Glottic Stenosis 

Updated: Dec 03, 2019
Author: Gauri Mankekar, MD, PhD; Chief Editor: Arlen D Meyers, MD, MBA 

Overview

Practice Essentials

Glottic stenosis is narrowing of the larynx at the level of the glottis (ie, vocal cords). It is caused by webbing, fibrosis, or scarring and most often involves the posterior glottis. The most common cause of stenosis is prolonged endotracheal intubation. In patients who are intubated for more than 10 days, the risk of developing posterior glottic stenosis is as high as 15%. Inflammation, infection, trauma, and congenital and iatrogenic causes also contribute to glottic stenosis. In all cases, the preoperative evaluation must include direct laryngoscopy as well as microlaryngoscopy with an assessment of vocal cord mobility. Treatment is based on the etiology of the stenosis and the thickness of the stenotic segment. Various medical and surgical methods are discussed according to the type of stenosis.[1, 2]

Anatomic regions of the larynx are shown in the image below.

Anatomical regions of the larynx. Anatomical regions of the larynx.

Signs and symptoms

Congenital glottic stenosis in the form of laryngeal webs typically manifests with symptoms of airway distress or obstruction, a weak or husky cry, and, occasionally, aphonia.

In general, a patient with posterior glottic scarring tends to present with dyspnea, while a patient with anterior glottic scarring presents with dysphonia.

Acquired anterior glottic webs may produce symptoms that range from hoarseness to respiratory distress. Posterior glottic stenosis can manifest as airway stenosis and may mimic bilateral vocal cord paralysis.[3]

Workup

Few diagnostic laboratory findings are associated with glottic stenosis, although performing a serologic workup is necessary if a granulomatous disease (eg, sarcoidosis, tuberculosis, syphilis, Wegener granulomatosis) or a systemic disease (eg, rheumatoid arthritis, amyloidosis) is suspected as the cause.

A computed tomography (CT) scan allows for evaluation of the length and thickness of the glottic stenotic segment in subglottic stenosis. A CT scan also allows for evaluation of the laryngeal framework in order to determine the presence of a fracture or other significant injury. Spiral CT scanning with 3-dimensional reconstruction is advisable for better surgical planning and outcome.[4]

Electromyography (EMG) can help to differentiate posterior glottic stenosis from bilateral vocal cord paralysis. It may also be used to evaluate the function of the intrinsic muscles of the larynx.

Under anesthesia, direct laryngoscopy and bronchoscopy in the operating room allow for careful evaluation of the laryngeal and distal airways and provide a means of assessing the cricoarytenoid joints.

Management

Treatment consists of medical therapy, intralesional injections, endolaryngeal procedures, and open surgical procedures. The treatment depends on the thickness of the glottic web. Thin anterior commissure webs can be successfully excised with a carbon dioxide laser or microdebrider followed by endoscopic keel placement, while thicker webs require laryngofissure, lysis of the web, and placement of a silicone or silastic keel.

When stenosis is due to an infection or inflammatory disorder, appropriate treatment in the form of antibiotics, corticosteroids, or both is important.

Surgery

Open surgical techniques involve an anterior laryngofissure or thyrotomy with grafting or placement of keels or stents.

In congenital glottic stenosis, the thickness of the webs determines the treatment modality. Thin webs that transilluminate respond well to endoscopic lysis (either sharply with microscissors or with a carbon dioxide laser or a microdebrider) or serial dilations. Thicker webs, in approximately 40% of patients, require tracheotomy with a subsequent open laryngeal repair.

Overall, the trend in glottic stenosis management is toward shorter stenting periods and less invasive techniques (eg, endoscopy, use of carbon dioxide laser, or a smaller laryngofissure).

