Laryngeal stenosis is a congenital or acquired narrowing of the airway that may affect the supraglottis, glottis, and/or subglottis. It can be defined as a partial or circumferential narrowing of the endolaryngeal airway and may be congenital or acquired. The subglottis is the most common site of involvement.
A formal endoscopic evaluation of the airway in the operating room is an essential part of evaluation. Treatment via an endoscopic or an open surgical approach is dependent on the patient’s symptoms, site of involvement, and the degree of stenosis. See the image below.
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Anatomical regions of the larynx.
Congenital laryngeal stenosis
Congenital laryngeal stenosis results from failure of the laryngeal lumen to recanalize. During normal development, the laryngeal lumen is obliterated to give rise to the epithelial lamina, which later recanalizes. By the 10th week of gestation, the laryngeal lumen is reestablished following recanalization. Incomplete recanalization results in various degrees of glottic and/or subglottic stenosis.
Congenital laryngeal atresia represents the most severe end of the spectrum of disease, arising from failed recanalization of the larynx and trachea during embryogenesis. Atresia can be diagnosed prenatally based on ultrasound by identifying signs of congenital high airway obstruction syndrome (CHAOS). Glottic and supraglottic atresia requires immediate tracheotomy at the time of delivery. Prenatal diagnosis of CHAOS allows for the use of the ex utero intrapartum treatment (EXIT) procedure to evaluate and secure the airway at birth. Laryngotracheal reconstruction to repair the atresia is necessary at a later stage.
Congenital laryngeal webs account for about 5% of congenital laryngeal anomalies. Seventy-five percent of these are at the glottic level. Treatment varies depending on the nature of the web and associated symptoms, ranging from division of thin membranous webs, staged dilations following incision, keel placement, open laryngotracheal reconstruction, and tracheostomy. Laryngeal webs often involve both the glottis and subglottis and may rarely involve the supraglottis. Glottic stenosis may also result from impaired vocal cord mobility or, rarely, complete fusion of the true vocal folds.
Congenital subglottic stenosis is the third most common congenital laryngeal anomaly after laryngomalacia and vocal fold paralysis. It is diagnosed where subglottic narrowing exists with no history of intubation or surgical trauma. Distinguishing congenital from acquired stenosis once a child has been intubated is difficult, but the suspected incidence is 5%. Congenital stenosis can be a contributing factor to acquired laryngeal stenosis.
Congenital subglottic stenosis may be divided into 2 types: membranous (fibrosis, submucous gland hyperplasia, granulation tissue) and cartilaginous. Membranous stenosis is more common than cartilaginous stenosis. Most commonly, membranous stenoses are circumferential and symmetric and may extend upward to include the true vocal cords. Cartilaginous stenosis is a deformity of the cricoid cartilage or tracheal ring projecting into the lumen. It may be symmetric (small but normal shaped cricoid or a nondistensible complete first tracheal ring trapped inside the cricoid) or asymmetric (elliptic or oval-shaped cricoid, isolated enlargement of either the anterior or posterior cricoid lamina, or laryngeal cleft).
Congenital subglottic stenosis is defined as a subglottic diameter of 4 mm or less in a full-term neonate (< 3.5 mm in the premature neonate). Diagnosis depends on exclusion of acquired stenosis.
Treatment is individualized. Mild cases of stenosis (grade I) are typically managed with a conservative approach consisting of regular follow-up care and aggressive medical management of upper respiratory infections.
Most patients with greater than 50% obstruction are likely to require some surgical intervention. These include both endoscopic (dilation, laser resection) and external approaches to cricoid expansion. Laser resection and dilation are rarely effective if the stenosis is cartilaginous.
Acquired laryngeal stenosis
Instrumentation of the airway for nonlaryngeal and nontracheal illnesses remains a primary cause for laryngeal stenoses. External trauma and infection have been supplanted by iatrogenic trauma as the most common cause of laryngotracheal stenosis in adults.
Approximately 15% of patients who are intubated for more than 10 days develop some degree of laryngeal stenosis. Ninety percent of acquired subglottic stenoses in infants and children are due to endotracheal intubation. The incidence of subglottic stenosis after intubation is reported to be 1-10%.
Extrinsic factors that contribute to the increased risk of stenosis following intubation include traumatic intubation, prolonged duration of intubation, multiple extubations and reintubations, use of an oversized endotracheal tube for intubation, motion of the patient or the tube, gastroesophageal reflux, and local infection. In the pediatric population, since the pediatric subglottis is the narrowest portion of the airway, it is predisposed to injury by intubation.
The above-mentioned extrinsic factors lead to such changes as submucosal edema and granulation tissue deposition from fibroblast proliferation. Ulceration due to pressure or trauma (ie, from endotracheal or nasogastric tube) can progress perichondritis or chondritis with associated scar formation and/or arytenoid fixation.
