Pediatric Anesthesia 2009 19 (Suppl. 1): 88–99 doi:10.1111/j.1460-9592.2009.03005.x

Review article Upper in children

IAIN A. BRUCE MD, FRCS (ORL-HNS) AND MICHAEL P. ROTHERA FRCS Department of Paediatric ENT, Royal Manchester Children’s Hospital, Manchester, UK

Introduction redundant arytenoid mucosa prolapsing into the glottis and a long curled (Figure 2). Surgical Poiseuille’s law is central to the understanding and management of the condition is largely based on management of all airway obstructions in children, correction of these anatomical anomalies. The natural with the clinical impact of even a small reduction in history of the inspiratory is to often worsen radius being compounded by the inverse relation- initially for 6–9 months, before gradually improving, ship of the resistance to the radius to the power 4. with most children being free of symptoms by Indeed deterioration from a ‘mild’ obstruction to life 18–24 months (1). In the absence of atypical symp- threatening airway compromise may be heralded by toms (e.g. cyanosis, altered cry, choking with feeds), slight decrease in airway diameter (Figure 1). Suc- which could suggest an alternative diagnosis or the cessful outcome in all cases of childhood airway presence of synchronous lesions elsewhere in the obstruction is dependant upon the efficient cooper- airway, the condition may be diagnosed by awake ation between suitably experienced otolaryngolo- flexible fibreoptic (FFL) in the outpa- gists, anesthetists, and intensivists. tient department. can be classified The aim of this article is to discuss the presenta- into three types dependant on site of the abnormality tion, assessment, and management of the common (1). Type 1 is due to prolapse of redundant arytenoid causes of childhood airway obstruction as seen in a mucosa into the glottis. Type 2 is a result of short tertiary level unit. Traditionally, airway manage- aryepiglottic folds and Type 3 is characterized by ment often comprised tracheostomy insertion, but collapse of the epiglottis posteriorly over the glottis. It the development of endoscopic techniques has is our departmental policy to perform rigid endos- superseded this in an ever increasing proportion of copy in the following circumstances: (i) severe pro- cases. Treatment strategies and principles will be gressive symptoms; (ii) atypical symptoms; (iii) FFL highlighted and placed in context with results inconclusive; and (iv) clinical or fibreoptic suspicion reported in the literature. of a synchronous airway lesion (SAL). The possibility of an SAL has lead some authors to advocate rigid Laryngomalacia endoscopy in all cases of suspected laryngomalacia (2). However, although the rate of SALs in the Laryngomalacia is the commonest cause of congenital literature is significant (20–30%) (1, 3, 4) the impact stridor. The presenting symptom is usually inspira- upon outcome and time to symptom resolution has tory stridor commencing within the first 2 weeks of been shown to be negligible (3, 4). Laryngomalacia, life, exacerbated by feeding, agitation, and lying in the like vocal cord palsy (VCP), is a dynamic condition supine position. The airway obstruction results from and therefore, if formal airway assessment is collapse of supraglottic structures on inspiration. The indicated, it should be performed under general etiology is not fully understood, but the condition is anesthesia with the child breathing spontaneously. consistently associated with certain anatomical Supraglottic collapse is most obvious during the abnormalities, namely short aryepiglottic folds, ‘waking phase’ at the end of the procedure. The majority of children will not require surgical Correspondence to: Iain A. Bruce, Department of Paediatric ENT, Royal Manchester Children’s Hospital, Manchester, UK (email: intervention, with the remaining 5–10% requiring [email protected]). some form of surgical treatment (1, 4). Surgical

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Figure 3 Figure 1 ‘Cold steel’ aryepiglottoplasty in laryngomalacia. Illustration of the increase in airway resistance with decrease in airway diameter. being a causal factor. A neurological form of the condition exists and may be seen in children with neurological or neuromuscular conditions, such as cerebral palsy. In such cases, surgical intervention should be approached with caution and it may be most appropriate to manage severe airway collapse with a tracheostomy.

