Pediatric Subglottis Stenosis Surgery 

  • Author: John E McClay, MD; Chief Editor: Glenn C Isaacson, MD, FACS, FAAP   more...
 
Updated: Dec 5, 2011
 

Background

Subglottic stenosis (SGS) is a narrowing of the subglottic airway (see image below), which is housed in the cricoid cartilage. The subglottic airway is the narrowest area of the airway because it is a complete, nonexpandable, and nonpliable ring, unlike the trachea, which has a posterior membranous section, and the larynx, which has a posterior muscular section.

Intraoperative endoscopic view of a normal subglotIntraoperative endoscopic view of a normal subglottis.

The term SGS implies a narrowing that is created or acquired, although the term is applied to both congenital lesions of the cricoid ring (see first 3 images below) and acquired SGS (see the remaining images below).

A glottic and subglottic view of a grade III subglA glottic and subglottic view of a grade III subglottic stenosis in an 18-year-old patient following a motor vehicle accident. The true vocal cords are seen in the foreground. Subglottic stenosis is seen in the center of the picture. An intraoperative view of granular subglottic stenAn intraoperative view of granular subglottic stenosis in a 3-month-old infant who was born premature, weighing 800 g. The area is still granular following cricoid split. This patient required tracheotomy and eventual reconstruction at age 3 years. True vocal cords are shown in the foreground (slightly blurry). Intraoperative laryngeal view of the true vocal coIntraoperative laryngeal view of the true vocal cords of a 9-year-old boy. Under the vocal cords, a spiraling subglottic stenosis can be seen. A close-up view of the stenosis in a 9-year-old boA close-up view of the stenosis in a 9-year-old boy with spiraling subglottic stenosis. This spiraling subglottic stenosis is not complete circumferentially. Laser therapy was the treatment choice and was successful after 2 laser treatments. Continued lasering of the subglottic stenosis in aContinued lasering of the subglottic stenosis in a 9-year-old boy with spiraling subglottic stenosis. The reflected red light is the aiming beam for the CO2 laser. Endoscopic view of the same patient (9-year-old boEndoscopic view of the same patient (9-year-old boy with spiraling subglottic stenosis) two months after surgery. Some mild residual posterior subglottic stenosis remains, but the child is asymptomatic and the airway is open overall. Preoperative view of a 4-month-old infant with acqPreoperative view of a 4-month-old infant with acquired grade III subglottic stenosis from intubation. Vocal cords are in the foreground. An endoscopic subglottic view of a 4-month-old witAn endoscopic subglottic view of a 4-month-old with grade III subglottic stenosis born premature at 26 weeks' gestation and intubated for 3 months. Postoperative view in a 4-month-old infant with acPostoperative view in a 4-month-old infant with acquired grade III subglottic stenosis from intubation. Following cricoid split, the patient had been intubated for 1 week and extubated for 1 week. A subglottic view of the same patient (a 4-month-oA subglottic view of the same patient (a 4-month-old infant with acquired grade III subglottic stenosis from intubation) following dilation with an endotracheal tube to lyse the thin web of scar and a short course (5-day) treatment with oral steroids. Postoperative view of the same patient (a 4-month-Postoperative view of the same patient (a 4-month-old infant with subglottic stenosis following cricoid split). This picture is 2 weeks after lysis of scar and steroids. Notice very mild recurrence of scaring at the site of previous scar. Overall, the airway is open and patent. The anterior superior area can be seen, with a small area of fibrosis where the cricoid split previously healed. Preoperative endoscopic subglottic view of a 2-yeaPreoperative endoscopic subglottic view of a 2-year-old patient with congenital and acquired vertical subglottic stenosis.

Acquired SGS is the most common acquired anomaly of the larynx in children and the most common abnormality requiring tracheotomy in children younger than 1 year. Correction of this abnormality requires expanding the lumen of the cricoid area to increase airflow and decrease obstructive breathing. Surgical correction of SGS has been performed with various techniques over the years.

Early in the 20th century, acquired SGS was usually related to trauma or infection from syphilis, tuberculosis, typhoid fever, or diphtheria. Also, children often had tracheotomies placed that caused laryngeal stenosis. In this era, attempted laryngeal dilation failed as a treatment for SGS.

Acquired SGS increasingly occurred in the late 1960s through the 1970s, after McDonald and Stocks introduced long-term intubation as a treatment method for neonates in need of prolonged ventilation for airway support.[1] The increased incidence of SGS focused new attention on the pediatric larynx, and airway reconstruction and expansion techniques were developed.

