Laryngeal Stenosis

Laryngeal Steis

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Laryngeal steis is a congenital or acquired narrowing of the airway that may affect the supglottis, 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 opeting 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 steis. See the below.

Congenital laryngeal steis results from failure of the laryngeal lumen to recanalize. During normal development, the laryngeal lumen is obliteted to give rise to the epithelial lamina, which later recanalizes. By the 0th week of gestation, the laryngeal lumen is reestablished following recanalization. Incomplete recanalization results in various degrees of glottic and/or subglottic steis.

Congenital laryngeal atresia represents the most severe end of the spectrum of disease, arising from failed recanalization of the larynx and tchea during embryogenesis. Atresia can be diaged prenatally based on ultsound by identifying signs of congenital high airway obstruction syndrome (CHAOS). Glottic and supglottic atresia requires immediate tracheotomy at the time of delivery. Prenatal diagis of CHAOS allows for the use of the ex utero intpartum treatment (EXIT) procedure to evaluate and secure the airway at birth. Laryngotcheal 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, nging from division of thin membnous webs, staged dilations following incision, keel placement, open laryngotcheal reconstruction, and tcheostomy. Laryngeal webs often involve both the glottis and subglottis and may rely involve the supglottis. Glottic stenosis may also result from impaired vocal cord mobility or, rely, complete fusion of the true vocal folds.

Congenital subglottic stenosis is the third most common congenital laryngeal anomaly after laryngomalacia and vocal fold palysis. It is diaged where subglottic narrowing exists with no history of intubation or surgical tuma. Distinguishing congenital from acquired steis once a child has been intubated is difficult, but the suspected incidence is 5%. Congenital steis can be a contributing factor to acquired laryngeal steis.

Congenital subglottic steis may be divided into 2 types: membnous (fibrosis, submucous gland hyperpl, gnulation tissue) and cartilaginous. Membnous steis is more common than cartilaginous steis. Most commonly, membnous stees are circumferential and symmetric and may extend upward to include the true vocal cords. Cartilaginous steis is a deformity of the cricoid cartilage or tcheal ring projecting into the lumen. It may be symmetric (small but normal shaped cricoid or a nondistensible complete first tcheal ring tpped inside the cricoid) or asymmetric (elliptic or oval-shaped cricoid, isolated enlargement of either the anterior or posterior cricoid lamina, or laryngeal cleft).

Treatment is individualized. Mild cases of steis (gde I) are typically managed with a conservative approach consisting of regular follow-up care and aggressive 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 rely effective if the steis is cartilaginous.

Instrumentation of the airway for nonlaryngeal and nontcheal illnesses remains a primary cause for laryngeal stees. External tuma and infection have been supplanted by iatrogenic tuma as the most common cause of laryngotcheal steis in adults.

Approximately 5% of patients who are intubated for more than 0 days develop some degree of laryngeal steis. Ninety percent of acquired subglottic stees in infants and children are due to endotcheal intubation. The incidence of subglottic steis after intubation is reported to be -0%.

Extrinsic factors that contribute to the increased risk of steis following intubation include tumatic intubation, prolonged dution of intubation, multiple extubations and reintubations, use of an oversized endotcheal 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 gnulation tissue deposition from fibroblast prolifetion. Ulcetion due to pressure or tuma (ie, from endotcheal or nasogastric tube) can progress perichondritis or chondritis with associated scar formation and/or arytenoid fixation.

Acquired posterior glottic steis, typically resulting from tuma due to endotcheal intubation, is the most common form of glottic steis.

Caustic ingestion, foreign bodies, and iatrogenic causes due to surgery on the larynx may also result in laryngeal steis.

Supglottic steis may result from tcheotomy or laryngotcheal reconstruction. This is thought to be due to disruption of the supglottic lymphatics and/or relaxation or injury to the suspensory muscles of the hyoid bone and hyoepiglottic ligament. Such disruption may occur during laryngotcheal surgery.

So far, laryngeal steis has not been found to occur at a higher te in percutaneous dilational tracheotomy compared with open tcheotomy.

The role of gastroesophageal reflux is not clearly delineated but is thought to be a complicating factor via chemical irritation.

For the diagis of idiopathic progressive subglottic steis to be considered, no history of recent intubation or tuma should exist. Sex has been implicated as a possible cause due to the prepondence of females afflicted with this condition, but sevel reports were not able to confirm the presence of estrogen receptors in the biopsies.

Less common autoimmune s such as cicatricial pemphigoid, systemic lupus erythematosus, Wegener granulomatosis, sarcoidosis, rheumatoid arthritis, and relapsing polychondritis may result in laryngeal steis 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 membne obstructing the glottis. Emergent tcheotomy 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 supglottic or subglottic level. Congenital laryngeal webs are re; one report identified 5 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 steis is reported to be as high as 5% in patients who are intubated for more than 0 days. [1] Factors that contribute to the increased risk of steis following intubation include tumatic intubation, prolonged dution of intubation, multiple extubations and reintubations, use of an oversized endotcheal tube for intubation, motion of the patient or the tube, gastroesophageal reflux, and local infection.

