Pediatric Subglottic stenosis

TITLE: Pediatric Congenital Subglottic Stenosis
SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
DATE: June 27, 2007
RESIDENT PHYSICIAN: Michael Briscoe, Jr., MD
FACULTY PHYSICIAN: Seckin Ulua= lp, MD
SERIES EDITORS: Francis B. Quinn, Jr., MD

"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 purp= ose of stimulating group discussion in a conference setting. No warranties, eit= her 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."

Introduction

There are many causes of noisy breathing in the neonate. Any site in the upper airway can become obstructed and cause noisy breathing as well as dyspnea.<= span style=3D'mso-spacerun:yes'> These include nasal causes such as= choanal atresia or nasal stenosis, pharyngeal causes including lingual thyroid, laryngeal causes such as laryngomalacia and subglottic stenosis, and tracheobronchial causes such as tracheal stenosis. Lesions in= the oropharynx may cause stertor, while lesions in the laryngotracheal tree will cause stridor. Subglottic ste= nosis is the third leading cause of congenital stridor in the neonate. Most cases are self limited, but s= ome require intervention that require a multidisciplinary approach, with the he= ad and neck surgeon taking a primary role.

Anatom= y

The subglottis is defined as the area extending = from the lower surface of the true vocal cords to the lower surface of the crico= id cartilage. In adults this corresponds to approximately 10 mm inferior to the anterior commissure and = 5 mm inferior to the posterior commissure.

The infant larynx differs significantly in size = and position when compared to the adult larynx. At birth, the infant larynx is approximately one third the size of the adult larynx, however, the infant larynx is proportionately larger than the adult larynx compared with the remainder of the tracheobronchial system.&= nbsp; The vocal process of the arytenoid takes up half the length of the v= ocal cord in the infant larynx, while it only takes up about ¼ of the len= gth of the vocal cord in the adult. The narrowest portion of the airway in the older child and adult is the glottic aperture, while the narrowest part of the airway in the infant is the subglottis. The subglottis in infants measures approximately = 4.5 by 7mm. A diameter of 4.0 mm is considered the lower limit of normal in a full term infant and 3.5 mm in a premature infant. One millime= ter of edema circumferentially in the subglottis reduces the cross-sectional area = by 60%.

The infant larynx is positioned higher in the ne= ck than the adult larynx. The su= perior border of the larynx of the infant is located at about the level of the fir= st cervical vertebrae with the cricoid positioned at about the fourth cervical vertebrae. In comparison, the= adult cricoid rests at about the level of the sixth cervical vertebrae. The structures of the infant laryn= x are more pliable and less fibrous making the infant airway more susceptible to narrowing from edema and less easily palpable.

Embryology

The anlagen of the larynx, trachea, bronchi and = lungs arise from the ventromedial diverticulum of the foregut called the tracheobronchial groove at day 25. The lining of the larynx and trachea are from endoderm, while the muscles and cartilage are derived from splanchnic mesenchyme. At day 33 the laryngeal primordia = appears, and the laryngeal aditus is formed by the growth of three tissue masses, the hypobranchial eminence from arches III and IV (epiglottis), and the paired ventral ends of arch IV (arytenoids), giving it a T-shape. This slit, extends to the first tr= acheal ring in the fifth and sixth week, and by week seven the cricoid ring is complete, and the cartilaginous hyoid is visible below the epiglottis. By the end of the embryonic period= , the larynx and trachea are well formed.

During the fetal period, the structures are refi= ned, and neurological reflexes are developed.&n= bsp; In the third month, the thyroid laminae fuse, cartilaginous vocal processes of the arytenoids are seen, and the ventricle and saccule are see= n. The fourth month reveals laryngeal tissue with goblet cells, and tracheal tissue with cilia. In the fifth and sixth months, the cuneiform and corniculate cartilages develop, and the epiglottis has fibroelastic cartilage. Throu= ghout the remaining fetal course, breathing becomes a more mature and coordinated event.