Vocal cord palsy Vocal cord palsy is a relatively common cause of airway obstruction in children that may be idio- pathic, iatrogenic, as a result of a neurological abnormality or birth trauma (8,9). Unilateral VCP presents with stridor, breathy cry (or voice) and feeding difficulties from birth or following surgical Figure 2 procedures in the thorax. The symptoms are often Supraglottic collapse in laryngomalacia. relatively mild and resolution of symptoms can usually be expected as compensation from the options include division of the aryepiglottic folds to contra-lateral vocal cord ensues over a period of ‘open’ the constricted supraglottis (Figure 3), resec- months. FFL in the awake child is often all that is tion of the redundant mucosa and suspension of the required to diagnose the problem in the absence of prolapsing epiglottis to uncover the laryngeal intro- other symptoms. Radiological assessment is also itus (5,6). Rates of complete resolution of stridor of important in both unilateral and bilateral VCP in over 80% have been reported following aryepiglot- order to diagnose associated central nervous system toplasty (6,7). A degree of gastro-esophageal reflux (e.g. Arnold-Chiari malformation) (10,11) and car- disease (GERD) is often associated with laryngoma- diovascular abnormalities (12). Supportive treatment lacia and all children should therefore receive anti- alone is often sufficient in unilateral VCP, with reflux medication (3). The exact relationship is not feeding via a nasogastric tube until the child devel- fully understood (1), with GERD possibly reflecting ops a ‘safe’ swallow and possibly chest physiother- changes in airway and intrathoracic pressures in apy until an adequate cough is obtained. Bilateral response to the airway obstruction, as opposed to VCP presents a far greater clinical challenge and can

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cause potentially life-threatening airway obstruction. Dysphonia is not usually found in bilateral VCP (8,11). Tracheostomy insertion may be required in the emergency situation to safeguard the airway. Tracheostomy may be necessary in approximately half of cases of bilateral VCP (8). Magnetic resonance imaging of the brain in cases of bilateral VCP is mandatory in order to exclude an Arnold-Chiari malformation with hydrocephalus (10). Diagnosis is once more by rigid airway endoscopy, under general anesthesia with spontaneous ventilation, and cord mobility is best assessed during the waking phase. Care should be taken to also assess passive vocal cord movements in order to diagnose cord immo- bility due to crico-arytenoid fixation (9), complicat- ing prolonged intubation or intubation injury to the . Vocal cord mobility may return to some degree in patients with VCP. Spontaneous recovery rates of up to 70% are reported (8) and therefore an Figure 4 interval of at least a year should be given before an Airway enlargement by laser arytenoidectomy in bilateral vocal cord palsy. E, epiglottis; VF, vocal fold; VP, vocal process of airway widening procedure is undertaken, with CO2 arytenoid cartilage; MP, muscular process of arytenoids cartilage; laser being the treatment modality of choice (9,11). AEF, aryepiglottic fold. Ultimately the aim of surgical treatment is to provide an adequate airway, facilitating tracheos- Virus types 6 and 11. Proliferations involving the tomy decannulation where present, while safeguard- larynx may present with childhood hoarseness and ing the best possible voice quality (9). Laser symptoms of progressive airway obstruction (Fig- arytenoidectomy has been shown to meet both of ure 5). Involvement of the tracheobronchial tree will these criteria in a study of six children from the also lead to airway obstruction and usually presents Great Ormond Street Hospital, in London (9). The a more significant management problem. The recur- improvement in airway was sufficient to facilitate rent nature of this condition often necessitates decannulation in the four children with tracheosto- multiple surgical procedures. mies preoperatively (9). A CO2 laser is used to widen The current management philosophy is toward a the airway by resecting the vocal process and part of more conservative approach, aimed at ameliorating the body of arytenoid cartilage on one side, paying airway symptoms while limiting subsequent scar- attention not to damage the membranous anterior ring of the larynx. Younger age at diagnosis has been 2 ⁄ 3 of the vocal cord (Figure 4). Improvement in shown to be a negative prognostic factor for remis- vocal cord function in idiopathic bilateral VCP can sion (14). Surgical debulking is the treatment of occur up to approximately 10 years of age and choice and several modalities have been used, therefore in such cases an endoscopic airway wid- including ‘cold steel’, microdebrider, CO2 laser and ening procedure should be delayed until the teenage radiofrequency ablation (15,16). The use of adjuvant years (8,13). medical treatments, such as intralesional cidofovir

remains controversial (17,18). CO2 laser treatment of Recurrent respiratory papillomatosis laryngeal papillomata has largely been superseded by other techniques, such as the microdebrider, due Recurrent respiratory papillomatosis is a benign to the increased risk of fibrosis and scarring subse- condition, of viral etiology, characterized by recur- quently impacting on the airway and voice quality. rent proliferations of squamous papillomata within Wherever possible the procedure should be under- the airway, anywhere from lips to . The viral taken with the child breathing spontaneously, pathogen is most commonly Human Papilloma without endotracheal intubation in order to limit

