---------------------------------------------------------------------------- TITLE: LARYNGOTRACHEAL STENOSIS SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: November 30, 1994 RESIDENT PHYSICIAN: Denise V. Guendert, M.D. FACULTY: Byron J. Bailey, M.D., F.A.C.S. DATABASE ADMINISTRATOR: Melinda McCracken, M.S. ---------------------------------------------------------------------------- "This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." HISTORY Congenital subglottic stenosis was first described by Rossi in 1826. Laryngeal stenosis resulting from inflammatory conditions (syphilis very predominant) described by Mackenzie in 1862. In the latter part of the 19th century Schroetter performed laryngeal dilatation with rigid vulcanite tube and used pewter plugs for stents. It wasn't until the early 1900s that Jackson described use of implanted cartilage for the correction of tracheal stenosis. In the first few decades of the 20th century, the most common cause of laryngotracheal stenosis in children was "high tracheotomy" for inflammatory illnesses such as diphtheria or croup. With world war I and II and the advent of antibiotics, things changed and most stenosis were the result of laryngeal trauma. Treatment of stenosis at this time consisted of multiple dilations. Initial experiments with open procedures were for cancer. In 1938 Negus described the technique of laryngofissure with dermal grafting for extensive laryngeal scarring. In 1953 Conley described surgical correction of subglottic stenosis in adults by segmental resection. Laryngeal stents, as we now know them, did not come into existence until 1965 when Montgomery developed the T-tube. EMBRYOLOGY The lower respiratory tract begins to develop 26 days after conception as the median laryngotracheal groove in the caudal end of the ventral pharynx. The laryngotracheal diverticulum becomes separated from the foregut by ridges called tracheoesophageal folds which fuse to form the tracheoesophageal septum. The septum divides the foregut into a ventral laryngotracheal tube and a dorsal esophagus. The larynx develops 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. Recanalization gives rise to the laryngeal ventricles, vocal folds, and vestibular folds. This is complete by the 10th week of gestation. Failure of the tracheoesophageal folds to fuse during the fourth to fifth weeks cause a defective tracheoesophageal septum which leaves a communication between the trachea and esophagus. The incidence of T-E fistula 1:2500 births. Tracheal atresia and stenosis are often associated with T-E fistula. LARYNGEAL STENOSIS A. Glottic stenosis 1. congenital laryngeal stenosis Occurs secondary to inadequate recanalization of the laryngeal lumen by the end of the third month of gestation. Findings will depend on degree of recanalization with absence of recanalization resulting in atresia and partial recanalization resulting in stenosis or webbing. Atresia and stenosis can occur at any level, though atresia usually results in closure at or above the vocal cords. Upon clamping the umbilical cord, the neonate with atresia is aphonic, deteriorates rapidly, and will die of asphyxia unless emergent tracheotomy is performed. Direct laryngoscopy is diagnostic. Incomplete atresia can be managed with tracheotomy over a bronchoscope. If there is an associated T-E fistula, the infant with atresia has less risk of immediate asphyxia. After the airway is established in atresia, the next step is to create laryngeal airway which is accomplished with laryngofissure. Important to attempt to provide laryngeal airway so that tracheotomy is not the only airway, especially in children since they are particularly at risk for tube occlusion and self extubation. The phonatory and protective mechanisms of the larynx usually remain poor after open repair. Laryngeal atresia is associated with a high incidence of other anomalies such as esophageal atresia, urinary tract abnormalities, and limb defects especially those involving the radius. Laryngeal webs account for approximately 5% of congenital laryngeal anomalies. 