History of the Procedure

Congenital subglottic stenosis was first described by Rossi in 1826. Mackenzie in 1862 described laryngeal stenosis that results from inflammatory conditions, especially syphilis, which was predominant then.[5] In the late 19th century, Von Schroetter performed laryngeal dilatation with rigid vulcanite tubes and used pewter plugs for stents.[6]

In 1924, Haslinger described an endoscopic technique for web excision with placement of a silver plate keel.[7] In 1935, Iglauer described the use of a spring ring from a watch chain as a keel after glottic stenosis excision.[8] In 1950, McNaught used a tantalum keel postglottic stenosis excision.[9]

In 1979 and 1980, Dedo and Lichtenberger, respectively, modified this technique for clinical use.[10, 11] In 1980, Lichtenberger introduced a technique for the treatment of anterior commissure webs. This technique involved endoscopically suturing a keel in place from inside the airway out to the neck. In 1994, Lichtenberger reported on a series of 13 patients who were treated for anterior commissure webs with a keel-fixing technique that involved the use of a specialized endo-extralaryngeal needle carrier.[11]

In 1968, Dedo and Sooy described an aryepiglottic fold mucosal flap. In 1984, they detailed the endoscopic use of the laser for mild posterior commissure stenosis and described the creation of a trapdoor flap.[10] In 1973, Montgomery recommended a superiorly based advancement mucosal flap from the interarytenoid area.[12] Multiple variations of the laryngofissure approach have been developed.

In 1993, Zalzal described an anterior laryngofissure technique with posterior cricoidotomy and cartilage grafting.[13] In 1995, Biavati et al successfully used, in 5 children, a single-stage procedure for the repair of congenital laryngeal webs that were associated with subglottic stenosis.[14] Recent work has centered around endoscopic techniques for repair, use of a carbon dioxide laser or microdebrider for excision of webs, topical application of mitomycin-C, and, lately, chitosan for prevention of restenosis.

Problem

Glottic stenosis may accompany subglottic stenosis or may be diagnosed as a separate entity. Glottic stenosis may be a congenital or an acquired condition, represented as anterior or posterior webs, interarytenoid adhesions with or without impaired vocal cord mobility, or complete fusion of the true vocal folds (rare).

Epidemiology

Frequency

Acquired posterior glottic stenosis is the most common form of glottic stenosis and typically results from trauma due to endotracheal intubation. The risk of developing posterior glottic stenosis is reported to be as high as 15% in patients who are intubated for more than 10 days. Factors that contribute to increased risk of stenosis related to intubation include traumatic intubation, prolonged duration of intubation, multiple extubations and reintubations, an oversized endotracheal tube used for intubation, motion of the patient or the endotracheal tube, gastroesophageal reflux, and local infection.

Congenital glottic stenosis is a rare disorder and may exist as a thin membranous stenosis, a thick anterior or posterior web, or as a complete fusion of the vocal cords. Congenital laryngeal webs are rare; the largest study identified 51 children over a 32-year period. In 2009, Cheng et al reported on 4 children with Shprintzen syndrome who had severe congenital anterior glottic web.[15] Crowe et al have reported on a rare case of glottic stenosis in an infant with Fraser syndrome.[16]

Etiology

Congenital glottic webs result from failure of the larynx to completely recanalize during gestation. Different degrees of failure of this separation can result in webs or, rarely, in complete atresia at the glottic level. Laryngeal webs account for approximately 5% of congenital laryngeal anomalies, and 75% of the webs occur at the glottic level.

Acquired glottic stenosis is most commonly due to trauma secondary to endotracheal intubation. Other causes include caustic ingestion, infections (eg, croup, syphilis, fungus, diphtheria), foreign bodies, irradiation, or external trauma. A study by Howard et al provides photodocumentation of the progression of intubation-related mucosal injury to granulation tissue and the subsequent development of posterior glottic stenosis; the investigators stress the importance of serial examination of patients who develop persistent voice change following intubation.[17]

Iatrogenic causes of acquired glottic stenosis include traumatic endoscopic manipulation, aggressive endolaryngeal laser surgery, and vocal cord stripping procedures.

Granulomatous diseases such as tuberculosis, sarcoidosis, rhinoscleroma, or Wegener granulomatosis may also cause laryngeal glottic stenosis. Tuberculosis commonly involves the interarytenoid space and the posterior vocal cords. Sarcoid usually involves the supraglottis, while Wegener, rhinoscleroma, and histoplasmosis primarily involve the subglottis. Long-term nasogastric intubation may contribute to mucosal erosion and ulceration in the postcricoid region, which progresses to posterior stenosis.