Acquired posterior glottic stenosis, typically resulting from trauma due to endotracheal intubation, is the most common form of glottic stenosis.
Caustic ingestion, foreign bodies, and iatrogenic causes due to surgery on the larynx may also result in laryngeal stenosis.
Supraglottic stenosis may result from tracheotomy or laryngotracheal reconstruction. This is thought to be due to disruption of the supraglottic lymphatics and/or relaxation or injury to the suspensory muscles of the hyoid bone and hyoepiglottic ligament. Such disruption may occur during laryngotracheal surgery.
So far, laryngeal stenosis has not been found to occur at a higher rate in percutaneous dilational tracheotomy compared with open tracheotomy.
The role of gastroesophageal reflux is not clearly delineated but is thought to be a complicating factor via chemical irritation.
For the diagnosis of idiopathic progressive subglottic stenosis to be considered, no history of recent intubation or trauma should exist. Sex hormones has been implicated as a possible cause due to the preponderance of females afflicted with this condition, but several reports were not able to confirm the presence of estrogen receptors in the biopsies.
Less common autoimmune disorders such as cicatricial pemphigoid, systemic lupus erythematosus, Wegener granulomatosis, sarcoidosis, rheumatoid arthritis, and relapsing polychondritis may result in laryngeal stenosis in addition to malignancy and other systemic diseases such as amyloidosis.
Congenital laryngeal atresia may be incomplete or complete. Incomplete atresia consists of a firm fibrous membrane obstructing the glottis. Emergent tracheotomy is necessary. Complete atresia may present as stillbirth.
Congenital laryngeal webs account for about 5% of congenital laryngeal anomalies. Seventy-five percent of these are at the glottic level. The rest are at the supraglottic or subglottic level. Congenital laryngeal webs are rare; one report identified 51 children with webs during a 32-year period. Few cases are significant enough to require immediate airway intervention. Laryngeal webs often involve both the glottis and subglottis.
The incidence of posterior glottic stenosis is reported to be as high as 15% in patients who are intubated for more than 10 days.[1] Factors that contribute to the increased risk of stenosis following intubation include traumatic intubation, prolonged duration of intubation, multiple extubations and reintubations, use of an oversized endotracheal tube for intubation, motion of the patient or the tube, gastroesophageal reflux, and local infection.
Supraglottic stenosis has recently been identified as a factor in chronic upper airway obstruction following tracheotomy or laryngotracheal reconstruction.
Approximately 15% of patients who are intubated for more than 10 days develop some degree of glottic stenosis. Ninety percent of acquired subglottic stenoses in infants and children are due to endotracheal intubation. The incidence of subglottic stenosis after intubation is reported to be 1-10%.
Congenital glottic stenosis is a rare disorder and may exist as a thin membranous stenosis, as a thick anterior or posterior web, or as a complete fusion of the vocal cords. Congenital laryngeal webs are rare; one report identified 51 children with webs during a 32-year period.
Sex and Race
In a retrospective, multi-institutional study, Gelbard et al reported an interesting degree of homogeneity between patients with idiopathic subglottic stenosis, finding that the vast majority of the 479 patients, from 10 participating centers, were female (98%) and Caucasian (95%).[2]
Causes of laryngeal stenosis include the following:
Size of airway - The pediatric subglottis is predisposed to injury by intubation because it is the narrowest portion of the pediatric airway. The subglottic airway is lined with pseudostratified, ciliated, columnar epithelium, with a submucosal layer composed of loose areolar tissue.
Submucosal edema - Caused by local trauma factors or infection, leads to luminal narrowing
Stenosis - Develops due to granulation tissue deposition and fibroblast proliferation
Gastroesophageal reflux - Thought to be a complicating factor, adding chemical irritation to the endotracheal tube-induced mechanical trauma
Acquired posterior glottic stenosis - Typically begins as ulceration of the mucosa, due to pressure from the endotracheal tube, followed by secondary infection, perichondritis, chondritis, and formation of granulation tissue, which leads to scar formation and possible arytenoid fixation
As a result of technological improvements, more premature infants are surviving due to prolonged endotracheal intubation. This now is the primary cause of subglottic stenosis in children, with the percentage estimated at 1-10%.
Congenital glottic webs and subglottic stenosis result from failure of the laryngeal lumen to recanalize. During normal development, the laryngeal lumen is obliterated by continued growth of the arytenoid masses and hypobranchial eminence. By the tenth week of gestation, the laryngeal lumen is reestablished when this condensation is recanalized. Incomplete recanalization results in various degrees of glottic and/or subglottic stenosis.