Etiology

I. Congenital SGS

&= nbsp; A. Membranous <= o:p>

&= nbsp; &= nbsp; 1. increased fibrous connective tissue

&= nbsp; &nbs= p; 2. hyperplastic submucous glands

&= nbsp; &nbs= p; 3. granulation tissue

&= nbsp; B. Cartilaginous

&= nbsp; &nbs= p; 1. cricoid cartilage deformity

&= nbsp; &= nbsp; &= nbsp; a. small cricoid

&= nbsp; &nbs= p; &= nbsp; b. elliptical cricoid

&= nbsp; &nbs= p; &= nbsp; c. large anterior lamina

&= nbsp; &nbs= p; &= nbsp; d. large posterior lamina

&= nbsp; &nbs= p; &= nbsp; e. generalized thickening

&= nbsp; &nbs= p; &= nbsp; f. submucous cleft

&= nbsp; &nbs= p; 2. trapped first tracheal ring

II. Acquired SGS

&= nbsp; A. Intubation

&= nbsp; B. Laryngeal trauma

&= nbsp; &= nbsp; a. previous airway surgery

&= nbsp; &nbs= p; - high tracheotomy

&= nbsp; &nbs= p; - cricothyroidotomy

&= nbsp; &nbs= p; - prior surgery for respiratory papillomatosis

&= nbsp; &nbs= p; - prior laser surgery for SGS

&= nbsp; &nbs= p; b. accidental

&= nbsp; &nbs= p; &= nbsp; 1. inhalational (thermal or caustic)

&= nbsp; &nbs= p; &= nbsp; 2. trauma (blunt or penetrating)

&= nbsp; C. Autoi= mmune

&= nbsp; D. Infection

&= nbsp; E. Gastroesophageal reflux (GER)

&= nbsp; F. Inflammatory diseases

&= nbsp; &= nbsp; a. Anti-neutrophil Cytoplasmic Autoantibodies (C-ANCA)

&= nbsp; &nbs= p; b. sarcoidosis

&= nbsp; &nbs= p; c. Systemic lupus erythematosis

&= nbsp; G. Neoplasms

III. &nb= sp; Idiopathic SGS

Congenital Subglottic Stenosis

Su= bglottic stenosis is the third most common cause of stridor in the neonate behind laryngomalacia and vocal cord paralysis.&n= bsp; Involves narrowing of the subglottic lumen in the absence of trauma (intubation). Normal diameter= of newborn trachea is 5mm, lumen of 4mm in full-term newborn (3mm in premature infant) represents subglottic stenosis.&nb= sp; Proposed mechanism is incomplete recannalization during embryogenesi= s.

There are two types of congenital subglottic ste= nosis: membranous and cartilaginous. Membranous is usually circumferential, soft and dilatable, in contra= st, the cartilaginous has a more variable appearance. Mild-normal shape with narrowed lu= men, or can have abnormal shape of cricoid cartilage with prominent lateral shel= ves giving an elliptical appearance to the lumen.

Symptoms

Symptoms of upper airway obstruction dominate, w= ith inspiratory stridor, progressing to biphasic as obstruction worsens. Stridor is an important sym= ptom of SGS as well as many other causes of neonatal obstruction. The characteristics of stridor can= be a clue as to where the obstruction is occurring. Three distinct zones have been identified, the supraglottic/supralaryngeal zone, the extrathoracic tracheal zone which includes the glottis and subglottis, and the intrathoracic trachea. Supraglottic stridor= is high-pitched, and inspiratory. An example of this is laryngomalacia, where the tissues are floppy and are suc= ked in during inspiration causing narrowing of the airway. Glottic and subglottic stridor is usually biphasic in nature because these structures are rigid, and there is= no collapse of tissue during either phase of respiration, there is a fixed obstruction. Intrathoracic st= ridor has a expiratory noise, this is due to the positive pressure exerted on the bronchial tissues by contraction of the thorax.

Causes of stridor in children according to site of ob= struction

I. = &nb= sp; Pharynx

a. = Congenital

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; i. &nb= sp; Lingual thyroid

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; ii. &n= bsp; Choanal atresia

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; iii. &= nbsp; Craniofacial anomalies

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; iv. &n= bsp; Cysts

b. Inflammatory

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; i. &nb= sp; Abscess

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; ii. &n= bsp; Allergic polyps

c. = Neoplasm

d. Adenotonsillar hypertrophy

e. = Foreign body

II. = Larynx

a. = Congenital

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; i. &nb= sp; Laryngomalacia

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; ii. &n= bsp; Webs, cysts, laryngocele

= &nb= sp; = &nb= sp; = iii. &= nbsp; Subglo= ttic stenosis

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; iv. &n= bsp; Laryngeal cleft

b. Inflammatory

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; i. &nb= sp; Croup, epiglottitis

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; ii. &n= bsp; Tb, rare infections

c. = Neoplasm

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; i. &nb= sp; Subglottic hemangioma

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; ii. &n= bsp; Laryngeal papilloma

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; iii. &= nbsp; Cystic hygroma