A study by Hillel et al reported that in intubated patients, risk factors for posterior glottic stenosis include ischemia, diabetes mellitus, length of intubation time, and large endotracheal tube size.[18]

Prevention

Prevention of glottic stenosis consists of performing atraumatic intubation with the smallest endotracheal tube acceptable, limiting total time of intubation, reducing motion of the tube while patient is intubated and treating gastric reflux. Prevention also involves the avoidance of inappropriate dissection or overzealous use of the laser in endolaryngeal surgery.

Pathophysiology

Acquired posterior glottic stenosis typically begins as ulceration of the mucosa due to pressure from an endotracheal tube. Secondary infection, perichondritis, chondritis, and formation of granulation tissue occur next, which leads to scar formation and possible arytenoid fixation. However, most posterior glottic injuries heal after extubation with re-epithelialization, leaving no scars.

Presentation

Congenital glottic stenosis in the form of laryngeal webs typically manifests with symptoms of airway distress or obstruction, a weak or husky cry, and, occasionally, aphonia. Patients may present with these lesions shortly after birth and may require emergent intubation or tracheotomy if the stenosis is severe.

Seventy-five percent of congenital webs are located (usually anteriorly) at the glottic level, with the remainder located in supraglottic and subglottic areas. Occasional extension to the glottic level may occur.

In general, a patient with posterior glottic scarring tends to present with dyspnea, while a patient with anterior glottic scarring presents with dysphonia. Acquired anterior glottic webs may produce symptoms that range from hoarseness to respiratory distress. Posterior glottic stenosis can manifest as airway stenosis and may mimic bilateral vocal cord paralysis.[3] Acquired posterior glottic stenosis is usually associated with tracheotomy dependence or difficulty performing extubation, along with a history of airway difficulty that requires intubation.

Indications

See Surgical therapy.

Relevant Anatomy

Embryology

The larynx develops in early intrauterine life from the cranial end of the laryngotracheal tube and surrounding mesenchyme of the fourth and sixth branchial arches. A rapid proliferation of the laryngeal epithelium causes temporary occlusion of the laryngeal lumen. Thus, the vocal cords adhere to each other during the seventh week of gestation. Over a period of 2 weeks, this epithelial fusion deteriorates and leaves an opening between the cords. Different degrees of failure of separation can result in glottic webs or, rarely, complete atresia at the level of the glottis.

Anatomy

The larynx is divided into 3 distinct anatomical regions as seen in the image below: the supraglottis, the glottis, and the subglottis. 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 the glottis from the supraglottic region. The inferior border is located at the inferior limit of the true vocal cord. The glottis is approximately 5 mm at the midportion of the true vocal cord, its longest point, and tapers to 2-3 mm at the anterior commissure.

See the image below.

Anatomical regions of the larynx. Anatomical regions of the larynx.

The posterior commissure is a strip of mucosa that measures approximately 5 mm in height. This strip extends across the interarytenoid space from one vocal process to the other. 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, while the posterior glottis shares respiratory epithelium with the subglottis.

Contraindications

In general, patients who require peak airway pressures above 35 mm Hg are poor surgical candidates. When reconstruction is necessary, surgery may be delayed if the patient's medical condition precludes prolonged anesthesia for any reason. Similarly, reconstruction in infants and children with a history of bronchopulmonary dysplasia may also be deferred until they experience a period without hospitalization for severe respiratory illness.

Guidelines for laryngotracheal reconstruction that are important to consider prior to repair include weight of at least 10 kg, no need for ventilatory support, and control of gastroesophageal reflux or asthma.

 

Workup

Laboratory Studies

Few diagnostic laboratory findings are associated with glottic stenosis, although performing a serologic workup is necessary if a granulomatous disease (eg, sarcoidosis, tuberculosis, syphilis, Wegener granulomatosis) or a systemic disease (eg, rheumatoid arthritis, amyloidosis) is suspected as the cause.

Imaging Studies

Routine plain upper airway and chest radiographs are of limited value in the diagnosis and treatment of glottic stenosis but may provide an initial assessment of laryngotracheal air column and coexisting pulmonary disease.

A CT scan allows for evaluation of the length and thickness of the glottic stenotic segment in subglottic stenosis. A CT scan also allows for evaluation of the laryngeal framework in order to determine the presence of a fracture or other significant injury.

