Updated: Feb 8, 2008
Partial or complete narrowing of the subglottic area may be congenital or acquired. The problem is rare and challenging, affecting soft tissue and cartilage support.
Iatrogenic injuries cause most of the problems seen. Often, subglottic stenosis has an insidious onset, and early manifestations are usually mistaken for other disorders (eg, asthma, bronchitis).
Congenital
Stenosis is said to be congenital in the absence of a history of intubation or other acquired causes. Congenital laryngeal webs account for approximately 5% of congenital anomalies of the larynx, with 75% occurring at the glottic level and the rest occurring at the subglottic or supraglottic level. Most severe cases are diagnosed in childhood.
Acquired
Trauma is the most common cause of stenosis in both children and adults. Approximately 90% of all cases of acquired chronic subglottic stenosis in children and adults result from endotracheal intubation. The reported rate of stenosis following intubation ranges from 0.9-8.3%.
Intubation causes injury at the level of the glottis due to pressure between the arytenoid cartilages. Intubation causes injury in the subglottis due to the complete cartilaginous ring or can cause injury distally in the trachea. Pressure and/or motion of the tube against the cartilage framework may cause ischemia and necrosis.
Duration of intubation is the most important factor in the development of stenosis. Severe injury has been reported after 17 hours, but it may occur much sooner. A 7-10 day period of ICU intubation is acceptable, but the risk of laryngotracheal injury increases drastically after that.
Size of the tube is also important. Tubes should be no larger than 7-8 mm in internal diameter for adult males. Tubes should be no larger than 6-7 mm in internal diameter for adult females. The size of the endotracheal tube needed correlates best with the patient's height.
Stenosis could also be secondary to foreign body, infection, inflammation, or chemical irritation. Respiratory epithelium is susceptible to injury. Initial edema, vascular congestion, and acute inflammation can progress to ulceration and local infection with growth of granulation tissue. Finally, fibroblast proliferation, scar formation, and contracture can occur and result in stenosis.
Systemic factors may increase the risk of injury and include the following:
Other causes include the following:
Chronic inflammatory diseases include the following:
Congenital stenosis has two main types, membranous and cartilaginous.
In membranous stenosis, fibrous soft tissue thickening is caused by increased connective tissue or hyperplastic dilated mucus glands with absence of inflammation. Membranous stenosis is usually circumferential and may extend upward to include the true vocal folds.
In cartilaginous stenosis, a thickening or deformity of the cricoid cartilage most commonly occurs, causing a shelflike plate of cartilage and leaving a small posterior opening. Cartilaginous stenosis is less common than membranous stenosis.
Acquired subglottic stenosis is secondary to localized trauma to subglottic structures. Usually, injury is caused by endotracheal intubation or high tracheostomy tube placement. If irritation persists, the original edema and inflammation progress to ulceration and granulation tissue formation. This may or may not involve chondritis with destruction of the underlying cricoid cartilage and loss of framework support.
When the source of irritation is removed, healing occurs with fibroblast proliferation, scar formation, and contracture, leading to stenosis or complete occlusion of the airway.
Adults with mild congenital stenosis are usually asymptomatic, and they are diagnosed after a difficult intubation or while undergoing endoscopy for other reasons.
Patients with acquired stenosis are diagnosed from a few days to 10 years or more following initial injury. The majority of cases are diagnosed within a year. Symptoms include the following:
Many patients would have been diagnosed with asthma and recurrent bronchitis prior to discovery of stenosis. A high index of suspicion is warranted with the onset of respiratory symptoms following intubation, regardless of the duration of intubation.
Indications for treatment are to improve compromised airways and progress toward decannulation. Speedy intervention prior to cartilage damage or scar contracture is preferred when the diagnosis is made early.
The subglottic area is circumferentially bound by the cricoid cartilage, which is part of the larynx. The adult trachea is 10-13 cm long and 17-24 mm in diameter and extends from the inferior border of the cricoid cartilage to the carinal spur.
The first tracheal cartilage is partly inset in the lower border of the cricoid and, on occasion, may be fused with it. All of the tracheal rings are incomplete posteriorly.
Primarily, arterial supply to the larynx comes from branches of the superior and inferior thyroid arteries. The superior thyroid artery sends a superior laryngeal branch through the thyrohyoid membrane. The inferior thyroid artery sends an inferior laryngeal branch with the recurrent laryngeal nerve to enter the larynx near the cricothyroid joint.
The tracheal blood supply is segmental. Branches of the inferior thyroid artery supply the upper trachea. Branches of the bronchial arteries, with contributions from subclavian, supreme intercostal, internal thoracic, and innominate arteries, supply the lower trachea. The branches arrive to the trachea via lateral pedicles.
Sensory innervation to the subglottic mucosa is by the recurrent laryngeal nerve. The thyroid gland is adherent to the trachea at the second and third tracheal rings, but the lateral lobes overlie the cricoid cartilage and can approximate the lower lateral thyroid laminae.
Most contraindications are relative and include the following:
Contraindications specific to long-term tracheostomy are debatable and include the following:
Contraindications reported for open repair include the following:
In the endoscopic management of the stenosis, mitomycin-C has become routinely used. The concentration is usually 0.4mg/ml and is applied topically on a cottonoid pledget. The length of application varies from 2-3 repeat applications of 2 minutes each to a single application of 5 minutes.
The handling and disposal of the mitomycin-C should be per the hospital protocol for chemotherapeutic agents. Care should be taken to avoid contact with unprotected skin.
Overall goals are improvement of airway function and preservation of laryngeal function.
The endoscopic approach was found to be successful in 57-90% of cases.
Intraluminal stents were found to be successful in 80% of cases.
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subglottic stenosis in adults, subglottic stenosis, acquired glottic stenosis, congenital glottic stenosis, narrowing of the subglottic area, acquired chronic subglottic stenosis, intubation, glottis, membranous stenosis, cartilaginous stenosis
James D Garnett, MD, Director of Voice and Swallowing Center, Associate Professor, Department of Otolaryngology-Head and Neck Surgery, University of Kansas Medical Center
James D Garnett, MD is a member of the following medical societies: American Academy of Otolaryngic Allergy and American Academy of Otolaryngology-Head and Neck Surgery
Disclosure: Nothing to disclose.
Anthony P Sclafani, MD, Director of Facial Plastic Surgery, The New York Eye and Ear Infirmary; Professor of Otolaryngology, New York Medical College
Anthony P Sclafani, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American College of Surgeons
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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Robert M Kellman, MD, Professor and Chair, Department of Otolaryngology and Communication Sciences, State University of New York Upstate Medical University
Robert M Kellman, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Physician Executives, American College of Surgeons, American Medical Association, American Society for Head and Neck Surgery, and Medical Society of the State of New York
Disclosure: Nothing to disclose.
Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.
Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: Advanced Headache Intervention Consulting fee Consulting; Covidien Corp Consulting fee Consulting
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