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; iv. &n= bsp; Malignant (chondrosarcoma, rhabdomyosarcoma)

d. Trauma

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; i. &nb= sp; Intubation

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; ii. &n= bsp; Foreign body

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; iii. &= nbsp; Neck trauma

e. = Vocal cord paralysis

f. = laryngospasm

III. = Tracheobronchial tree

a. = Congenital

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; i. &nb= sp; Vascular anomalies

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; ii. &n= bsp; Webs, cysts

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; iii. &= nbsp; Tracheal stenosis

b. Neoplasm

c. = Foreign body

d. Trauma

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; i. &nb= sp; Intubation

&nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; ii. &n= bsp; Tracheotomy

In addition to stridor, may show intercostal or xyphoid retractions and have a barking cough. Mild-moderate SGS is exacerbated b= y URI, and these children tend to have recurrent croup.

Diagnosis

When these children present, it is important to perform a thorough history and physical exam. Birth injury, or intubation, as we= ll as prematurity are important to note. The timing, onset, and duration of stridor, voice/cry quality, feedi= ng abnormalities or failure to thrive, cyanosis, and possible foreign body aspiration are important to document. Also, recurrent croup = or hospitalizations for respiratory illnesses. The physical exam should include a thorough head and neck exam, as well as careful characterization of stridor, and signs of respiratory distress. A flexible laryngoscopic exam should also be performed. At that time, an assessment of lar= yngomalacia, vocal cord paralysis, laryngopharyngeal refluxx, or other laryngeal patholo= gy can be ellicited.

Differential diagnosis of laryngotracheal stenosis

I. Congenita= l

&= nbsp; A. Tracheomalacia

&= nbsp; B. Laryngomalacia

&= nbsp; C. Vocal cord paralysis

&= nbsp; D. Laryngeal cleft

&= nbsp; E. Congenital cysts

&= nbsp; D. External compression from congenital abnormality or lesion

&= nbsp; &nbs= p; 1. Vascular compression

&= nbsp; &nbs= p; &= nbsp; a. innominate artery compression (most &= nbsp; &nbs= p; &= nbsp; &nbs= p; &= nbsp; &nbs= p; &= nbsp; common)

&= nbsp; &nbs= p; &= nbsp; b. right-sided aortic arch with persistent ductus = ; &n= bsp; = ; = = arteriosus

&= nbsp; &nbs= p; &= nbsp; c. aberrant left pulmonary atery

&= nbsp; &nbs= p; 2. Mass

&= nbsp; &nbs= p; &= nbsp; a. teratoma

&= nbsp; &nbs= p; &= nbsp; b. cystic hygroma

&= nbsp; &nbs= p; &= nbsp; c. hemangioma

<= /o:p>

II. Infectious/inflammatory

&= nbsp; A. Viral laryngotracheobronchitis (croup)

&= nbsp; B. Retropharyngeal abscess

&= nbsp; C. GER

&= nbsp; D. Tracheitis

<= /o:p>

III. Neoplas= tic

&= nbsp; A. Subglottic hemangioma

&= nbsp; B. Recurrent respiratory papillomatosis

<= /o:p>

IV. Traumati= c

&= nbsp; External compression

&= nbsp; Foreign body

The gold standard for diagnosis of any laryngotr= acheal abnormalities is direct laryngoscopy and tracheobronchoscopy under general anesthesia. This should be performed in the operating room with an experienced anesthesiologist. It is important to delay endoscopy for at least two weeks following an acute epis= ode of croup to minimize the risk of postoperative airway obstruction. The potential need for tracheotomy should be discussed with the patient (adults) or patient's family (children) prior to endoscopy. A rigid bronchoscope or a rod lens telescope may be use= d to assess the airway. The important things to document during endoscopy are as follows: (1) the outer diamet= er of the largest bronchoscope or endotracheal tube that can be passed through the stenotic segment, (2) the location/subsites (glottis, subglottis, trachea) and length of the stenosis, (3) other separate sites of stenosis, (4) other airway anomalies in infants (clefts, webs, cricoaryteno= id joint fixation, neoplasms, etc.), and (5) reflux changes. After removing the sizing endotrac= heal tube or bronchoscope it is important to observe the stenotic segment for ed= ema which may result in the need for tracheostomy

There are two widely excepted staging systems for classifying subglottic stenosis: Myer-Cotton grading system and the McCaffrey system. Other systems have been desc= ribed as well, however, none are universally applicable or useful. At this time, no staging system ex= ists that allows comparison of patients treated at different institutions.