Spiral CT scanning with 3-dimensional reconstruction is advisable for better surgical planning and outcome, and it is complementary to rigid endoscopy in the management of these conditions.[4]

Other Tests

Pulmonary function tests (ie, maximum inspiration and expiration flow rates, flow volume loops, pressure flow loops) show characteristic changes in upper airway stenosis and may be used to compare preoperative and postoperative results.

Electromyography (EMG) can help to differentiate posterior glottic stenosis from bilateral vocal cord paralysis. It may also be used to evaluate the function of the intrinsic muscles of the larynx.

Twenty four-hour pH studies help to evaluate coexistent gastroesophageal reflux.

Diagnostic Procedures

First, the conscious patient's vocal cord mobility is assessed using either indirect laryngoscopy or fiberoptic laryngoscopy. Currently many clinicians are advocating early evaluation of the larynx (ie, within the first few hours after extubation) to diagnose and commence treatment of lesions caused by prolonged endotracheal intubation.

Subsequently, under anesthesia, direct laryngoscopy and bronchoscopy in the operating room allow for careful evaluation of the laryngeal and distal airways and provide a means of assessing the cricoarytenoid joints.

Microlaryngoscopic assessment helps to identify the extent and character of the stenosis and the degree of arytenoid mobility and to determine if cricoarytenoid joint fixation is present. Posterior glottis stenosis or interarytenoid adhesion has sometimes been misdiagnosed as cord paralysis. Laryngoscopy and laryngeal electromyography studies are the two diagnostic aids in this condition.[19]

Other important aspects of the evaluation include assessment of inflammatory changes in the larynx, the size of the airway, and evidence of gastroesophageal reflux (eg, interarytenoid edema, erythema).

Histologic Findings

In rare cases of glottic stenosis caused by a granulomatous or systemic infection or disease, biopsy is necessary to make the diagnosis. The presence or absence of caseous necrosis or vasculitis differentiates tuberculosis, sarcoidosis, and Wegener granulomatosis. Identification of causative organisms can also be accomplished using the biopsy specimen.

Staging

Cohen’s classification is as follows:[20]

  • Type I : This is the mildest form of the web. It involves less than 35% of the glottis. It is usually thin and uniform in thickness with no subglottic extension. The true vocal cords are usually well seen through the web. The patient usually has an adequate airway and only slight voice change.

  • Type II: The web involves 35-50% of the glottis and can be thin or thick, but the vocal cords can usually be seen within the web. These may be associated with some subglottic extension of stenosis. Patients usually don't have too much airway obstruction or airway symptoms.

  • Type III: This type involves 50-75% of the glottis. The web is usually very thick anteriorly and may thin out as it extends posteriorly. The true vocal cords may or may not be visible within the web; these almost always have a subglottic component to them. Patients have marked vocal dysfunction and have moderate-to-severe airway symptoms.

  • Type IV: This is the most severe form. The web involves 75-90% or more of the glottis and is uniformly thick both anteriorly and posteriorly. The true vocal cords are not identifiable within the web and may be one continuous, thick band. The patient is usually aphonic. Severe airway obstruction is usually present and almost always requires an emergency tracheotomy.

 

Treatment

Medical Therapy

The primary goals of treatment are the development of an adequate airway and preservation or improvement in voice quality.

Treatment consists of medical therapy, intralesional injections, endolaryngeal procedures, and open surgical procedures. The treatment depends on the thickness of the glottic web. Thin anterior commissure webs can be successfully excised with a carbon dioxide laser or microdebrider followed by endoscopic keel placement, while thicker webs require laryngofissure, lysis of the web, and placement of a silicone or silastic keel.

Sharouny and Omar recommended that when a keel is used for anterior glottic stenosis, it be adequately sutured to the anterior laryngeal wall to prevent complications. They described a case in which a patient returned to the clinic two weeks after placement of a custom-made keel, having aspirated it. Flexible bronchoscopy revealed that the silastic sheet from which the keel was made was in the right main bronchus; the object was removed via a flexible bronchoscope passed through the tracheostomy.[21]

When stenosis is due to an infection or inflammatory disorder, appropriate treatment in the form of antibiotics, corticosteroids, or both is important.

The use of systemic steroids in glottic stenosis is controversial. These agents tend to decrease scar formation but may delay wound healing. Treatment should be individualized.