Surgery without cartilage expansion

In 1971, Rethi and Rhan described a procedure for vertical division of the posterior lamina of the cricoid cartilage with Aboulker stent placement. A metal tracheotomy tube was attached to the Aboulker stent with wires, and the anterior cartilaginous incision was closed. In 1974, Evanston and Todd described success with a castellated incision of the anterior cricoid cartilage and upper trachea, which was sewn open, and a stent made of a rolled silicone sheet was placed in it for 6 weeks. In 1980, Cotton and Seid described a procedure in which tracheotomy is avoided called the anterior cricoid split (ACS).[2] The procedure was designed for use in neonates (usually, those born prematurely) with anterior SGS or SGS who had airway distress after extubation. The cricoid ring was divided anteriorly and a laryngofissure was created in an attempt to expand the airway without a tracheotomy. Holinger et al also described success with this procedure in 1987.[3]

Surgery with cartilage-grafting reconstruction

In 1974, Fearon and Cotton described the successful use of cartilage grafts to enlarge the subglottic lumen in African green monkeys and in children with severe laryngotracheal stenosis.[4] All augmentation materials were evaluated, including thyroid cartilage, septal cartilage, auricular cartilage, costal cartilage, hyoid bone, and sternocleidomastoid myocutaneous flaps. After significant work, it appeared that costal cartilage grafts had the highest success rate.

In the 1980s, Cotton reported his experience with laryngeal expansion with cartilage grafting.[5, 6, 7, 2] His success rates depended on degree of stenosis. More severe forms of stenosis required multiple surgical procedures. Cotton used the Aboulker stent.

In 1991, Seid et al described a form of single-stage laryngotracheal reconstruction in which cartilage was placed anteriorly to expand the subglottis and upper trachea to avoid a tracheotomy.[8]

In 1992, Cotton et al described a 4-quadrant cricoid split, along with anterior and posterior grafting.[9] In 1993, Zalzal reported 90% decannulation with any degree of SGS with his first surgical procedure.[10] Zalzal customized the reconstruction on an individual basis, and most patients received Aboulker stents for stabilization.

Cricotracheal resection

In 1993, Monnier described partial cricotracheal resection with primary anastomoses for severe SGS because grade III and grade IV SGS (ie, severe SGS) often requires multiple (3-4) surgical augmentations for decannulation.[11] In 1997, Stern described his experience with the procedure, reporting a decannulation rate higher than 90% for primary and rescue cricotracheal resection.[12]

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Pathophysiology

The pathophysiology of congenital SGS is a malformed cricoid cartilage in utero. The cause of congenital SGS is in utero malformation of the cricoid cartilage.

The etiology of acquired SGS is related to trauma of the subglottic mucosa. Injury can be caused by infection or mechanical trauma, usually from endotracheal intubation but also from blunt, penetrating, or other trauma. Historically, acquired SGS has been related to infections such as tuberculosis and diphtheria. Over the past 40 years, the condition has typically been related to mechanical trauma.

Factors implicated in the development of SGS include the size of the endotracheal tube relative to the child's larynx, the duration of intubation, the motion of the tube, and repeated intubations. Additional factors that affect wound healing include systemic illness, malnutrition, anemia, and hypoxia.

Local bacterial infection may play an important role in the development of SGS. Gastroesophageal reflux (GER) may play an adjuvant role in the development of SGS because it causes the subglottis to be continually bathed in acid, which irritates and inflames the area and prevents it from correctly healing. A systemic or GI allergy may cause the airway to be more reactive, creating a greater chance of developing stenosis.

Acquired SGS is often caused by endotracheal intubation. Mechanical trauma from an endotracheal tube, as it passes through or remains for long periods in the narrowed neonatal and subglottic airway, can lead to mucosal edema and hyperemia. These conditions then can progress to pressure necrosis of the mucosa. These changes have been observed within a few hours of intubation and may progress to expose the perichondrium of the cricoid cartilage. Infection of the perichondrium can result in a subglottic scar.

This series of events can be hastened if an oversized endotracheal tube is used. Always check for an air leak after placing an endotracheal tube because of the risk of necrosis of the mucosa, even in short surgical procedures. This practice is common among anesthesiologists. Usually, the pressure of the air leak should be less than 20 cm of water, so that no additional pressure necrosis occurs in the mucosa of the subglottis.

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Epidemiology

Frequency

United States

No known frequency has been reported for congenital SGS; the incidence of acquired SGS has greatly decreased over the past 40 years.