75% occur at the glottic level. Most present within the first few months of life and do not require airway support. Benjamin created the following classification for webs: Glottic: Thin and membranous;thick at the anterior commissure; or severe with subglottic involvement Subglottic: With or without cricoid cartilage involvement, 7% of webs Congenital: Interarytenoid fixation Supraglottic: Extremely rare <2% congenital webs Thin webs can be excised with the CO2 laser or microscissors, addressing one side of larynx at a time to avoid further webbing. Thicker webs are often associated with subglottic narrowing and are more difficult to treat, they often require tracheotomy ( 40%) followed by laryngofissure with division of web possibly cricoid cartilage and closure over a keel or stent. Timing of correction controversial. Much more difficult procedures in smaller children but you do not want to leave a small child with the tracheotomy being there sole airway as the risk of decannulation and tube obstruction in this age group is high. 2. Acquired glottic stenosis The most common cause of acquired glottic stenosis in both children and adults is external laryngeal trauma. Trauma results in a collection of blood within the soft tissues of the larynx and this can lead to organization into fibrous tissue. Trauma can also result in mucosal tears and cartilage fractures with subsequent stenosis. The degree of stenosis and dysfunction can be reduced by early intervention of mucosal tears and cartilage fractures Intubation either prolonged or traumatic may also lead to glottic stenosis though most commonly results in subglottic stenosis. Adults tend to acquire stenosis at posterior commissure secondary to traumatic intubation causing mucosal disruption which later scars and contracts resulting in fixation of the arytenoids towards the midline. The keys to avoiding intubation induced glottic stenosis are performing atraumatic intubation with smallest tube acceptable, limiting total time of intubation, reducing motion of tube while patient intubated, and treating gastric reflux. Other potential causes of acquired glottic stenosis are several. Cricothyrotomy and high tracheotomy place the glottis at risk and it is very important to revise these immediately and perform DL to assess for laryngeal injury as in laryngeal trauma. Glottic surgery, especially that which addresses the anterior commissure often leads to narrowing secondary to webbing. XRT may result in chondroradionecrosis with subsequent stenosis up to 20 years after XRT. Prolonged presence of a nasogastric tube may result in stenosis secondary to compression of the mucosa between the cervical vertebrae and the cricoid cartilage. Other causes include: inhalation burns, caustic ingestions, syphilis, TB, leprosy, mycosis,sarcoid, Wegener's granulomatosis, SLE, relapsing polychiondritis, amyloidosis etc... TB most commonly involves the intraarytenoid space and posterior vocal cords. Sarcoid usually involves the supraglottis with nodules at first then scarring and stenosis. Wegeners primarily involves the subglottis, histoplasmosis the anterior TVCs and epiglottis, coccidiomycosis the posterior commissure, false vocal cords, and aryepiglottic folds. Symptoms of acquired glottic stenosis include variable degrees of hoarseness or complete aphonia, inspiratory stridor which may become biphasic as severity increases, and dyspnea that is either mild and associated with URIs or dramatic. Diagnosis can be made with IDL or flexible scope though, intraoperative laryngoscopy and tracheoscopy necessary. Types of acquired glottic stenosis include anterior glottic stenosis, posterior glottic stenosis, and complete glottic stenosis. Anterior glottic stenosis can be thin involving only the TVCs or thick and involve the TVCs, FVCs, and ventricles.Thin webs are usually secondary to glottic surgery at the anterior commissure. Thick webs are usually the result of external laryngeal trauma. Posterior glottic stenosis is usually secondary to either traumatic or prolonged endotracheal intubation and is usually associated with some degree of subglottic involvement. Mucosal injury results in formation of granulation tissue with subsequent scarring of the interarytenoid region. These patients may also have associated fixation of the cricoarytenoid joint and/or subglottic stenosis. The vocal quality is usually good because the cords are adducted but the airway usually compromised to some degree. This is often confused with bilateral vocal cord paralysis on indirect laryngoscopy and EMG can differentiate posterior glottic stenosis from paralysis. It is important to palpate the arytenoids during direct laryngoscopy. Complete glottic stenosis is rare without associated subglottic or supraglottic involvement. Most commonly this occurs secondary to delayed or inadequate treatment of laryngeal trauma. Management options for acquired glottic stenosis vary with the thickness of the stenosis and the site of involvement. Medical management includes humidification, antibiotics, and steroids in a closely monitored setting. The two basic forms of surgicalmanagement include endoscopic techniques and open techniques. Endoscopic techniques include dilatation, laser or cold steel incision of mucosa, and the microtrapdoor mucosal flap(MTD flap). CO2 laser removal of stenotic regions usually