Steroid injection into the posterior glottic scar may be useful in cases of inflammation during the very early stages. These injections are technically difficult, and cartilage resorption may be a serious complication. Inhalational steroids are sometimes used to reduce granulation tissue formation after stent removal.

Supportive therapy includes humidified oxygen and close airway monitoring in a supervised setting.

Always manage gastroesophageal reflux prior to any surgical intervention.

Surgical Therapy

Surgical methods that rely solely on dilation are generally unsuccessful for all webs except the most translucent membranous ones.

A study by Rosen et al indicated that early posterior glottic stenosis can be better treated with teardrop-shaped laryngeal dilation than with round dilation, since the glottis is itself teardrop shaped. Teardrop dilation was performed by inserting a triangular static stent into the anterior glottis, with a round balloon dilator simultaneously employed in the posterior glottis. Results in the study patients included improved breathing, a reduced Dyspnea Index score, and decannulation. The investigators found the teardrop dilation method preferable to round dilation of the larynx because the latter compresses the membranous vocal folds (risking injury) and only minimally expands the posterior larynx.[22]

The use of advancement rotation flaps for the management of anterior commissure cicatrization and webs resulting from a variety of clinical conditions has been described.

In 1924, endoscopic division of webs and subsequent keel placement were first described. Since that time, multiple modifications of both the technique and keel material have been made.

Open techniques involve an anterior laryngofissure or thyrotomy with grafting or placement of keels or stents.

Arytenoidectomy and cordectomy are frrquently used to manage glottic stenosis. However, they are associated with poor quality of voice. Zeitels et al reported on the successful use of a less invasive treatment, insertion of a silastic T-tube, modified into a self-retaining interarytenoid spring, into patients with acquired posterior glottic stenosis. Of the study’s five patients, four were tracheotomy dependent (for the most part due to glottic stenosis). The spring permitted tracheotomy tube decannulation, and patient voice quality subsequent to the procedure was considered excellent.[23]   

In congenital glottic stenosis, the thickness of the webs determines the treatment modality. Thin webs that transilluminate respond well to endoscopic lysis (either sharply with microscissors or with a carbon dioxide laser or a microdebrider) or serial dilations. Thicker webs, in approximately 40% of patients, require tracheotomy with a subsequent open laryngeal repair.

Bogdasarian and Olson (1980) classified the extent of posterior glottic stenosis into the following 4 types:[24]

  • Type I - Vocal process adhesion

  • Type II - Posterior commissure stenosis with scarring in the interarytenoid plane and internal surface of the posterior cricoid lamina

  • Type III - Posterior commissure stenosis with unilateral cricoarytenoid joint ankylosis

  • Type IV - Posterior commissure stenosis with bilateral cricoarytenoid joint ankylosis

Bogdasarian and Olson recommend a graded surgical approach based on this classification scheme. They also recommend, in mild cases (type I and type II), performing scar excision, resurfacing with mucosa or split-thickness skin graft, and stenting. Arytenoidectomy and hyoid interposition have been recommended in cases of joint fixation.

Overall, the trend in glottic stenosis management is toward shorter stenting periods and less invasive techniques (eg, endoscopy, use of carbon dioxide laser, or a smaller laryngofissure).

In a literature review, Lahav et al recommended that surgical intervention for glottic stenosis begin with a discussion of expectations with the patient regarding voice versus airway functions. In addition, careful planning for anesthesia administration is required, as the surgeon and anesthetist must each understand tubeless jet ventilation options.[25]

Intraoperative Details

The key to successful repair of webs is the adequate coverage of denuded surfaces.

Endoscopic techniques include manual or laser scar division or microdebrider web or scar lysis, endoscopic arytenoid abduction lateroplexy (EAAL), classic vocal cord laterofixation (VCL), transverse cordotomy (TC), arytenoidectomy (AE), laser arytenoidectomy, and microtrapdoor (MTD) flaps. In a study of 34 patients with glottic stenosis (33 with pure glottic stenosis, 1 with accompanying supraglottic stenosis) who underwent unilateral or bilateral microtrapdoor flap surgery, Yilmaz et al found that 33 of them were dyspnea-free on exertion at 1-year follow-up.[26]

Recently, endoscopic techniques have been used with good results to perform posterior cricoid splits and rib grafting.