  • In the late 1960s, when endotracheal intubation and long-term ventilation for premature infants began, the incidence of acquired SGS was as high as 24% in patients who required such care.
  • In the 1970s and 1980s, estimates of the incidence of SGS were 1-8%.
  • In 2000, Choi reported that the incidence of SGS had remained constant at the Children's National Medical Center in Washington DC, accounting for approximately 1-2% of the children who had graduated from the neonatal ICU (NICU).[13]
  • Walner reported that, among 504 neonates who were admitted to the level III NICU at the University of Chicago in 1997, 281 were intubated for an average of 11 days; over a 3-year period, no patients developed SGS.[14]
  • In 1996, a report from France also described no incidence of SGS in the neonatal population who were intubated with very small endotracheal tubes (2.5 mm internal diameter) in attempts to prevent trauma to the airway.

International

International frequency is the same as that of the United States.

Mortality/Morbidity

Patients can die if they have significant SGS that is left untreated. Difficulty breathing and exercise intolerance can occur with mild, moderate, or severe SGS.

Race

No racial predilection is noted.

Sex

Equal sex distribution is noted.

Age

SGS is observed more often in premature infants because they may require mechanical ventilation for other system or pulmonary problems secondary to their prematurity. The mechanical ventilation can result in airway trauma and, potentially, SGS.

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Contributor Information and Disclosures
Author

John E McClay, MD  Associate Professor of Pediatric Otolaryngology, Department of Otolaryngology-Head and Neck Surgery, Children's Hospital of Dallas, University of Texas Southwestern Medical School

John E McClay, MD is a member of the following medical societies: American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, and American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Orval Brown, MD  Director of Otolaryngology Clinic, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Texas Southwestern Medical Center at Dallas

Orval Brown, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American Bronchoesophagological Association, American College of Surgeons, American Medical Association, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat Advances in Children, and Society of University Otolaryngologists-Head and Neck Surgeons

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Alan D Murray  MD, Pediatric Otolaryngologist, ENT for Children; Full-Time Staff, Medical City Dallas Children's Hospital; Consulting Staff, Department of Otolaryngology, Medical Center of Lewisville, Children's Medical Center at Dallas, Cook Children's Medical Center; Full-Time Staff, Texas Pediatric Surgery Center, Cook Children's Pediatric Surgery Center Plano

Alan D Murray is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American College of Surgeons, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat Advances in Children, and Texas Medical Association

Disclosure: Nothing to disclose.

Paul D Petry, DO, FACOP, FAAP  Consulting Staff, Freeman Pediatric Care, Freeman Health System

Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Chief Editor

Glenn C Isaacson, MD, FACS, FAAP  Professor of Otolaryngology-Head and Neck Surgery and Pediatrics, Temple University School of Medicine

Glenn C Isaacson, MD, FACS, FAAP is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American Bronchoesophagological Association, American College of Surgeons, American Laryngological Rhinological and Otological Society, American Society of Pediatric Otolaryngology, and Society of University Otolaryngologists-Head and Neck Surgeons