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Figure 5 Laryngeal recurrent respiratory papillomatosis involving the glottis. the chance of distal seeding of the papilloma. Microdebrider and radiofrequency ablation wands are now available designed to allow access to the larynx and as far distally as the carina (16). Figure 6 (a) Preoperatively subglottic cyst. (b) Postmarsupilization of the Subglottic cysts subglottic cyst. Subglottic cysts are a rare, but increasingly encoun- tered, cause of stridor in children, representing 7% necessitate tracheostomy insertion. The exact rela- of the airway pathologies identified at direct laryn- tionship between subglottic cysts and SGS is not gotracheobronchoscopy (DLTB) over a 2 year peri- known, with both either representing the conse- od, at our unit (19). All of the children with quences of the same subglottic trauma, or cysts subglottic cysts in this study had been intubated in resulting from the additional risk of mucosal trauma the neonatal period. Importantly, the same study in SGS, even with an age-appropriate endotracheal also identified a median delay of 4.25 months to the tube. onset of symptoms (range 1–13 months) (1). Their Again an unobstructed view of the operative site anatomical location means that the stridor is char- is achieved under general anesthesia with the acteristically biphasic in nature. The etiology of patient breathing spontaneously. The cysts may be subglottic cysts is thought to be mucosal damage marsupialized using laryngeal micro-instruments, from endotracheal intubation, especially in ex-pre- CO2 laser or a microdebrider (19) (Figure 6a,b). mature children. The length of intubation is not Despite adequate initial treatment cysts may recur in necessarily critical to cyst formation with children up to 50% of cases (19–21) and therefore interval identified following intubation for a single day reassessment should be performed 6–8 weeks later. (19,20). Concurrent (SGS) should Supraglottic cysts are even rarer and are treated by also be considered (19,20) and may on occasion marsupilization (Figure 7).

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‘nonsurgical’ treatment is corticosteroids, delivered either systemically or intra-lesionally. ‘Surgical’ options comprise either, excision of the abnormal

tissue (CO2 laser excision or an open approach with submucosal resection) or bypassing the developing airway narrowing while awaiting the natural regres- sion of the lesion (tracheostomy). Each modality has pros and cons, and in practice more than one modality is often employed. Systemic and intrale- sional steroids have both been reported to success- fully treat subglottic hemangiomas. Meeuwis et al. reported six children successfully treated with int- ralesional corticosteroid injection and intubation, avoiding tracheostomy over an average follow-up period of 3.3 years. The average total duration of intubation was however 19 days (7–36) (24). Sys- temic corticosteroids alone may be successful in a third of patients, providing the airway narrowing is Figure 7 not circumferential and does not exceed 50% (22). Supraglottic cyst. Systemic complications resulting from prolonged corticosteroid usage, such as growth retardation and Cushing syndrome, are well recognized (22,24) and Subglottic hemangioma the involvement of a pediatric endocrinologist is A subglottic hemangioma is a vascular anomaly essential if a prolonged course is anticipated. Laser resulting from endothelial hyperplasia (22). It is vaporization has also been reported to be successful usually characterized by the onset of biphasic stridor but is associated with a risk of iatrogenic SGS (25). within the first 6 weeks to 6 months of age. Initially Open surgical excision has been demonstrated to the hemangioma continues to enlarge (proliferative provide a ‘one stop’ treatment in noncircumferential phase) for up to 1 year (23) with resultant progres- subglottic hemangiomas (26) (Figure 8a,b). Success- sion of symptoms of airway obstruction. However, ful outcome, in terms of avoiding tracheostomy the tumor eventually enters a period of regression insertion or decannulation of existing tracheostomy, (involution phase) with gradual resolution of symp- has been reported in over 90% of cases (26). An toms over a 2–5 year period. The exact etiology of anterior cartilage graft may also be required if there the condition is not understood (22). The diagnostic are concerns about the development of a SGS (26). pathway begins with ascertaining the exact nature Although tracheostomy will protect the airway until and onset of the stridor and physical examination the tumor involutes, it is itself associated with may reveal a cutaneous hemangioma in association significant potential complications, including acci- with a subglottic hemangioma in approximately half dental decannulation or tube obstruction with the of cases (24). Airway endoscopy with spontaneous risk of cerebral hypoxia and death. The author’s ventilation is mandatory for all cases of biphasic protocol for the management of subglottic heman- stridor, as discussed earlier, and will demonstrate a giomas is illustrated in Figure 9. compressible subglottic swelling, often found poste- riorly on the left side, that may blanch in response to Laryngeal clefts topical epinephrine. Following diagnosis various treatment options are Laryngeal clefts result from failure of either the available dependant upon the age of the child, the posterior cricoid lamina or the septum between the degree of subglottic narrowing, distribution of the trachea and esophagus to develop, and are a rare hemangiomatous tissue within the subglottis cause of childhood airway symptoms. The anomaly and the presence of co-morbidities. The principal usually presents with a combination of stridor,