Acquired glottic stenosis most commonly is due to trauma secondary to endotracheal intubation. Other causes include caustic ingestion, infections (such as croup), foreign bodies, external trauma, and iatrogenic causes due to surgery on the larynx. Long-term nasogastric intubation also may contribute to mucosal erosion and ulceration in the postcricoid region, progressing to posterior glottic stenosis.
Supraglottic stenosis or collapse is thought to be due to disruption of the supraglottic lymphatics and/or relaxation or injury to the suspensory muscles of the hyoid bone and hyoepiglottic ligament. Such disruption may occur during laryngotracheal surgery.
Supraglottic stenosis can also associated with external-beam radiation or autoimmune disorders, with a majority of patients also having coexisting dysphagia, often associated with pharyngeal or esophageal stricture. Although patient response to endoscopic treatment is generally favorable, additional procedures are typically needed, owing to a recurrence of the stenosis. The stenosis can be treated endoscopically in the operating room with a carbon dioxide laser, but it can also be treated in the office with a pulsed KTP laser, which actually appears to be a potentially safer option.[3]
The clinical presentation of laryngeal stenosis is variable depending on the age, medical condition, and activity level of the patient and the extent of stenosis. Stridor is a common presenting sign in laryngeal obstruction. Supraglottic or glottic obstruction generally presents as inspiratory stridor, while narrowing between the glottis through the trachea is associated with biphasic stridor.
Other symptoms include episodes of apnea, suprasternal and subcostal retractions, tachypnea, and dyspnea. Hypoxia can result in cyanosis and anxiety. If the glottis is involved, symptoms of hoarseness or weak husky cry, aphonia, or dysphagia may be noted.
In children, failure to thrive and feeding problems are often noted. Mild-to-moderate stenosis may be asymptomatic until an upper respiratory tract infection leads to airway edema and thickened secretions which further compromise the airway. Recurrent or persistent croup is also a typical finding in children with subglottic stenosis. Also, children may be asymptomatic but difficult to intubate for anesthesia, as may be the case in children with Down syndrome. Any individual with a history of endotracheal intubation or laryngeal trauma can potentially develop subglottic stenosis. In general, congenital stenoses are less severe than acquired ones.
The history should include an assessment of dyspnea and stridor, including the characteristics of the stridor, time of onset, and relieving and aggravating factors. Voice quality should also be assessed. History should also include questions to identify possible etiological factors, such as a history of prolonged intubation, prior surgery (airway or otherwise), trauma, or caustic ingestion.
In general, while anterior glottic scarring results in dysphonia, posterior glottic scarring tends to present with dyspnea. Acquired posterior glottic stenosis usually presents as difficulty on extubation or tracheotomy dependence.
In children, supraglottic stenosis typically presents as persistent upper airway obstruction following tracheotomy or laryngotracheal reconstruction. This problem has recently been identified as a major factor in preventing decannulation following laryngotracheal reconstruction in the pediatric patient.
The normal subglottic lumen diameter is 4.5-5.5 mm in the full-term neonate and about 3.5 mm in premature neonates. A subglottic diameter of 4 mm or less in a full-term baby is considered to be narrow. In children, the subglottic region (cricoid cartilage) is the narrowest portion of the airway. It is most susceptible to injury from endotracheal intubation.
The proximal subglottic airway is bounded by the thyroid cartilage anteriorly and by the posterior plate of the cricoid cartilage laterally and posteriorly. Distally, the cricoid ring circumferentially surrounds the subglottic airway. This area is lined with pseudostratified ciliated columnar epithelium.
The glottic segment of the larynx is composed of the true vocal cords, the anterior and posterior commissures, and the vocal processes of the arytenoid cartilages. The superior border of the glottis is the ventricle, which separates it from the supraglottis. The inferior border is the inferior limit of the true vocal cord. The posterior glottis consists of the posterior third of the vocal cords, the posterior commissure with the interarytenoid muscle, the cricoid lamina, the cricoarytenoid joints, the arytenoids, and the overlying mucosa. The anterior glottis is lined with squamous epithelium, and the posterior glottis shares respiratory epithelium with the subglottis.
Patients with a need for ventilatory support are generally poor surgical candidates. Pulmonary status must be maximized prior to any airway intervention. Infants and children with a history of bronchopulmonary dysplasia may need to demonstrate a season without hospitalization for severe respiratory illness before consideration for reconstruction. A tracheotomy for airway control may be necessary until pulmonary reserve is optimized.
Some authors recommend a minimum patient weight of 10 kg before laryngotracheal reconstruction, as this allows adequate growth, maturity of the immune system, and stabilization of pulmonary disease.
Control of gastroesophageal reflux and asthma is essential prior to treatment.