Open techniques require laryngofissure with web division and coverage of the raw area using a variety of flaps, including native mucosa, nasal septal mucosa, buccal mucosa, perichondrocutaneous grafts, skin grafts, and cartilage grafts. An investigational technique that may become favorable to traditional open techniques involves an anterior window laryngoplasty. This method is expected to provide closer and more direct exposure than endoscopic techniques and to have fewer possible complications than traditional laryngofissure.

The MTD technique for anterior webs involves elevating the web unilaterally, ablating the scar, and redraping the preserved mucosa over the vocal cord to resurface the raw area. This technique is most successful in cases in which webs are of thin-to-moderate size (ie, < 1 cm thick). Posterior glottic webs may also be treated in a similar manner using the MTD technique, but these may require several procedures for adequate treatment.

Thin webs can be excised with the carbon dioxide laser, microscissors, or microdebrider, addressing one side of larynx at a time to avoid further webbing as well as application of either mitomycin-C or chitosan to prevent re-webbing. Thicker webs are often associated with subglottic narrowing and are more difficult to treat; they often require tracheostomy followed by laryngofissure with division of web and possibly cricoid cartilage and then closure over a keel or stent. The timing for correction is controversial.

Several techniques have been described for the management of interarytenoid fusion, including division by sharp dissection or carbon dioxide laser with stent placement. In 1994, Lichtenberger et al described a successful keel-fixing technique for the endoscopic repair of anterior commissure webs in 13 patients. This technique involves precise keel placement using an endo-extralaryngeal needle carrier. The results of Lichtenberger's study showed improved airway and voice in all patients treated, without the need for tracheotomy.

Beswick et al reported on a technique for endolaryngeal keel placement in patients with anterior glottic webs in which an endoscopic suture retriever is inserted through a percutaneously placed angiocatheter, precluding the need for a Lichtenberger needle passer. This exo-endolaryngeal technique uses materials that are readily available in most operating rooms.[27]

Chitose et al (2009) have described the use of a posterior mucosal flap for the treatment of posterior glottic stenosis.[28] Using endoscopic microscissors, they separated the posterior commissure and interarytenoid scar tissue submucosally. The bilateral corniculate cartilages of the superior arytenoids were then debulked using a CO2 laser. A posteriorly based mucosal flap obtained from the postcricoid region was extended approximately to the mucosa of the posterior commissure. The mucosal flap was sutured to the inferior subglottic mucosa by two 4-0 polyglactin absorbable sutures.

Rovó et al (2008) have described endoscopic arytenoid lateropexy for isolated posterior glottic stenosis.[29] Using a CO2 laser and endoscopic approach, they transected the scar between the arytenoid cartilages. A right-angled endolaryngeal scythe was used to transect the scars that had spread into the cricoarytenoid joint. A reinforced Lichtenberger needle carrier instrument was used to perform the lateropexy of the adequately mobilized arytenoid cartilages, with consideration of the real abduction of the cricoarytenoid joint.

Scar incision, posterior cricoidotomy with stenting, and cartilage grafting have been used together to treat posterior glottic fixation, with excellent 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 cricoidotomy to the hypopharyngeal mucosa, and cartilage grafting between the arytenoids.[13] Zalzal's report detailed the treatment of 12 tracheotomy-dependent patients with glottic stenosis from endotracheal intubation; all patients were decannulated successfully after the described procedure.

Schaefer et al reported the successful mobilization of fixated arytenoids without arytenoidectomy in 4 patients with type IV posterior glottic stenosis.[30] The procedure described involves a midline thyrotomy with the advancement of superiorly based mucosal flaps and cricoarytenoid joint exploration with lysis of adhesions. The patients were stented postoperatively for 2-3 weeks and subsequently underwent endoscopic stent removal under general anesthesia.

A 1-stage procedure for the repair of major congenital laryngeal webs with associated subglottic stenosis has been successfully used in 5 children. The advantage of this technique is the avoidance of morbidity associated with stents, keels, and tracheotomies. Biavati et al describe this technique, which involves anterior laryngofissure with division of the web.[14] Careful mucosal coverage of raw surfaces, submucous resection of the stenotic area, and costal cartilage grafting complete this technique. Postoperative endotracheal tube stenting is required for 5-7 days.