The Myer-Cotton staging system is useful for mature, firm, circumferential sten= osis confined to the subglottis. It describes the stenosis based on the percent relative reduction in cross-sectional area of the subglottis which is determined by differing siz= ed endotracheal tubes. Four grad= es of stenosis are described with this system:&n= bsp; grade I lesions have less than 50% obstruction, grade II lesions have 51% to 70% obstruction, grade III lesions have 71% to 9= 9% obstruction, and grade IV lesions have no detectable lumen or comple= te stenosis.

The McCaffrey system classifies laryngotracheal stenosis based on the subsites involved and the length of the stenosis. Four stages are described: stage I lesions are confine= d to the subglottis or trachea and are less than 1cm long, stage II lesio= ns are isolated to the subglottis and are greater then 1 cm long, stage III= are subglottic/tracheal lesions not involving the glottis, and stage IV = lesions involve the glottis.

Management

The management of congenital SGS ranges from observation with supportive care in times of exacerbations, to complicated surgical reconstructions of the patients airway. Most grade I and II lesions are ma= naged with observation. If a grade = II lesion becomes symptomatic, causing a decrease in exercise tolerance or respiratory distress, then endoscopic repair, dilation, or an expansion procedure can be undertaken. = KTP and CO2 laser has also been used for lesions that are thin, and circumferential. Failures ten= d to occur with thick, circumferential cicatricial scarring greater then 1 cm in vertical dimension, and posterior commissure involvement. Complications of laser include chondritis, and perichondritis, as well as re-stenosis. With high grade stenosis, grade II= I-IV will need an open surgical procedure.

Surgical treatment options for high grade subglottic stenosis:

I. Tracheostomy

<= /o:p>

II. Open procedure

A. Expansion procedure (one-stage or with stent placement)=

        &= nbsp;           &= nbsp;   1. Anterior cricoid split with or without cartilage graft

        &= nbsp;           &nbs= p;   2. Posterior cricoid split with or without cartilage graft
        &= nbsp;           &nbs= p;   3. Anterior and posterior cricoid split with cartilage graft=

        &= nbsp;           &nbs= p;   4. Four quadrant LTR

        &= nbsp;   B. Segmental resection (cricotracheal resection - CTR)

        &= nbsp;           &nbs= p;   1. Primary CTR

        &= nbsp;           &nbs= p;   2. Salvage CTR

        &= nbsp;           &nbs= p;   3. Extended CTR – CTR with and expansion

        &= nbsp;           &= nbsp;           &= nbsp;   procedure, arytenoid lateralization, or

        &= nbsp;           &nbs= p;            &= nbsp; aytenoidectomy

The goal of surgery is to have patients with ade= quate airway to allow for normal activity without the need for tracheostomy. Secondary goal to have single-stage procedure, minimal postoperative morbidity, and minimal hospital stay. Most surgeries are performed in sp= ring and summer, when chance of developing RSV is lower.

Anterior Cricoid Split

The anterior cricoid split (ACS) procedure was originally described for a neonate who has had multiple failed extubations instead of performing a tracheostomy (Cotton and Seid, 1980). This procedure is also used for ol= der infants and those who are have already been tracheotomized. Indications were later expanded to patients with congenital subglottic stenosis. The lesion responsive to this proc= edure is a mild anterior subglottic narrowing with extensive fibrosis but a normal cricoid. ACS may also be used= to decompress subglottic cysts. = Strict criteria for ACS have been established by Cotton and include: extubation failure on two occasions or more due to laryngeal pathology, weight >150= 0g, no assisted ventilation for 10 days prior to evaluation, O2 requirements <30%, no CHF for one month prior to evaluation, no acute respiratory tra= ct infection, no antihypertensive medications ten days prior to evaluation. The procedure is performed after d= irect laryngoscopic and bronchoscopic confirmation of the diagnosis. All other airway pathology must be ruled-out.

A vertical midline incision is made through the cricoid cartilage and first two tracheal rings as well as the lower thyroid cartilage. This allows the cartilages to spring open and allow edematous mucosa to drain, increasing a= irway size. Prolene stay sutures are placed on either side of the cricoid cartilage and the skin is re-approxima= ted after placement of a drain. T= he child is then left intubated, sedated and paralyzed in the ICU for 7-14 days. Cotton has guidelines f= or endotracheal tube sizes for stenting and for duration of stenting based on the infants weight.