only successful in granulomatous stage of scarring, some also inject kenalog at this stage. Dedo and Sooy pioneered the laser epithelial preservation techniques using the CO2 laser to develop a microtrapdoor flap. The MTD flap is indicated for thin stenosis 10mm or less in vertical height, involving the posterior commissure. Dedo and Sooy also reported the use of the MTD flap in thin stenosis of the subglottis and trachea. Endoscopic techniques do not work on mature scars except for perhaps temporary airway improvement. Many feel that traumatizing mature scars endoscopically leads to further scar deposition. Though thin anterior commissure webs can be successfully treated with the CO2 laser followed by endoscopic keel placement, thicker webs are better managed with median thyrotomy lysis of web, and placement of either Montgomery silicone keel or silastic keel. The silastic keel has the advantage of later endoscopic removal whereas the silicone requires open approach. Posterior glottic stenosis is approached through a median thyrotomy. The posterior scar is excised , the interarytenoid muscle is divided, and the area is covered with either mucosal advancement flaps from the hypopharynx or free skin graft. A stent is not necessary. Complete glottic stenosis is also approached through a midline thyrotomy starting at the cricothyroid membrane over a kelly to incise the anterior scar. The posterior scar is either incised or excised and again covered with skin graft or mucosal flaps. Most surgeons place a keel though some use stents. B. Subglottic stenosis 1. Congenital By definition this is narrowing in the region bounded superiorly by a plane of 0.5 cm below the glottis and inferiorly by the lower edge of the cricoid cartilage that occurs in the absence of a history of intubation, trauma, tracheitis etc....The normal newborn subglottic diameter is 4.5 to 5.5 mm. In premature infants it is 3.5mm. A subglottic diameter less than 4mm in a fullterm infant is considered narrow. Congenital subglottic stenosis is thought to be secondary to failure of the lumen to recanalize properly during embryogenesis. Cotton categorized subglottic stenosis into membranous and cartilaginous. Membranous stenosis is a fibrous soft-tissue thickening secondary to either increased fibrous tissue or hyperplastic mucus glands, it is usually circumferential and may involve the TVCs. Cartilaginous stenosis is more variable, but the most common results from thickening of the anterior lamina of the cricoid cartilage causing an anterior subglottic shelf though other malformations may be present as well including lateral bulges which produce a slitlike opening and trapped first tracheal ring. The severity of symptoms depends on degree of narrowing. Membranous stenosis is usually less severe. Subglottic stenosis is the third most common cause of congenital stridor following laryngomalacia and vocal cord paralysis. Stridor, when present (62%)is usually biphasic. The second most common finding is that of recurrent croup(38%). Patients may present at birth or several months later. Diagnosis based on history and physical with endoscopy. AP and lateral neck film if obtained may reveal funnel shape narrowing and give idea of the length of stenosis. Fluoroscopy may give indication of laryngeal mechanics and reveal TVC paralysis. Endoscopy is necessary for proper diagnosis. Flexible scope gives information regarding vocal cord mobility. Congenital subglottic stenosis is often associated with other head and neck abnormalities and or Down's syndrome Congenital subglottic stenosis is not only less common but is usually less severe than the acquired form of stenosis and can often be managed by watchful waiting and early treatment of URIs. At times a tracheotomy is needed until the subglottic diameter has increased with age. Fearon reported that 76 of 153 patients required a tracheotomy, but all were decannulated by 6 yrs. Rosenfield studied congenital subglottic stenosis and found resolution of tracheotomy dependence of 19% at 6 months, 39% at 12 months, 69% at 18 months. Holinger has previously reported a mean cannulation time of 18 months. The older a child is at presentation (likely the less severe the stenosis), the shorter the time of trach dependency). An anterior cricoid split or laryngotracheoplasty may be required in select cases especially if cricoid abnormalities exist. (see below for techniques). It is very important to inform parents of potential risks of longterm tracheotomy including tube obstruction and accidental decannulation verses those of laryngeal expansion surgery. Treatment should be individualized. 