Krimsky et al have reported 3 cases of glottic and subglottic narrowing treated with spray cryotherapy alone or in combination with balloon dilation.[31]

A study by Zeitels and Hillman indicated that endolaryngeal mobilization of local fibromucosal soft tissue flaps can help to lengthen the anterior glottic aperture in patients with anterior commissure glottic webs not covered by excessive redundant papillomatosis. In the procedure, which can be performed without the use of stents or other devices, flaps can be derived from the glottic web, contralateral vocal fold, medial aspect of the thyroid lamina, and infrapetiolar area.[32]

Postoperative Details

Keels or stents typically remain in place for 4-6 weeks postoperatively and may be removed endoscopically.

Postoperative paralytic agents are avoided whenever possible, especially in children, for the following reasons:

  • Accidentally extubated patients are unable to breathe spontaneously.

  • Sedatives and analgesics are easily titrated.

  • Patients with a dislodged or obstructed tube are unable to show respiratory distress when paralyzed.

  • Prolonged weakness that occurs after long-term paralysis has been documented.

After open procedures, monitor patients closely for the development of a pneumothorax or neck hematoma. Because of possible complications, include the use of drains to allow the escape of air following an open airway procedure. Always obtain a postoperative chest radiograph and daily examine any costal cartilage harvest site. Administer antibiotics for 2-3 weeks after any open procedure and while a keel or stent is in place. The patient should follow an antireflux regimen. Some authors recommend periodic endoscopy every 4 weeks to assess the stent location and monitor formation of granulation tissue. Closely monitor systemic diseases (eg, diabetes) that may impede tissue revascularization.

Follow-up

Close follow-up care is necessary to monitor airway patency, stenosis recurrence, and granulation tissue formation.

Granulation tissue may be treated with aerosolized steroids (dexamethasone 1 mg/kg/d) orally or through the tracheotomy tube.

Multiple recurrences after serial dilations may necessitate an open laryngeal procedure.

Most speaking patients (ie, noninfant patients) should also undergo 4-6 weeks of postoperative voice therapy. In most cases, oral intake may be resumed once the patient is extubated.

Repeat endoscopy is performed 2-4 weeks after stent or keel removal. Repeat endoscopy is often performed when signs or symptoms of airway difficulty return.

Complications

Emergent complications include airway obstruction, stent aspiration, hematoma formation, and pneumothorax. Airway obstruction is often caused by a mucus plug that 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 depending on the technique used for treatment and include recurrence, aspiration, infection, keel extrusion, chondritis, granulation tissue formation, dysphonia, and tracheotomy dependence.

Outcome and Prognosis

Involvement of the glottis in subglottic stenosis has been found to have an unfavorable effect on outcome. In addition, using multivariate analysis, a prospective study by Pullens et al indicated that in patients who undergo surgery for laryngotracheal stenosis, involvement of the glottis and the existence of comorbidities are the only factors that significantly increase the risk of a poor long-term functional outcome.[33]

Similarly, a study by Xie et al indicated that in adults with laryngotracheal stenosis, open airway reconstruction is less likely to result in decannulation when posterior glottic stenosis or a larger red blood cell distribution width is present.[34]

However, isolated glottic stenosis tends to have a significantly better outcome when compared with other areas of laryngeal stenosis.

Voice outcomes vary according to the method of treatment but are generally either unchanged or improved.

In adult-acquired laryngeal stenosis, the most important factors in predicting the rate and time of decannulation include the length of the stenotic segment and the anatomical site.

The applications of mitomycin-C or chitosan are being extensively investigated in canine subglottic stenosis and have shown promising anecdotal results in human subglottic stenosis.

In a cadaver morphometric study, Sztano et al[35] found that endoscopic arytenoid Abduction lateroplexy was more effective in improving posterior glottis configuration, although arytenoidectomy and vocal cord lateral fixation were also beneficial.

Future and Controversies

Postoperative movement of the arytenoids in a patient with a stent may have a negative effect on the healing process.

Further investigation of the use of different stent materials and designs or botulinum toxin (in cases of vocal cord paralysis) is needed.

Recent reports suggest that mitomycin-C application is associated with airway complications from delayed wound healing in rabbits.[36] This should be considered during the use of mitomycin-C in clinical practice.