Laryngotracheal Expansion Surgery

Laryngotracheal expansion surgery involves scar division with distraction of the edges by interposition of graft material (augmentation) to widen the airway lumen.&= nbsp; It is important to avoid removing scar which results in a large surf= ace area of denuded mucosa and leads to restenosis. Cotton recommends augmenting the a= irway with grafts when the distraction of the laryngotracheal framework must be greater than approximately 3mm. There are several techniques depending on t= he location and severity of the stenosis. Laryngotracheoplasty can be performed with a tracheostomy and formal stenting or by using the endotracheal tube a= s a stent, the latter known as a single-stage LTP (SS-LTP). Gustafson et all performed a retrospective chart review of 200 patients undergoing SS-LTP. There was a 96% successful decannu= lation rate, with 29% requiring reintubation.&nbs= p; Those undergoing both posterior and anterior grafting had more complications than those undergoing either anterior or posterior grafting alone. Younis et al, performe= d a retrospective chart review of 46 patients undergoing anterior/posterior SS-= LTP and had a 83% decannulation rate. Thus, this procedure should be used for either anterior or posterior stenosis, but other procedures should be considered if there is anterior and posterior stenosis.

Several stents have been used in the past, but t= he aboulker stent (teflon) is the most used. It has the benefit of being rigid, = and having a lumen with a sufficient diameter for aggressive pulmonary toilet.<= span style=3D'mso-spacerun:yes'> The duration of stenting depends o= n the length of the prior stenosis, and the grade of stenosis. Stenting can last from four weeks = to greater than two months. (Cable et al 2004)

Graft material has included rib cartilage, auric= ular cartilage, thyroid cartilage hyoid bone, and irradiated cartilage. Autogenous cartilage is the materi= al of choice for grafting, most commonly costal or auricular cartilage. Cartilage is better material becau= se it has a lower rate of resorption, is easy to carve, and is viable without a vascular pedicle. They also r= etain bulk even without functional use. Hyoid bone requires vascular pedicle, can resorb, and is difficult to carve.

Anterior laryngofissure with anterior lumen augmentat= ion

This technique is good for anterior subglottic stenosis or anterior tracheal wall collapse. The lesion should not involve = the glottis. Other procedures sho= uld be considered if there the cricoid cartilage is deformed or weak. Anterior grafts are made considera= bly larger and thicker than grafts placed posteriorly. The perichondrium is oriented to t= he luminal side to allow for epithelialization. The perichondrium is also a good b= arrier against infection. A large ex= ternal flange is created to prevent the graft from prolapsing into the airway.

Laryngofissure with division of posterior cricoid lam= ina

This is indicated for patients with posterior subglottic stenosis, posterior glottic stenosis that extends to the glottis, complete or circumferential stenosis, or if there is significant cricoid deformity. Division of the an= terior and posterior cricoid must be carried out for this procedure. If possible, one should avoid a co= mplete laryngofissure to avoid damaging the anterior commissure, however this is o= ften needed for posterior glottic involvement for access. The posterior cricoid cartilage is incised in a manner that is vertically oriented to the cartilage to allow maximal purchase for the graft. The incision is extended superiorly to the interarytenoid area and inferiorly 5 to10 mm into the membranous trachea. The graft is elliptical in shape. It should not be too thick as it c= an cause swallowing difficulties and can lead to aspiration. The width of the graft is determin= ed by the desired distraction of the cut edges of the incised posterior cricoid cartilage. 0.05 to 1.00 mm of distraction can be obtained for each year of age, up to 1 cm. It is sutured in place with absorb= able suture on a small cutting needle. The knots should be buried so that they remain extraluminal to preve= nt development of granulation tissue. Long-term stenting is usually necessary (3-6 months).

Laryngofissure and division of posterior cricoid lami= na with anterior and posterior grafts

This should be used for patients who have SGS si= milar to those above but with a significant amount of stenosis posteriorly such t= hat grafting is necessary to maintain the adequate separation.

Once the grafts have been sutured into place in = any of the above procedures, the decision must be made on whether it should be sin= gle or double-staged. Cotton and = Walner (1999) recommend a double-staged procedure for patients with severe stenose= s, history of reactive airway, or poor pulmonary function. This should also be considered at institutions with inadequate intensive care facilities. Double-stage procedure implies pla= cement of stent above the tracheostomy tube instead of using an endotracheal tube = as the stent (single-staged procedure). Once this decision is made, the strap muscles are closed to provide blood supply to the outer surface of the anterior graft.