Lateral soft tissue radiographs of the neck allow an assessment of the general structure of the larynx, approximate size of the airway column, and the length of stenosis. High-kilovoltage anteroposterior projections of the neck allow an assessment of the subglottic airway. Narrowing of the air column should not be confused with the normal right lateral deviation of the trachea just below the thoracic inlet from the aortic arch on the left. Plain films are useful in the diagnosis of retropharyngeal abscess, croup, and epiglottitis.
Airway fluoroscopy may be useful if true inspiratory and expiratory views are difficult to obtain.
Obtain chest radiographs in all patients with airway abnormalities to help define concomitant cardiopulmonary problems.
A CT scan allows an evaluation of the laryngeal framework and length of stenosis. CT scan and MRI are not routinely ordered unless specific information is required after evaluation of the airway by rigid endoscopy. Recent reports describe the use of helical CT imaging on a double-detector helical CT system with sagittal multiplanar and volume-rending reformations and with axial cross-sectional stenotic areas determined. Symptoms were found to have a high degree of correlation with radiologic findings. Care must be taken to avoid undervaluing the degree of stenosis using 2-dimensional algorithms.
Barium esophagram may be indicated to assess feeding problems but rarely rules out external compression of the trachea, as might be the case from vascular anomalies. Other congenital lesions such as lymphatic malformations or duplication cysts may case external compression and secondary tracheomalacia.
Pulmonary function tests reveal characteristic changes in upper airway stenosis, and may be used to compare the postoperative results with preoperative figures. These tests are not essential to preoperative workup, as reliable data are difficult to obtain in children. In the institutions equipped with facilities for pulmonary function testing in infants and young children, the tidal or forced flow volume loop may show abnormalities such as truncation of inspiratory and/or expiratory component suggesting obstruction. The extent of truncation changes after surgical correction.
Voice and speech evaluation is performed when possible.
Genetic testing if indicated. Velocardiofacial syndrome has been associated with anterior glottic webs.
Flexible fiberoptic endoscopy in the awake patient is performed to assess for supraglottic and glottic pathology such as vocal cord paralysis and laryngomalacia.
Direct laryngoscopy and bronchoscopy with the patient under general anesthesia remains the criterion standard of diagnosis by allowing careful evaluation of each segment of the airway: supraglottis, glottis, subglottis, and trachea. The outer diameter of the largest bronchoscope that can pass through the stenosis should be noted as well as the length of the stenotic segment, its location, thickness, and composition. Use of the telescope without the bronchoscope allows dynamic assessment. Rule out secondary sites of stenosis and palpate arytenoids for cricoarytenoid joint fixation. Laryngeal electromyography may be useful.
Determine the size of the airway visually and objectively by using endotracheal tubes. An individual’s endotracheal tube size is the largest tube that permits an air leak at less than 30 cm of water pressure.
Evaluate for gastroesophageal reflux (pH probe) in all surgical candidates.
Assess vocal status (with the assistance of speech pathologists) preoperatively in older children and adults.
Subglottic stenosis may be histopathologically classified as cartilaginous or membranous. The latter may be due to submucosal fibrosis, submucosal gland hyperplasia, or granulation tissue.
Rarely, when laryngeal stenosis is caused by granulomatous infections or systemic diseases, biopsy is necessary to make the diagnosis. For example, the presence or absence of caseating necrosis or vasculitis differentiates between tuberculosis, sarcoidosis, and Wegener granulomatosis. Identification of causative organisms can also be accomplished using the biopsy specimen.
Regarding acquired stenosis due to iatrogenic trauma, histologically, studies suggest that collagen type I may be responsible for the structural integrity of normal tracheal and cricoid rings since in stenosis resection specimens, increased amounts of collagen type II are found deposited by regenerative fibroblasts, lowering the ratio of collage type I to type II.
The classification of glottic webs as described by Cohen is as follows:
Type I is an anterior web involving 35% or less of the glottis with visible true cords and no subglottic extension. Airway and voice symptoms are mild.
Type II is an anterior web involving 35-50% of the glottis. Minimal involvement of subglottis. Mild airway and voice symptoms.
Type III is an anterior web involving 50-75% of the glottis with associated cricoid abnormalities. True vocal cords may not be visualized. Severe airways symptoms with marked vocal dysfunction. Airway intervention may be necessary.
Type IV is a web occluding 75-90% of the glottis. True vocal cords are not identifiable. Subglottis is narrowed. The patient is aphonic. Immediate airway management is required.
Posterior glottic stenosis may be defined as one of the following 4 types: (Bogdasarian and Olson).
Type I is vocal process adhesion from an interarytenoid scar with a mucosally lined posterior sinus tract.
Type II is a posterior commissure stenosis involving the submucosa of the posterior commissure, interarytenoid region, and internal surface of the posterior cricoid lamina.
Type II and IV stenosis are posterior commissure scars involving the cricoarytenoid joint unilaterally or bilaterally, respectively.