2. Acquired subglottic stenosis Acquired subglottic stenosis is usually secondary to prolonged endotracheal intubation, (>90% of cases).There really is no safe time of intubation though, since subglottic stenosis has been reported after 17 hours of intubation(Bergstrom 1962). The incidence following prolonged endotracheal intubation ranges from 0.9-8.3%. Trauma as a cause is much more unusual in children than adults. Premature infants tolerate intubation for longer periods of time than fullterm infants or adults, this is thought to be secondary to the pliability of immature cartilage. The French, who report a lower incidence of subglottic stenosis than US, advocate the following tube sizes to lessen the risk of stenosis: 2.5 mm in children <2500g, 3.0 mm in children 2500-4000g, and 3.5 mm in children > 4000g, as they determined the size of an endotracheal tube to be a major risk factor for development of subglottic stenosis in the neonate The pathogenesis of ET Tube induced stenosis is as follows: pressure necrosis occurs with ulceration over the vocal processes and the posterior and lateral subglottic mucosa with subsequent cricoid chondritis, healing then leads to the formation of granulation tissue and fibrosis of the exposed submucosa. The likelihood of subglottic stenosis increases with increased motion of tube, infection, repeated intubation, compromise of immune status, reflux and presence of nasogastric tubes. The symptoms though usually more severe are similar to congenital subglottic stenosis and diagnosis is based on endoscopy. There are separate classifications of subglottic stenosis for adults and for children. Cotton proposed a staging system for children based on the relative relation in cross sectional area of the stenosis that predicts the rate of successful decannulation. Cotton's system is as follows: Grade 1 - compromise of <70% cross sectional area, Grade 2 - 70-90%, Grade 3 - >90%, Grade 4 - complete obliteration of lumen. Children with grade 4 stenosis not only are less likely to be successfully decanulated and require more than one procedure, but also have worse post-operative vocal quality. McCaffrey studied subglottic stenosis in adults and determined that cross sectional area was not a predictive factor of subsequent decannulation as it is in children. He devised the following classification system instead: Stage 1 lesions are stenotic areas <1 cm in length that are membranous and these can effectively be treated with dilation, Stage 2 SGS are lesions > 1 cm in length that do not extend to the glottis or trachea. Stage 3 SGS are lesions that extend to the upper trachea. Stage 4 SGS involves the glottis with fixation or paralysis of the TVCs. Management options for subglottic stenosis are several. Endoscopic techniques including dilatation, CO2 laser mucosal incisions, mucosal trapdoor flaps, should only be considered in cases of mild stenosis (Grade 1 and 2). Factors associated with failure of endoscopic techniques include: failure of previous endoscopic procedures, significant loss of cartilaginous support, combined laryngeal and tracheal stenosis, fibrotic scar tissue in the intraarytenoid region, bacterial tracheitis following tracheotomy, exposure of cartilage following previous laser work, circumferential scarring, and vertical scar length >1 cm. Reported success rates with the laser on grade 1 and 2 stenosis are 66-80%. Open procedures have been developed to avoid tracheotomy and include anterior cricoid split in the neonate and one stage laryngotracheoplasty in older infants/children. There are also two stage laryngotracheoplasties using various forms of grafting materials with stenting. Contraindications to open procedures include absolute contraindication to general anesthesia and uncontrolled gastroesophageal reflux. It is imperative to r/o TVC paralysis and/or other airway abnormalities prior to proceeding with management of stenosis. Cartilage is the most commonly used graft material for airway reconstruction. Sources of cartilage include the rib, thyroid cartilage, septum, and conchal bowl. Grafts can also be fashioned form iliac crest, hyoid bone, and composite clavicular bone muscle skin flaps. Hirano reported good results with the use of hydroxyapatite in reconstructing the laryngotracheal framework, thus avoiding donor site morbidity. Stents include endotracheal tubes, the foam finger cot, rolled silastic, the Montgomery T-tube, the Aboulker stent, and the Jackson stent and tracheotomy tube combination to name a few and are usually left in place for 6 weeks with removal dependent upon findings at subsequent endoscopy. Longer stenting (4-6 months) reserved for four quadrant cricoid split or those cases where cricoid significantly ossified or lacks rigidity. The three principles of stenting include: provide