spreads to cover the vocal cords and subglottis
- Respiratory tract edema with subsequent upper airway obstruction may develop — the leading cause of death in untreated laryngeal diphtheria
- "Croup of diphtheria" historically described — the thick membrane can cast off and cause sudden complete obstruction
Bull-neck sign: Massive cervical lymphadenopathy with brawny soft-tissue edema of the neck — indicates severe toxin-producing infection with high mortality.
Diagnosis
Clinical Case Definition:
- Suspect case: Pharyngitis/laryngitis with low-grade fever + adherent gray pseudomembrane that bleeds when manipulated
- Probable case: Above + stridor, bull-neck, toxic circulatory collapse, myocarditis, or relevant epidemiological link
Laboratory:
- Throat and nasopharyngeal swabs on tellurite selective culture medium (routine cultures do NOT identify C. diphtheriae — laboratory must be notified)
- Colony morphology + microscopy + fermentation reactions for definitive ID
- Elek test (CDC) for toxin A; PCR for toxin structural gene (more sensitive)
- ECG: ST-T wave changes, AV block; Troponin: elevated with myocarditis
- Leukocytosis, mild thrombocytopenia, proteinuria (common but nonspecific)
Differential Diagnosis of Respiratory Diphtheria:
Streptococcal pharyngitis, viral pharyngitis (EBV, adenovirus, HSV), infectious mononucleosis, tonsillitis, acute epiglottitis, candidiasis (thrush), peritonsillar abscess, ANUG
Key distinguishing features of diphtheria membrane: darker gray, more fibrous, more firmly adherent, bleeds on removal — unlike the white-yellow looser exudate of streptococcal or viral tonsillitis. Epiglottitis has rapid onset without membrane. — Rosen's Emergency Medicine
Complications
| Complication | Onset | Notes |
|---|---|---|
| Airway obstruction | Early | Primary cause of early death |
| Myocarditis | 1–2 weeks | Dilated or hypertrophic cardiomyopathy; AV block; mortality 7% |
| Malignant diphtheria (with bull-neck) | Early | 26% mortality |
| Demyelinating polyneuropathy | 2–8 weeks | Palatal palsy (nasal voice, regurgitation) → oculomotor palsy → peripheral motor neuropathy; diaphragmatic paralysis |
| Tubular necrosis | Variable | Acute renal insufficiency |
| Cardiac conduction disturbances | 1–2 weeks | All degrees of AV block, dysrhythmias |
Management
- Respiratory isolation — immediately
- Secure the airway — early intubation for laryngeal involvement; tracheostomy if membrane prevents intubation
- Diphtheria antitoxin (DAT) — neutralizes unbound toxin; most critical intervention; given as soon as clinical diagnosis is made (do not wait for culture); dose based on site, severity, and duration of illness; administer IV or IM after sensitivity testing
- Antibiotics — eliminate the organism and halt toxin production:
- Penicillin G (IV/IM) or amoxicillin (oral) for 14 days
- Erythromycin or azithromycin (for penicillin allergy) for 14 days
- Cardiac monitoring — ECG, troponin; treat arrhythmias; pacemaker for complete AV block
- Fluid management — assess for fluid responsiveness; the toxin's myocardial effect may result in heart failure
- Vaccination — post-recovery vaccination (infection may not confer lasting immunity); household contacts — prophylaxis and immunization
Key principle: Antitoxin must be given immediately on clinical grounds — laboratory confirmation takes too long and circulating toxin must be neutralized before it is internalized by cells. — Rosen's Emergency Medicine
Summary Table: Acute Laryngeal Diseases
| Disease | Age | Causative Agent | Onset | Key Feature | Stridor | Membrane | Treatment |
|---|---|---|---|---|---|---|---|
| Acute laryngitis | Any | Viral/bacterial/reflux | Gradual | Hoarseness | Absent | None | Voice rest, symptomatic |
| Croup | 6 mo – 3 yr | Parainfluenza virus | Gradual | Barking cough, steeple sign | Inspiratory | None | Dexamethasone, nebulized epinephrine |
| Epiglottitis | 2–7 yr (any) | H. influenzae type b | Sudden | Drooling, tripod, thumbprint sign | Inspiratory | None | Airway, IV antibiotics |
| Laryngeal edema | Any | Anaphylaxis, allergy, burns | Minutes–hours | Variable; anaphylaxis signs | Inspiratory | None | Epinephrine, steroids, airway |
| Laryngeal stenosis | Any | Post-intubation, trauma, GPA | Gradual | Fixed airway obstruction | Biphasic | None | Endoscopic/open repair, tracheostomy |
| Laryngeal diphtheria | Unvaccinated | C. diphtheriae | Gradual (2–4 days) | Gray adherent pseudomembrane, bull-neck | Inspiratory | Yes (gray, bleeds) | Antitoxin + antibiotics + airway |
Sources:
- Gray's Anatomy for Students (anatomy, physiology, laryngoscopy sections)
- Cummings Otolaryngology Head and Neck Surgery (imaging, physical examination, voice)
- Robbins, Cotran & Kumar Pathologic Basis of Disease (inflammatory lesions, croup, diphtheria)
- Rosen's Emergency Medicine (diphtheria clinical features, management, differential diagnosis)
- Morgan and Mikhail's Clinical Anesthesiology (post-intubation complications, stenosis)
- Fishman's Pulmonary Diseases and Disorders (post-tracheostomy complications)
- Pfenninger and Fowler's Procedures for Primary Care (indirect mirror laryngoscopy)
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