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).
An image depicting subglottic stenosis can be seen below.
View Image | Preoperative view of subglottic stenosis via an endoscopic approach. |
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.
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:
A retrospective study by Fang et al found that among 41 patients with idiopathic subglottic stenosis who underwent esophageal pH impedance testing, 19 (46.3%) had gastroesophageal reflux disease, including 15 (36.6%) who had a predominantly upright reflux condition.[2]
A study by Gnagi et al found that time to diagnosis differed significantly between patients with acquired subglottic stenosis and those with idiopathic subglottic and tracheal stenosis. While 32% of the acquired stenosis patients were diagnosed within 3 months of symptom onset, just 2% of the other group were diagnosed within this time. The study involved a total of 160 patients.[3]
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:
See the list below:
See the list below:
See the list below:
See the list below:
Any underlying medical cause must be addressed (eg, control of infectious etiology, inflammatory causes such as Wegener granulomatosis).
This includes the following
Use of systemic steroids in early stenosis is an option but has not been thoroughly investigated. In active inflammatory states of the subglottis, such as that manifesting as granulation tissue, inhaled steroids are of potential benefit (eg, fluticasone propionate [Flovent HFA 220 mcg], two puffs twice a day for 2 weeks; this is an off-label use based on the author's own experience).
Transcervical or transoral (via a channeled scope) injection of steroids such as triamcinolone acetonide (Kenalog-40) is now being used by many centers, with good early results in the control of subglottic inflammation and, in some cases, diminution of the subglottic scar.
The interval of injection has not been fully elucidated and varies from once a month for 6 months, then every 6 months afterward as needed (Simpson, CB; San Antonio, Texas; personal communication), to every three months as needed (author's experience). Although early reports have suggested that this approach is safe and effective, the steroids' long-term effects on cartilage integrity is unknown.[4, 5, 6]
Steroid injection may offer improvement in surgical interval or even serve as a primary treatment in minor grade stenosis in adults.
See the list below:
These include the following:
A study by Deckard et al indicated that, as in pediatric patients, two-stage laryngotracheal reconstruction (LTR) can be successfully used to treat subglottic stenosis in adults, offering a means to avoid the complications of cricotracheal resection. In the study, 14 adult patients, most of whom had high-grade (grade III or IV) stenosis, underwent LTR, with 12 of them achieving decannulation. One of these patients, however, subsequently required salvage surgery and was decannulated again only after cricotracheal resection. Thus, 11 patients (79%) achieved decannulation with LTR alone.[7]
See the list below:
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.
See the list below:
View Image | Postoperative view of subglottic stenosis after 4-quadrant carbon dioxide laser division and endoscopic balloon dilation. Note the excellent view of d.... |
See the list below:
See the list below:
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.
In a study of 109 patients with subglottic stenosis, D’Andrilli et al reported that the long-term results of laryngotracheal resection demonstrate it to be the definitive curative treatment for the condition, with 94.5% of the patients having good to excellent outcomes from the surgery.[8]
End-to-end anastomosis was found to be successful in 80-90% of cases. Mortality was reported at 10-20%; it has decreased with experience. Morbidity is 20-50%, secondary to the effect on laryngeal function and swallowing.
Successful case rates of 60-96% have been reported. Grafts are susceptible to infection, resorption, displacement, and extrusion.