Supglottic steis has recently been identified as a factor in chronic upper airway obstruction following tcheotomy or laryngotcheal reconstruction.

Approximately 5% of patients who are intubated for more than 0 days develop some degree of glottic steis. Ninety percent of acquired subglottic stees in infants and children are due to endotcheal intubation. The incidence of subglottic steis after intubation is reported to be -0%.

Congenital glottic steis is a re and may exist as a thin membnous steis, as a thick anterior or posterior web, or as a complete fusion of the vocal cords. Congenital laryngeal webs are re; one report identified 5 children with webs during a 32-year period.

In a retrospective, multi-institutional study, Gelbard et al reported an interesting degree of homogeneity between patients with idiopathic subglottic steis, finding that the vast majority of the 479 patients, from 0 participating centers, were female (98%) and Caucn (95%). [2]

Causes of laryngeal steis 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 pseudosttified, ciliated, columnar epithelium, with a submucosal layer composed of loose areolar tissue.

Submucosal edema – Caused by local tuma factors or infection, leads to luminal narrowing

Steis – Develops due to gnulation tissue deposition and fibroblast prolifetion

Gastroesophageal reflux – Thought to be a complicating factor, adding chemical irritation to the endotcheal tube-induced mechanical tuma

Acquired posterior glottic steis – Typically begins as ulcetion of the mucosa, due to pressure from the endotcheal tube, followed by secondary infection, perichondritis, chondritis, and formation of gnulation tissue, which leads to scar formation and possible arytenoid fixation

As a result of technological improvements, more premature infants are surviving due to prolonged endotcheal intubation. This now is the primary cause of subglottic steis in children, with the percentage estimated at -0%.

Congenital glottic webs and subglottic steis result from failure of the laryngeal lumen to recanalize. During normal development, the laryngeal lumen is obliteted by continued growth of the arytenoid masses and hypobnchial 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 steis.

Acquired glottic steis most commonly is due to tuma secondary to endotcheal intubation. Other causes include caustic ingestion, infections (such as croup), foreign bodies, external tuma, and iatrogenic causes due to surgery on the larynx. Long-term nasogastric intubation also may contribute to mucosal erosion and ulcetion in the postcricoid region, progressing to posterior glottic steis.

Supglottic steis or collapse is thought to be due to disruption of the supglottic lymphatics and/or relaxation or injury to the suspensory muscles of the hyoid bone and hyoepiglottic ligament. Such disruption may occur during laryngotcheal surgery.

Supglottic steis can also associated with external-beam diation or autoimmune s, with a majority of patients also having coexisting dysphagia, often associated with pharyngeal or esophageal stricture. Although patient response to endoscopic treatment is genelly favoble, additional procedures are typically needed, owing to a recurrence of the steis. The steis can be treated endoscopically in the opeting 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 steis is variable depending on the age, condition, and activity level of the patient and the extent of steis. Stridor is a common presenting sign in laryngeal obstruction. Supglottic or glottic obstruction genelly presents as inspitory stridor, while narrowing between the glottis through the tchea is associated with biphasic stridor.

Other symptoms include episodes of apnea, supsternal and subcostal retctions, tachypnea, and dyspnea. Hypoxia can result in cyais 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 are often noted. Mild-to-modete steis may be asymptomatic until an upper respitory tct infection leads to airway edema and thickened secretions which further compromise the airway. Re or persistent croup is also a typical finding in children with subglottic steis. 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 endotcheal intubation or laryngeal tuma can potentially develop subglottic steis. In genel, congenital stees are less severe than acquired ones.

The history should include an assessment of dyspnea and stridor, including the chacteristics of the stridor, time of onset, and relieving and aggvating 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), tuma, or caustic ingestion.

In genel, while anterior glottic scarring results in dysphonia, posterior glottic scarring tends to present with dyspnea. Acquired posterior glottic steis usually presents as difficulty on extubation or tcheotomy dependence.

In children, supglottic steis typically presents as persistent upper airway obstruction following tcheotomy or laryngotcheal reconstruction. This problem has recently been identified as a major factor in preventing decannulation following laryngotcheal reconstruction in the pediatric patient.

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

Treatment can be organized as follows into 4 broad categories:

Observation

Intlesional injections or applications

Endolaryngeal procedures

Open surgical procedures

Treatment depends on the ovell condition of the patient, symptoms, and extent of steis.

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 endotcheal intubation.

The proximal subglottic airway is bounded by the thyroid cartilage anteriorly and by the posterior plate of the cricoid cartilage latelly and posteriorly. Distally, the cricoid ring circumferentially surrounds the subglottic airway. This area is lined with pseudosttified 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 sepates it from the supglottis. 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 interytenoid 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 respitory epithelium with the subglottis.