Segmental resection/Cricotracheal resection (CTR) with thyrotracheal anastomosis

The first CTR was performed by Conley in 1953 in= a patient undergoing surgery for chondroma of the cricoid cartilage. It was later popularized by Ogura = and powers (1964) as a technique for treatment of traumatic stenosis. In the 1970s it became the treatme= nt of choice in adults with acquired subglottic stenosis from long term intubation. Until recently, surgeons were reluctant to perform this procedure in the pediatric patients because of the risk of anastamotic dehiscence and recurrent laryngeal nerve injury, and disturbing the normal growth of the larynx. The first successful CTR performed= in a child was occurred in 1978 (Savary). In 2005, White et al performed a retrospective chart review of 96 patients undergoing CTR. 89 of these patients had grade III/IV stenosis, and they achieved a 94% decannula= tion rate. They found that vocal f= old dysfunction was the only significant risk factor for failure to decannulate after one procedure.

This technique is indicated if there is severe deformity of the cricoid making grafting very likely to fail. Most say that there must be at lea= st 10 mm of normal airway below the glottis, however Cotton states that the resec= tion can be up to the vocal folds but to expect prolonged edema. This technique is technically diff= icult due to the close proximity of the vocal cords and recurrent laryngeal nerves. Stenosis less than 4 = cm can be resected by laryngeal release and cervical tracheal mobilization. Stenting is not required and the trachetomy tube can usually be removed at around 4 weeks.

Complications

These include bleeding, pneumothorax, pneumomediastinum, recurrent laryngeal nerve injury, slipped graft, slipped stent, plugged stent, wound infection, keloid formation, suprastomal/infrastomal collapse, re-stenosis, tracheocutaneous fistula, granulation tissue and death.

Factors contributing to LTR failure (Choi et al 1999)=

  =           Preoperati= ve - inadequate assessment of posterior laryngotracheal stenosis

  =           Intraopera= tive – duration of stent, type of stent, correct assessment with failure to address posterior stenosis, type of graft, and length of stent.

  =           Postoperat= ive – keloid formation, anterior suprastomal collapse, poor follow-up, slipped stent, broken stent, GERD, no discernable factors.

Postoperative Care

Patients should be admitted to intensive care un= it, and care must be coordinated with the ICU team, pediatrics, and otolaryngology. Patients requ= ire sedation, but the length of sedation will vary on the age of the child, and= the procedure performed. In child= ren over 4 years old, there is a better chance of weaning sedation within 48 ho= urs after the procedure. Aggressi= ve and meticulous thracheostomy care and pulmonary toilet needs to be undertaken.<= span style=3D'mso-spacerun:yes'> Post operative antibiotics, antire= flux medications and dexamethasone are also indicated.

Conclusions

Approximately five percent of children undergoing procedures will require a smaller then expected endotracheal tube due to mi= ld subglottic stenosis. Most of = these children will never present to the otolaryngologist, but for more severe ca= ses, these children present a challenging problem for the head and neck surgeon. It is imperative to perform detailed history, physical, and characterization of the extent and severity of the stenosis. Rig= id endoscopy is essential for preoperative planning for any of the surgical pr= ocedures that can be used for correction. Choice of operation is dependent on surgeon comfort, postoperative capabilities, and severity of disease.&nbs= p; For high grade stenosis, the single-stage laryngotracheal resection,= or the cricotracheal resection are the best options. CTR is also available as a salvage= to LTR failures. Remember that t= he goal of surgery is to allow for an adequate airway for normal activity with= out the need for tracheostomy.

References

Bath AP, Panarese A, Thevasagayam M, Bull PD= . Paediatric subglottic stenosis.= Clinical Otolaryngol 1999; 24(2):117-121

Bosely et al. “Pediatric partial CTR: = a new technique for posterior anastomisis.”Oto Head and Neck Surgery 2006. = 135; 318-322

Cable et al. Pediatric airway reconstruction= : Principles in decision-making and outcomes at The University of Iowa Hospitals and clinics. Ann Otolo RhinolLaryngol 113:2004; 289-293

Choi et al. “Pitfalls in LTR” Ar= ch Otolaryng Head Neck Surgery. 1999 125, 650-53.

Cotton RT, O'Connor DM. Paediatric laryngotracheal reconst= ruction: 20 years experience. Acta Otorhinolaryngol Belg 199= 5; 49:367-372

Fayou et al. “Thyroid alar cartilage in paediatric LTR.” International Journal of Pediatric Otorhinolaryngolo= gy 2006; 70, 717-724.

Gustafson et al. “SSLTR in children: a= review of 200 cases. Otol Head and N= eck; Vol.123;4 430-434, 2000

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