The Myer-Cotton Grading system for subglottic stenosis is the most frequently used and is based on the leak pressure, tube size, and age of the patient, as follows:
Grade I - Less than 50% laryngeal lumen obstruction
Grade II - 50-70% obstruction
Grade III - 71-99% obstruction with an identifiable lumen present
Overall, the trend in management of glottic and subglottic stenosis is shorter stenting periods and less-invasive techniques.[4]
Glottic stenosis endoscopic methods
In congenital glottic stenosis, the thickness of the web determines the treatment modality; thin webs that transilluminate respond well to endoscopic lysis (either sharply or with a carbon dioxide laser) or serial dilations. Thicker webs may require an open procedure. Endoscopic techniques have been used to perform a posterior cricoid split[5] and rib grafting,[6] with good results.[7, 8, 9]
In the treatment of bilateral recurrent nerve paralysis, the patient may be treated endoscopically with posterior cricoid split and rib grafting, arytenoidectomy, or posterior cordectomy.
A retrospective study by Yilmaz et al reported that the microtrapdoor flap technique can successfully be used to treat short-segment laryngeal stenosis. The study involved 34 patients with glottic stenosis, including one with combined supraglottic and glottic stenosis. One year postoperatively, 33 patients (97%) had no breathing difficulty on exertion.[10]
Glottic stenosis open methods
Open techniques involve an anterior laryngofissure with grafting or placement of laryngeal keels or stents. A tracheotomy may be necessary in approximately 40% of patients with a subsequent open laryngeal repair.
Subglottic stenosis endoscopic methods
Soft subglottic stenoses may respond well to serial endoscopic dilations. Dilation has little role in the management of cartilaginous stenosis. Endoscopic scar excision with cauterization, cryosurgery, and serial electrosurgical resection has been used with limited success. The carbon dioxide laser can be useful for treating early stenosis with granulation tissue. This treatment may improve the airway without causing significant bleeding or edema.
Endoscopic treatment is not successful in cases of the following:
Circumferential cicatricial scarring
Abundant scar tissue more than 1 cm in length
Severe bacterial infection
Exposed perichondrium or cartilage after use of the carbon dioxide laser
Combined laryngotracheal stenoses
Previous failed endoscopic procedures
In the treatment of idiopathic progressive subglottic stenosis (IPSS), Dedo recommends against segmental resection; Dedo instead performs a CO2 laser submucosal resection with local mucosal rotation flaps technique that addresses half of the stenosis endoscopically every 2 months with the goal of ameliorating the condition, not curing it.[11]
For IPSS, others perform CO2 laser radial incisions with dilation, intralesional steroid injections, and application of mitomycin-C. Greater success is achieved with this technique if the stenoses are more than 1 cm thick.
A retrospective study by Maldonado et al indicated that CO 2 laser vaporization of fibrotic scar tissue can effectively control symptoms in idiopathic subglottic stenosis. The investigators also noted, however, that over a 5-year follow-up period, the stenosis recurred in 60% of patients, although their research suggested that aggressive medical management can reduce the recurrence rate.[12]
According to a study by Taylor et al, the likelihood of undergoing a tracheotomy owing to disease-related complications, as well as the likelihood of needing additional dilation after open airway reconstruction, was greater in individuals with Wegener granulomatosis – associated subglottic stenosis than in those with idiopathic subglottic stenosis.[13]
Mitomycin-C is an antineoplastic antibiotic that acts as an alkylating agent inhibiting cell division, protein synthesis, and fibroblast proliferation. It is applied topically for a 4-minute period after incisions are made. It can be beneficial in the modulation of wound healing and in decreasing scar formation. However, stenoses most amenable to mitomycin tend to be thin. Long-term relapse with mitomycin-C has been reported, and, while a second application 3-6 weeks apart has been shown to slow the rate of relapse for 2-3 years, at 5 years, the relapse rate is equivalent.
Recently, balloon dilation has been described as a safe and effective method to manage adults with idiopathic subglottic stenosis with findings of a single discrete stenotic area on microlaryngoscopy and bronchoscopy.[14] Dilations with a 10-mm to 14-mm balloon in a single procedure or in 2 consecutive dilations within 7 days were performed. Patients who underwent a single procedure in this study have remained symptom free for up to 30 months after balloon dilation.[15]
Subglottic stenosis open methods
In general grades III and IV subglottic stenosis require open methods. A tracheotomy is often required prior to definitive open surgical repair. Multiple techniques exist for expansion of the airway, combining the use of laryngeal and cricoid splits, cartilage grafts, and stenting.