support for soft tissue grafts, provide support for cartilaginous framework, and prevent scar contracture or luminal narrowing. The ideal stent should conform to lumen, be stable and exert pressure but not cause ischemia Though originally described for neonatal acquired subglottic stenosis that is moderate or severe in a patient who has not undergone tracheotomy, anterior cricoid split is now also indicated for older infants with progressive respiratory pathology and those status-post tracheotomy. The criteria for ACS are the following: extubation failure on at least two occasions secondary to the laryngeal pathology, >1500 gm birth weight, no assisted ventilation for 10 days prior to evaluation, supplemental O2 requirements less than 30%, no congestive heart failure one month prior to evaluation, no acute upper or lower respiratory tract infection, no antihypertensive medications for ten days prior to evaluation, and presence of adequately trained ICU personnel and necessary ICU equipment. Cotton's method of anterior cricoid split is as follows: Upon completion of flexible laryngoscopy and intraoperative direct laryngoscopy with tracheoscopy that confirms subglottic stenosis without other airway pathology such as glottic or tracheal stenosis, tracheomalacia, TVC paralysis, and choanal atresia , an incision is made over the cricoid cartilage. A vertical midline incision is made through the cricoid cartilage, first 2 tracheal rings, and lower thyroid cartilage. Prolene stay sutures are placed on either side of the cricoid and the skin is approximated over a rubber band drain. The patient is left intubated, sedated and paralyzed in the ICU. At 7-14 days (infants <2500 gm - 14 days, infants >2500 gms - 7 days) the patient is taken to the OR and extubated in a controlled fashion. Steroids (1mg/kg/day) are given 24 hrs prior to extubation and continued for 5 days (1mg/kg/day). Paralytic agents should be tapered starting 2 days prior to extubation. Cotton reports a 76% success rate with this procedure The three primary forms of presently used laryngotraceoplasty for acquired pediatric subglottic stenosis include: laryngotracheoplasty with costal cartilage, laryngofissure with division of the posterior cricoid, and 4 quadrant division of cricoid. Laryngotracheoplasty with costal cartilage can be performed with formal stent or with endotracheal tube as a stent, the latter as a one stage procedure. In laryngotracheoplasty with anterior graft, a midline cut is made through the cricoid and first 2 tracheal rings. A boat shaped piece of costal cartilage is placed so the perichondrium faces the lumen. Prolene sutures are placed extramucosally. Beveling of graft helps to prevent prolapse into lumen. Laryngofissure with division of the posterior cricoid is used with 1. combined posterior glottic and subglottic stenosis, 2. moderate subglottic stenosis and tracheal stenosis with loss of cartilaginous framework, 3. complete glottic and subglottic stenosis. In this procedure, cartilage can be placed just anteriorly or both anteriorly and posteriorly, the latter is done if significant narrowing results from the posterior scar. An Aboulker stent with Holinger metal trach tube is left in place for 1-6 mos. depending on severity. 4 quadrant division of the cricoid cartilage is usually used for complete congenital cricoid stenosis. The stent is left in place 6 months. Cincinnati reports a 76% success rate with this procedure. Cotton recommends posterior grafting in addition to anterior grafting in patients with scarring of the posterior glottis with extension into one or both cricoarytenoid joints, grade 3 subglottic stenosis in which the majority of scarring is posterior, grade 4 stenosis, loss of cartilaginous framework, congenital subglottic stenosis with prominent lateral shelves creating an elliptically shaped airway, and patients with an associated laryngeal cleft. Segmental resection with primary anastomosis though reported with good results, is very difficult in the subglottic region in most hands secondary to the proximity of the vocal cords and places the recurrent laryngeal nerves at risk for injury. Segmental resection in subglottic stenosis is indicated when architecture of cricoid is so destroyed that grafting is impossible. If a centimeter or more of normal airway exists below the vocal cords, a partial cricoid resection with thyrotracheal anastomosis may be performed. Dissection should be in the subperichondrial plane. Infrahyoid release allows tension free closure. If posterior scar is present, a posterior tracheal flap can be performed after resection of subglottic scar. Another option for repair of subglottic stenosis is the sternocleidomastoid myoperiosteal flap, though