Laryngeal stenosis refers to a pathological condition characterized by the narrowing or obstruction of the laryngeal lumen due to various causes, resulting in impaired breathing and phonation. This condition is relatively common and shows a trend of increasing incidence. It is often a composite lesion involving both the larynx and the cervical segment of the trachea, particularly in cases of subglottic scar-related stenosis that frequently extends to the cervical trachea. This condition is referred to as laryngeal and tracheal stenosis and is classified as either congenital or acquired.
Etiology
Congenital Causes
These are primarily observed in neonates and young children and include conditions such as laryngomalacia, vocal cord paralysis, laryngeal web, stenotic laryngeal malformations, vascular anomalies causing compression, tracheomalacia, and laryngotracheoesophageal clefts.
Trauma
Traumatic causes include closed or open laryngeal injuries, high tracheostomy, partial laryngectomy, long-term endotracheal intubation, excessive cuff pressure, or oversized tracheostomy tubes. Such trauma can result in damage to the laryngeal cartilaginous framework, mucosal injuries, or hematoma formation, which subsequently leads to collagen deposition and scar formation during the organization of the hematoma.
Chemical and Physical Injuries
These include injuries from laryngeal radiotherapy and chemical burns caused by strong acids or alkalis.
Specific Inflammatory Conditions
Conditions such as syphilis, tuberculosis, lupus, leprosy, and scleroderma can lead to scar formation and result in laryngeal stenosis after healing.
Nonspecific Inflammatory Conditions
Granulomatosis with polyangiitis (Wegener’s granulomatosis), collagen vascular diseases, and post-necrosis laryngeal chondritis can cause scarring and narrowing of the laryngeal or tracheal lumen.
Pathophysiology
The laryngeal mucosa provides the blood supply for the laryngeal cartilage and acts as its protective barrier. In cases of trauma or other pathological conditions resulting in mucosal damage, this barrier is disrupted, allowing bacterial invasion. This can lead to inflammation of the laryngeal cartilage and perichondrium, cartilage destruction, or even cartilage loss.
Inflammation triggers exudation, granulation tissue growth, and fibrosis, leading to scar formation and airway remodeling. Loss of laryngeal cartilage further exacerbates narrowing or complete closure of the laryngeal airway.
Classification
Classification by Location
This condition can be classified into:
- Supraglottic stenosis: Commonly caused by chemical burns to the larynx or cervical trauma (e.g., vehicular accidents).
- Glottic stenosis: Often results from vocal fold mucosal loss due to direct laryngoscopy or vocal cord surgery, leading to anterior commissure adhesion.
- Subglottic stenosis: The most frequently encountered type.
- Laryngeal and tracheal stenosis: Stenosis may extend from the supraglottic region to the subglottic region and/or the cervical trachea.
Classification by Severity (Myers-Cotton Classification)
This condition can be classified into:
- Grade I: Lumen obstruction occupies 0%–50% of the total lumen area.
- Grade II: Lumen obstruction occupies 51%–70% of the total lumen area.
- Grade III: Lumen obstruction occupies 71%–99% of the total lumen area.
- Grade IV: Complete airway obstruction.
Grades I and II are classified as mild stenosis, while Grades III and IV are classified as severe stenosis.
Clinical Manifestations
Hoarseness or Voice Loss
Glottic stenosis typically presents with hoarseness, weak voice, or aphonia. In cases of stenosis involving both the glottis and adjacent regions with accompanying vocal cord paralysis, hoarseness may also occur along with choking and coughing. Severe subglottic or tracheal stenosis or complete obstruction can result in aphonia due to airway blockage.
Stridor and Cough
Accumulated secretions may provoke paroxysmal coughing. Inspiratory stridor occurs due to airflow obstruction, which becomes worse during sleep.
Dyspnea
The degree of dyspnea varies with the severity of the stenosis. Symptoms may be minimal at rest but worsen with activity. As laryngeal stenosis often develops gradually, patients may adapt to mild dyspnea and experience no sense of breathlessness until the condition becomes severe, ultimately leading to cyanosis or even suffocation. Patients with an existing tracheostomy may experience difficulty in tube occlusion or decannulation.
Laryngoscopic examination often reveals bands, membranes, or rings of scar tissue in the larynx or trachea. These may affect the supraglottic, glottic, or subglottic regions. Deformation of the laryngeal lumen, vocal cord fixation, deformity of the ventricular folds and vocal folds, narrowing or closure of the glottis, adhesion in the subglottic region, and cervical tracheal stenosis may also be observed. In some cases, only small openings remain, with retained viscous secretions.
Diagnosis
The gradual progression of the disease, combined with history, symptoms, and findings from laryngoscopic or tracheostomy examinations, generally facilitates diagnosis. Imaging studies such as lateral neck radiographs or CT scans can identify the location, extent, and severity of the stenosis. Contrast-enhanced CT or MRI may be used to determine the presence of any space-occupying lesions in the larynx or trachea. For patients with unexplained laryngeal or tracheal stenosis, evaluations for autoimmune diseases may be necessary. Differential diagnoses include vocal cord paralysis and laryngeal masses.
Treatment
Medication
Corticosteroids and zinc sulfate may be used to suppress scar formation.
Surgical Intervention
The choice of surgical procedure depends on the underlying cause, location, and severity of the stenosis.
For mild stenosis, microinstruments or a CO2 laser may be used via suspension laryngoscopy to remove scar tissue, followed by balloon dilatation of the stenotic segment. The lumen's width determines the placement of an appropriately sized T-shaped silicone tube through the tracheostomy site to prevent scar retraction and restenosis. The T-tube is typically retained for three months.
For severe stenosis, low tracheostomy may be performed initially. If the cartilaginous framework is relatively intact, laryngotracheal reconstruction can be conducted using autologous cartilage or muscle-pedicled flaps (e.g., sternohyoid muscle-hyoid flap or sternocleidomastoid muscle-periosteal flap). A T-tube is generally retained for over three months. In cases of significant cricoid or tracheal framework defects, partial resection of the cricoid or trachea may be performed, followed by end-to-end anastomosis of normal airway segments. The T-tube is retained for at least 12 months.