The anterior cricoid split technique is most often used in cases of congenital subglottic stenosis due to a small cricoid ring or localized submucosal fibrosis with a normal cricoid cartilage in neonates who have failed extubation. Anterior cricoid decompression with cartilage grafting is used for anteriorly based subglottic stenosis. A combined laryngofissure with posterior cricoid split is the method of choice for combined posterior glottic and subglottic stenoses, moderate subglottic stenosis with loss of cartilaginous support, and complete glottic and subglottic stenoses. Scar removal is unnecessary in this procedure.
Autogenous costal cartilage is the graft material of choice in children when augmentation of cricoid cartilage is needed. Auricular or thyroid ala cartilage may be used in selected cases.
Stents are used to hold the reconstructed area in place and are necessary when using grafts to expand stenosed areas of the airway. The airway may be stented postoperatively with an endotracheal tube, or a molded silicone or Teflon stent may be placed intraoperatively.
Partial cricotracheal resection can be performed in cases of severe circumferential subglottic stenosis. Patients with vocal cord paralysis may require more than one procedure prior to decannulation, but overall decannulation rates with cricotracheal resection are high.
Buccal mucosa graft over a posterior cricoid split for subglottic stenosis has also been described with an overall success rate of 80%. However, it should be noted that poor postoperative voice outcomes with significant postoperative posterior glottic chinks occur if division of the interarytenoid muscle with stent placement is performed for concomitant posterior glottic stenosis.
Small anterior webs less than 2-3 mm wide that produce minimal or no symptoms do not generally require surgery. Successful repair of webs requires adequate coverage of denuded surfaces.
Glottic stenosis endoscopic methods
The tissue is dilated with round smooth dilators, and systemic steroids are often supplemented. Thin anterior webs may be managed successfully by microendoscopic incision of the web with a knife or carbon dioxide laser. The procedure should be staged for each side separately to avoid recurrence. Endoscopic keel placement in children is generally unsuccessful. In contrast, most glottic stenosis in adults can be treated endoscopically with or without a keel. Posterior glottic stenosis may be divided endoscopically if it is due to a simple interarytenoid adhesion with a mucosally lined sinus tract present posteriorly. Scarring involving the cricoarytenoid joints requires open techniques.
Glottic stenosis open methods
Tracheotomy with laryngofissure and keel placement is necessary in cases of longer, thick, anterior glottic scars. Scar resection should be kept to a minimum to reduce mucosal loss. A keel is placed to prevent restenosis in the anterior commissure during reepithelialization.[16] The keel is designed to avoid contact with the posterior glottis to minimize scarring. Bilateral vocal cord paralysis associated with acquired glottic stenosis requires an arytenoidectomy with vocal cord lateralization in addition to correction of the glottic stenosis. Open techniques require a laryngofissure with web division and coverage of the raw area with various flaps.
Investigational techniques involve an anterior window laryngoplasty, which may become favorable to traditional open techniques. This method is expected to provide closer and more direct exposure than endoscopic techniques and to carry fewer possible complications than traditional laryngofissure.
Posterior glottic fixation has been treated by scar incision, posterior cricoidectomy with stenting, and cartilage grafting with good airway and voice outcomes. Described by Zalzal in 1993, this technique involves an anterior laryngofissure with incision of the posterior glottic scar in the midline, posterior vertical cricoidectomy down to the hypopharyngeal mucosa, and cartilage grafting between the arytenoids.[1]
A one-stage procedure for the repair of major congenital laryngeal webs with associated subglottic stenosis has been used successfully in 5 children. This technique, reported by Biavati et al, involves anterior laryngofissure that includes division of the web with careful mucosal coverage of raw surfaces, submucous resection of the area of stenosis, costal cartilage grafting, and postoperative endotracheal tube stenting for 5-7 days.[17]
Subglottic stenosis endoscopic methods
Gentle periodic endoscopic dilation with well-lubricated, round, tracheal dilators has been recommended to treat soft congenital subglottic stenoses. The CO2 laser is most frequently used in cases of early stenoses with granulation tissue, thin circumferential webs, and crescent-shaped bands. Microcauterization and cryosurgery have fallen into disfavor due to inconsistent results.
Another therapy, balloon laryngotracheoplasty, can serve as either an alternative or adjunct treatment in pediatric patients with subglottic or laryngeal stenosis. Considered a low-risk therapy, it can reduce the chance of morbidity associated with open surgery. However, the procedure's success depends on early identification and treatment of laryngotracheal stenoses.[18]
A case series reported by Blanchard et al indicated that congenital laryngeal stenosis can be treated safely and effectively using endoscopic laryngoplasty with incision of the subglottic laryngeal cartilages with cold steel instruments and balloon dilation. According to the investigators, this operation may be viable as a first-line procedure, with appropriate prolonged follow-up, and an alternative to open laryngoplasty (which could subsequently be used if the endoscopic procedure failed).[19]
Subglottic stenosis open methods
Open techniques generally are required for grade III and IV stenoses and many grade II stenoses. These techniques may be classified broadly into splits, augmentations, and resections.