this tends to be used more for upper tracheal defects secondary to trauma or invasive thyroid carcinoma, this requires long term T-tube placement. The periosteum forms bone providing a rigid framework, but defect repair is limited by size of SCM periosteal attachment. Other options include the rotary door flap where a vascularized myocutaneous flap of the sternohyoid muscle with overlying skin is used for reconstruction, and the hyoid interposition either using free or pedicled hyoid grafts. Overall success rates for repair of subglottic stenosis are 75- 100%. The success rate following first repair ranges from 72-79%. The most significant complication by numbers is that of abnormal voice with an incidence of significant abnormality ranging from 21-50%. Some vocal dysfunction can be prevented by avoiding division of the anterior commissure and by performing meticulous reapproximation of Broyles ligament when detached. IV. Tracheal stenosis A. Congenital By definition this is stenosis below the lower edge of the cricoid cartilage that is present at birth. This is a rare anomaly, with ~ 70 cases reported in literature. It is often due to complete tracheal rings. Narrowing may be present anywhere in the trachea and extend into bronchi. It is often associated with other congenital anomalies especially cardiac and vascular anomalies. Typically, the more severe the stenosis the more likely there will be associated anomalies of the heart or lungs. The mortality of this condition is reported to be as high as 77%. The majority of cases present within the first 3 months of age. Congenital tracheal stenosis has been classified by Hoffer (1994) into 3 groups. Class one is defined as small segmental stenotic areas and few associated anomalies. Class one stenosis responds well to conservative management or tracheotomy as the symptoms usually resolve with growth. In class two the stenosis is extensive and associated with any one anomaly or multiple anomalies except significant cardiac or pulmonary disease. Class two disease usually requires tracheoplasty. Class three is any stenotic lesion with significant cardiac or pulmonary anomaly and according to Hoffer's classification requires tracheoplasty or segmental resection. Congenital tracheal stenosis secondary to complete rings often managed with castellated anterior tracheal incision with division of rings posteriorly as well. Stenting is performed with endotracheal tube and pericardial patch is placed anteriorly. The castellated incision helps prevent sagging of the pericardium during inspiration. The endotracheal tube is typically left in for 3-4 weeks. B. Acquired There are several potential causes of acquired tracheal stenosis, the most common of which include: h/o prolonged intubation, tracheotomy, repair of T-E fistula, external trauma. The reported incidence following tracheotomy ranges from 0.6 to 21% and the reported incidence following endotracheal intubation ranges from 6 to 21%. Cases are more severe and more frequent following endotracheal intubation with subsequent tracheotomy. Stenosis may be cicatricial membranous stenosis, anterior wall collapse, or complete stenosis. The management of tracheal stenosis is based on the severity, site and presence of associated airway lesions. Emergency treatment of airway compromise should be with rigid bronchoscopy through stenotic segment with dilatation verses intubation with small endotracheal tube while awaiting definitive management. The last resort is to perform tracheotomy as this increases the length of trachea which will need to be resected or augmented. Treatment types may be divided into endoscopic and open procedures. Indicators of poor outcome with endoscopic techniques include the presence of circumferential scarring, loss of cartilaginous support, and stenosis greater than 1 cm in length. Open techniques are associated with a 2% mortality rate and a 5% failure rate. Open procedures can be broken down into two categories: excision with end to end anastomosis and midline split with augmentation. The latter requires grafting and stenting as in the treatment of subglottic stenosis and will not be discussed further here. One option for repair not discussed previously is the sternocleidomastoid muscle composite flap. Osteotomies are made in the clavicle corresponding to the needed length of supporting tissue. The outer half of the clavicle is harvested with SCM attached. The majority of cancellous bone is removed with a curette, leaving a thin layer behind for vascular support of a mucosal graft for luminal lining. A T-tube is placed and the graft is sutured into place. This procedure works well for defects of 4- 5cm. Disadvantage is the risk of future clavicular