Patients with a need for ventilatory support are genelly poor surgical candidates. Pulmonary status must be maximized prior to any airway intervention. Infants and children with a history of bronchopulmonary dyspl may need to demonstte a season without hospitalization for severe respitory illness before considetion for reconstruction. A tcheotomy for airway control may be necessary until pulmonary reserve is optimized.

Some authors recommend a minimum patient weight of 0 kg before laryngotcheal 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.

Zalzal GH. Posterior glottic steis. Int J Pediatr Otorhinolaryngol. 999 Oct 5. 49 Suppl :S279-82. [Medline].

Gelbard A, Donovan DT, Ongkasuwan J, et al. Disease homogeneity and treatment heterogeneity in idiopathic subglottic steis. Laryngoscope. 205 Nov 4. [Medline].

Stevens MS, Chang A, Simpson CB. Supglottic steis: etiology and treatment of a re condition. Ann Otol Rhinol Laryngol. 203 Mar. 22(3):205-9. [Medline].

Parker NP, Bandyopadhyay D, Misono S, et al. Endoscopic cold incision, balloon dilation, mitomycin C application, and steroid injection for adult laryngotcheal steis. Laryngoscope. 203 Jan. 23():220-5. [Medline].

Liberman M, Mathisen DJ. Tailored cricoplasty: an improved modification for reconstruction in subglottic tcheal steis. J Thoc Cardiovasc Surg. 2009 Mar. 37(3):573-8; discussion 578-9. [Medline].

Ter RM, Minamoto H, Carneiro F, Pego-Fernandes PM, Jatene FB. Laryngeal split and rib cartilage interpositional gfting: treatment option for glottic/subglottic steis in adults. J Thoc Cardiovasc Surg. 2009 Apr. 37(4):88-23. [Medline].

Xu W, Han D, Hu H, et al. Endoscopic mucosal suturing of vocal fold with placement of stent for the treatment of glottic stees. Head Neck. 2009 Jun. 3(6):732-7. [Medline].

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Yilmaz T, Suslu N, Gunaydin RO, et al. Microtpdoor Flap Technique for Treatment of Glottic Laryngeal Steis: Experience With 34 Cases. J Voice. 205 Aug 28. [Medline].

Dedo HH, Sooy CD. Endoscopic laser repair of posterior glottic, subglottic and tcheal steis by division or micro-tpdoor flap. Laryngoscope. 984 Apr. 94(4):445-50. [Medline].

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Taylor SC, Clayburgh DR, Rosenbaum JT, et al. Clinical manifestations and treatment of idiopathic and Wegener gnulomatosis-associated subglottic steis. JAMA Otolaryngol Head Neck Surg. 203 Jan. 39():76-8. [Medline].

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Timman ST, Schoemaker C, Li WWL, et al. Functional outcome after (laryngo)tcheal resection and reconstruction for acquired benign (laryngo)tcheal steis. Ann Cardiothoc Surg. 208 Mar. 7 (2):227-36. [Medline]. [Full Text].

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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

Mark E Gerber, MD is a member of the following societies: American Academy of Otolaryngology-Head and Neck Surgery, American Bronchoesophagological Association, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat Advances in Children, American Academy of Pediatrics, American Rhinologic Society

Disclosure: Nothing to disclose.

Judy L Chen, MD Attending Physician, Department of Otolaryngology-Head and Neck Surgery, NorthShore University HealthSystem

Judy L Chen, MD is a member of the following societies: American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery

Disclosure: Nothing to disclose.

Fncisco Talave, PharmD, PhD Adjunct Assistant Professor, University of Nebska Center College of Pharmacy; Editor-in-Chief, Medscape Drug

Disclosure: Received salary from Medscape for employment. for: Medscape.

Stephen G Batuello, MD Consulting Staff, Colodo ENT Specialists

Stephen G Batuello, MD is a member of the following societies: American Academy of Otolaryngology-Head and Neck Surgery, American Association for Physician Leadership, American Medical Association, Colorado Medical Society

Disclosure: Nothing to disclose.

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colodo School of Medicine

Arlen D Meyers, MD, MBA is a member of the following societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;Preacute Population Health Management;The Physicians Edge
Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa
Received stock from RxRevu; Received ownership interest from Cerescan for consulting; for: Rxblockchain;Bridge Health.

Clark A Rosen, MD Director, University of Pittsburgh Voice Center; Professor, Department of Otolaryngology and Communication Science and s, University of Pittsburgh School of Medicine

Clark A Rosen, MD is a member of the following societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, Pennsylvania Medical Society

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Merz North America Inc
Received consulting fee from Merz North America Inc for consulting; Received consulting fee from Merz North America Inc for speaking and teaching.

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