The anterior cricoid split procedure generally is performed on a neonate who meets certain specific criteria. The procedure is used to avoid tracheotomy in neonates. A median vertical incision is made through the first 2 tracheal rings, cricoid cartilage, and the bottom one-third of the thyroid cartilage. The split permits distraction of the cricoid ring up to 3 mm with an endotracheal tube stenting the laryngeal framework for 7-14 days postoperatively. Other split procedures consist of posterior and lateral divisions of the cricoid.
Although anterior cricoid split has been considered the first alternative to tracheostomy in infants less than 6 months of age, single-stage laryngotracheoplasty has been demonstrated as an equally viable first alternative to tracheostomy if subglottic stenosis is the primary airway lesion.[20]
Augmentation procedures are required when distraction of the laryngeal framework greater than 3 mm is necessary. Autogenous costal cartilage is the graft material of choice in children because of its size and rigidity. A 4-cm section of the fifth rib is routinely obtained. This technique can be performed as a single-stage laryngotracheoplasty with postoperative stenting by a nasotracheal tube or as a 2-stage procedure, leaving the tracheotomy in place and placing an endolaryngeal stent. The larynx may be augmented anteriorly, posteriorly, or both.
A cartilage graft in the posterior glottis or subglottis may be necessary in cases of posterior glottic stenosis, subglottic stenosis, or both; isolated subglottic shelves; circumferential subglottic stenosis; and total or near-total obstruction at the glottic or subglottic level.
Stents are used to provide stability to the reconstructed airway, counteract scar contractures, and promote a scaffold for epithelium to cover the lumen of the airway. Stenting is necessary when a graft has been used to expand the airway.
The most commonly used stent is the endotracheal tube. Duration of stenting depends on the function of the stent. Nasotracheal tubes after single-stage laryngotracheoplasty are typically removed after one week. When the larynx has been distracted but not grafted, stenting is usually required for 3-6 months. The Cotton-Lorenz stent (rigid Teflon) is commonly used in children because it is inert, does not adhere to tissue, and provides firm support.
Individualization of laryngeal stent use in patients following reconstructive surgery must take into account the severity and location of the stenosis, as well as the type and length of the stent and how long it will be used. Preliminary data analyses from a comparison of open Aboulker stents with soft silastic stents indicated that the two devices have equal decannulation rates and that the soft silastic stents are associated with better postoperative feeding. However, the silastic stents were also associated with increased granulation tissue development and seemed to extend the time needed for decannulation. Laryngeal stents must be monitored to make sure that their position is stable and that they are removed in a timely fashion. In addition, persistent evaluations for the development of granulation tissue are necessary.[21]
Short-segment severe stenoses of the cricotracheal region may be resected with partial resection of the anterior cricoid and primary anastomosis. This procedure is for cases of isolated severe subglottic or upper tracheal stenosis with a normal lumen of at least 10 mm below the glottis but can be combined with other procedures. The dissection is performed in the subperichondrial plane to resect cricoid cartilage, if needed. The risk of recurrent laryngeal nerve injury is present because of its proximity to the resected portion. Many times, stenting is not necessary.
Excellent intensive care unit support is absolutely essential to the success of open laryngeal surgery, particularly with single-stage procedures.
Steroids (dexamethasone 1 mg/kg/d) are begun 16-24 hours before planned extubation and typically are continued 48-72 hours after extubation.
Aggressive pulmonary toilet may be necessary after extubation, including racemic epinephrine treatments, humidification, and chest physiotherapy.
The airway is endoscopically evaluated prior to extubation. If the patient is not sedated, he or she may be extubated immediately afterward. The patient may be extubated the next day after placing an endotracheal tube one-half size smaller.
Keels or stents typically remain in place for 2-6 weeks postoperatively.
When an endotracheal tube is used as a stent, the patient typically is extubated 7 days postoperatively. When posterior grafts are placed, the patient usually is extubated 14 days postoperatively.
After open procedures, monitor patients closely for the development of a pneumothorax or neck hematoma.
Because of the possible complications, all open airway procedures should include the use of drains to allow the escape of air to prevent subcutaneous emphysema.
A postoperative chest radiograph is obtained to check endotracheal tube placement and evaluate for pneumothorax.
Any costal cartilage harvest site should be examined daily.
Antibiotics should be administered for 2-3 weeks after any open procedure and while a keel or stent is in place, and an antireflux regimen should be followed.
Systemic diseases (eg, diabetes) that may impede tissue revascularization must be monitored closely.
Periodic endoscopy is recommended every 4 weeks postoperatively to assess stent location and monitor formation of granulation tissue.