fracture. The approach for segmental resection depends on site of lesion, either cervical, cervicosternotomy, or thoracotomy. Segmental resection with end to end anastomosis is indicated for severe circumferential stenosis exceeding 1 cm in length. The maximum average length that can be resected is 5-6 cm (9-10 rings), though this varies considerably with patient age and morphology. The main principles for success with this procedure are: complete resection of fibrotic area with anastomosis of healthy trachea, pre-operative treatment and resolution of gastroesophageal reflux and infection, mucomucosal approximation at the anastomosis which is facilitated by dividing the trachea between cartilage, the use of resorbable monofilament suture with knots placed outside the lumen, and a tension free closure. It is additionally crucial when dissecting around the trachea to dissect directly on the cartilage to prevent injury to the recurrent laryngeal nerves. The head should be flexed during the procedure and postoperatively to reduce tension. The latter can be done by placing 0-prolene sutures through chin to chest. In children, post-operative sedation and paralysis often required. Tensionless closure of the tracheal defect in segmental resection is allowed by various release procedures including the suprahyoid release (permits 2-3 cm length), intralaryngeal release or infrahyoid release, and extensive mobilization of the right hilus with division of the pulmonary ligament, intrapericardial dissection of pulmonary vessels, and division of intracartilaginous tracheal ligament (allows 3-4 cm length). Stenosis <4cm in length can be resected and reanastomosed safely with laryngeal release and cervical tracheal mobilization alone. Combined cervicomediastinal approach may be required for stenosis >3-4 cm, if stenosis is within the thoracic inlet, or if adequate mobilization not achieved with cervical approach. Tracheal stenosis with subglottic involvement is best treated with resection and cricotracheal anastomosis using the preserved posterior portion of the cricoid ring. If there is total destruction of the cricoid ring, a laryngotracheal anastomosis over a T-tube should be performed. DISCUSSION BY RONALD W. DESKIN, FACULTY: Acquired subglottic stenosis in infants due to prolong intubation of the premature infants has declined in numbers presumably due to Surfactant treatment of the premature lung problem with a decrease in an incidence of bronchopulmonary dysplasia. We are seeing more required subglottic stenosis in children who have prolonged intubation for neurologic and cardiac problems however. In children the stenosis is mostly anterior and if grade one and two we will try usually conservative endoscopic management with dilatation and laser treatment. If this is unsuccessful an open procedure may be required. An open procedure is often required on grade 3 and grade 4 stenosis. These are grading by the Cotton method with grade 1 being less than 70% stenosis, grade 2 70-90% stenosis, grade 3 90% stenosis but a visible lumen and grade 4 no visible lumen. A stent is usually used if the stenosis is severe such as grade 4 or if it involves the larynx as well as the subglottic area, if there is loss of cartilage support and if a posterior cricoid division is necessary. The stent material available is a Montgomery T-Tube which is silastic and produces some granulation tissue and is not available always in appropriate pediatric sizes, teflon Aboulker stents that are wired through a metal tracheotomy tube which have the disadvantage of technical difficulty in constructing this stent as well as the inability to change the trach tube during the time the stent is in place. More recently one stage laryngotracheoplasty has been used more extensively with removal of the tracheotomy stoma at the time of the costal cartilage graft and placement of a endotracheal tube for about a week. This has the disadvantage of the need to either paralyze or sedate for a week in the ICU and there is some associated problems with that method. A new material that is a newer plastic polymer in a design as the Montgomery-Healy stent has been produced and it is a T-tube design with an inner cannula and a more rigid material than silastic and also apparently produces less granulation than silastic. ---------------------------------------------------------------------------- BIBLIOGRAPHY Anand V. K. etal Surgical Considerations in Tracheal Stenosis, Laryngoscope, March 1992;102:237-243 Bailey, B.J. and Biller, H. F. Surgery of the Larynx, W.B. Saunders Company, 1985, Philadelphia, pgs. 155-175 Bailey, B.J. Head and Neck Surgery-Otolaryngology Volume one, J.B. 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