Disclosure: Covidien Honoraria Consulting

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Intraoperative endoscopic view of a normal subglottis.
A glottic and subglottic view of a grade III subglottic stenosis in an 18-year-old patient following a motor vehicle accident. The true vocal cords are seen in the foreground. Subglottic stenosis is seen in the center of the picture.
Endoscopic view of the true vocal cords in the foreground and the elliptical congenital subglottic stenosis (SGS) in the center of the picture.
Endoscopic subglottic view of congenital elliptical subglottic stenosis, a close-up of subglottic stenosis.
An intraoperative view of a split cricoid in a patient with elliptical congenital subglottic stenosis. The open airway can be seen in the center of the picture. The wound extends to the inferior one third of the thyroid cartilage. The first 2 tracheal rings also are divided.
Rib graft for reconstruction of subglottic stenosis carved in boat type anterior graft. The diamond-shaped internal intraluminal component with perichondrium still present is seen on the top section of the rib and the shape of the rib is seen on the backside of the carved out diamond shape.
An intraoperative aerial view of an anterior cartilage graft in place over the wound. Note external component of the graft still looks like a portion of the rib. The internal component has been carved in a diamond shape. This is an intraoperative photo of the patient with elliptical congenital subglottic stenosis. The cartilage graft (rib graft for reconstruction of subglottic stenosis carved in boat type anterior graft) was used in this patient for reconstruction.
An intraoperative side view of the neck with cartilage graft (rib graft for reconstruction of subglottic stenosis carved in boat type anterior graft) to be placed into the posterior cricoid suspended and having all sutures in position, ready to be tied. All the sutures are placed prior to lowering the graft into position. Then, the sutures are tied.
A 1-week postoperative subglottic view of the surgical repair with an anterior graft of a congential elliptical subglottic stenosis. The white areas to the left and right are the true vocal cords. The graft is seen at the superior and mid area.
Subglottic view of very mild congenital subglottic stenosis. Laterally, the area looks only slightly narrow. When endotracheal tubes were used to determine its size, it was found to be 30% narrowed.
An intraoperative view of granular subglottic stenosis in a 3-month-old infant who was born premature, weighing 800 g. The area is still granular following cricoid split. This patient required tracheotomy and eventual reconstruction at age 3 years. True vocal cords are shown in the foreground (slightly blurry).
Intraoperative laryngeal view of the true vocal cords of a 9-year-old boy. Under the vocal cords, a spiraling subglottic stenosis can be seen.
A close-up view of the stenosis in a 9-year-old boy with spiraling subglottic stenosis. This spiraling subglottic stenosis is not complete circumferentially. Laser therapy was the treatment choice and was successful after 2 laser treatments.
Continued lasering of the subglottic stenosis in a 9-year-old boy with spiraling subglottic stenosis. The reflected red light is the aiming beam for the CO2 laser.
Endoscopic view of the same patient (9-year-old boy with spiraling subglottic stenosis) two months after surgery. Some mild residual posterior subglottic stenosis remains, but the child is asymptomatic and the airway is open overall.
Preoperative view of a 4-month-old infant with acquired grade III subglottic stenosis from intubation. Vocal cords are in the foreground.
An endoscopic subglottic view of a 4-month-old with grade III subglottic stenosis born premature at 26 weeks' gestation and intubated for 3 months.
Postoperative view in a 4-month-old infant with acquired grade III subglottic stenosis from intubation. Following cricoid split, the patient had been intubated for 1 week and extubated for 1 week.
A subglottic view of the same patient (a 4-month-old infant with acquired grade III subglottic stenosis from intubation) following dilation with an endotracheal tube to lyse the thin web of scar and a short course (5-day) treatment with oral steroids.
Postoperative view of the same patient (a 4-month-old infant with subglottic stenosis following cricoid split). This picture is 2 weeks after lysis of scar and steroids. Notice very mild recurrence of scaring at the site of previous scar. Overall, the airway is open and patent. The anterior superior area can be seen, with a small area of fibrosis where the cricoid split previously healed.
Anterior rib graft with a diamond shape. Note it measures approximately 1.7 mm in length. Intraluminal site is facing up. Flanges of rib are carved to remain on the outside of the trachea to prevent prolapse into the trachea.
Representative (noninclusive) sample of varying sizes of Aboulker stents (range of 3-15 mm). These stents are hollow and coated in Teflon.
A glottic endoscopic view of the top of Aboulker stent in the larynx protruding through and above the true and false vocal cords. The arytenoids and epiglottic folds are seen.
Diagram of a long Aboulker stent wired to a metal Jackson tracheotomy tube.
A Jackson tracheotomy tube wired to a long Aboulker stent.
A 7-mm Montgomery tracheotomy tube with caps
A subglottic endoscopic view of granulation tissue (superior center portion of the picture) that occurred at the graft site 10 days following a laryngotracheal reconstruction performed with an anterior graft. Granulation tissue is at the superior center portion of the picture.
Intraoperative suspended view through a subglottoscope of the subglottis, showing the granulation tissue just prior to removal with cup forceps and laser. This was taken in a patient who developed granulation tissue that occurred at the graft site 10 days following a laryngotracheal reconstruction performed with an anterior graft.
Postexcision view of granulation tissue through the subglottoscope. This was taken in a patient who developed granulation tissue that occurred at the graft site 10 days following a laryngotracheal reconstruction performed with an anterior graft.
Preoperative view of glottic stenosis and small glottic chink in a 2-year-old child who underwent anterior and posterior grafting. The child's glottic narrowing is tight, and scarring of the right arytenoid has occurred.
Preoperative endoscopic subglottic view of a 2-year-old patient with congenital and acquired vertical subglottic stenosis.
Postoperative view of the glottic larynx in a child who underwent anterior and posterior grafting for subglottic stenosis. The child had glottic narrowing that is more open and in neutral position after the surgery. The scarring of the right true vocal cord appears improved, and her voice is more normal.
Postoperative close-up view of the true vocal cords in the patient with congenital and acquired vertical subglottic stenosis.
A 3-month postoperative subglottic view of the patient with congenital and acquired vertical subglottic stenosis, who underwent anterior and posterior costal cartilage grafting with successful decannulation showing open subglottis with some very mild damage to the anterior wall and the suprastomal area where the tracheostomy tube had been placed.
End view of an Aboulker stent showing the central opening. These stents are hollow and coated in Teflon.
 
 
 
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