Postoperative paralytics should be avoided if at all possible for the following reasons:
Sedatives and analgesics may be easily titrated.
Prolonged postparalytic neuromuscular weakness has been documented.
Patients are unable to breathe spontaneously if accidentally extubated.
Patients cannot show evidence of respiratory distress early in cases of an occluded airway.
Emergent complications include airway obstruction, stent aspiration, hematoma formation, and pneumothorax.
Airway obstruction is often caused by a mucus plug, which should be suctioned immediately.
Stent aspiration requires bronchoscopy under anesthesia for foreign body removal.
Manage hematoma and pneumothorax with drainage and chest tube placement, as indicated.
Other potential complications vary according to the technique and include recurrence, aspiration, infection, keel extrusion, chondritis, granulation tissue formation, dysphonia, and tracheotomy dependence.
Involvement of the glottis in subglottic stenosis has been found to have an unfavorable effect on outcome, although isolated glottic stenosis tends to have a significantly better outcome when compared with other areas of laryngeal stenosis.
In adults, resection of laryngotracheal stenosis with primary anastomotic reconstruction can achieve decannulation rates up to 97%. Advanced age may be correlated with unsuccessful airway patency, but other parameters, such as chronic obstructive lung disease, diabetes, grade of stenosis, and revision versus primary surgery, did not correlate with airway patency, according to Wolf et al.[22] Partial cricoidectomy with primary thyrotracheal anastomosis can achieve similar results. In adults, there is a high rate of reoperation and need for tracheotomy if a single-stage laryngotracheal reconstruction with cartilage grafting without stenting is undertaken.
The anterior cricoid split procedure consistently yields a higher than 70% success rate (decannulation) when specific criteria are followed.
In a study of endoscopic posterior cricoid split with costal cartilage graft placement, Gerber et al reported good success with regard to decannulation rates and tracheostomy avoidance for children with subglottic and/or glottic stenosis.[23]
In 16 patients undergoing partial cricotracheal resection with primary anastomosis for grade III or IV subglottic stenosis, Stern et al report a 94% decannulation rate. Younis et al report a series of 21 pediatric patients undergoing single-stage laryngotracheal reconstruction, with anterior rib grafts, without stenting, and with immediate postoperative extubation in 20 of 21 patients.
A study by Timman et al indicated that in the treatment of laryngotracheal or tracheal stenosis, laryngotracheal resection and reconstruction and segmental tracheal resection (STR) with either end-to-end tracheal anastomosis (ETE) or cricotracheal anastomosis are safe and effective approaches; the overall success rate in the study was 92%. However, compared with STR-ETE, laryngotracheal resection and reconstruction was more commonly associated with airway-related complications (7% vs 30%, respectively).[24]
Voice outcomes vary according to the method of treatment and degree of stenosis but generally are unchanged or improved. However, in the above-mentioned study by Timman and colleagues, 34% of laryngotracheal resection patients experienced early voice alterations without recurrent laryngeal nerve palsy, compared with 16% of patients who underwent STR-ETE.[24]
An increased understanding of voice outcomes has become possible with the help of new technologies and improvements in the quantification of dysphonia. Research has indicated that an association exists between voice outcomes and various surgical factors, such as the use of laryngofissures, posterior graft placement, and the duration of stenting. Significant surgical advances that have influenced voice outcome have included less frequent use of complete laryngofissures, the employment of smaller posterior grafts, and the reduction of stenting periods.
Stent placement, duration, and material are controversial issues. Postoperative movement of the arytenoids on a stent may have a negative effect on the healing process.
Mark E Gerber, MD, Clinical Associate Professor of Surgery, University of Chicago Pritzker School of Medicine; Division Head, Otolaryngology-Head and Neck Surgery; Director, Pediatric Otolaryngology-Head and Neck Surgery, NorthShore University Health System
Disclosure: Nothing to disclose.
Coauthor(s)
Judy L Chen, MD, Attending Physician, Department of Otolaryngology-Head and Neck Surgery, NorthShore University HealthSystem
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Stephen G Batuello, MD, Consulting Staff, Colorado ENT Specialists
Disclosure: Nothing to disclose.
Chief Editor
Arlen D Meyers, MD, MBA, Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;The Physicians Edge;Sync-n-Scale;mCharts<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; .
Additional Contributors
Clark A Rosen, MD, Director, University of Pittsburgh Voice Center; Professor, Department of Otolaryngology and Communication Science and Disorders, University of Pittsburgh School of Medicine
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Merz North America Inc<br/>Received consulting fee from Merz North America Inc for consulting; Received consulting fee from Merz North America Inc for speaking and teaching.
Acknowledgements
The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors Debbie A Eaton, MD, and Alan D Murray, MD, to the development and writing of this article.
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