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the cricoid cartilage and the sternal notch (29) (Figure 10). Type 1 clefts can be managed conservatively in most cases, with endoscopic suture repair of the cleft reserved for those children who remain symptom- atic despite conservative measures. Endoscopic repair is facilitated by suspension microlaryngos- copy with a nasopharyngeal tube and spontaneous ventilation. The management of a cleft extending into the thorax (Type 4) requires collaboration between otolaryngologists and cardiothoracic sur- geons and is accompanied by a high mortality rate. The management of ‘intermediate’ clefts (Types 2 and 3), confined to the cervical trachea, remains controversial with some surgeons advocating an open approach via an anterior laryngotracheal fis- sure, similar to the technique described for laryngo- tracheal reconstruction (LTR). Alternatively, the endoscopic approach is gaining support (27,28) with the aim of avoiding both a period of postoperative intubation, the need for a ‘covering’ tracheostomy and the possibility of destabilizing the laryngeal framework (Figure 11a,b). Sandu and Monnier have reported the successful endoscopic treatment of four children with Type 3 clefts, with no sign of residual aspiration at a mean follow-up of 48 months. Each child subsequently had a good voice, but a mild degree of exertional dyspnoea (27). Rahbar et al., following a retrospec- tive study, reported the successful endoscopic treat- ment of six patients (three with Type 1, two with Figure 8 Type 2, and one with Type 3) with laryngeal clefts. (a) Right subglottic hemangioma. (b) Rigid endoscopy following In the same study 15 of 16 open repairs appear to open excision of the right subglottic hemangioma seen in Fig. 8a. have been successful from the perspective of feeding without difficulty (28). feeding difficulty, choking episodes, recurrent chest infections and possibly cyanotic episodes. The range Subglottic stenosis and laryngotracheal and severity of symptoms vary with the extent of the reconstruction communication between the airway and esophagus. Laryngeal clefts may be found in association with Subglottic stenosis (SGS) continues to present a Opitz–Frias and Pallister–Hall syndromes (27). The significant airway management problem. SGS may gold standard investigation is suspension laryngos- be congenital (e.g. Down syndrome) or acquired copy under general anesthesia and spontaneous (e.g. Postintubation laryngeal injury). The presenting ventilation, with palpation of the inter-arytenoid features of the condition are stridor (usually bipha- notch and examination of the tracheobronchial tree sic), recurrent , exertional dyspnoea, failure to (28). The most commonly used classification system thrive and recurrent lower infec- is that described by Benjamin and Inglis, whereby tions (30). SGS is diagnosed by conventional DLTB each cleft is classified into one of four catergories with the child breathing spontaneously and the dependant upon the length of the cleft in relation to airway sized using endotracheal tubes of increasing

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Figure 9 A protocol for the management of subglottic hemangioma. diameter. The system described by Myer and Cotton of the airway augmentation, and subsequent heal- is used to classify the degree of stenosis and helps in ing, the patient is decannulated between 3–6 months treatment planning (31). Grade 1 does not exceed after the original surgery. A tracheostomy is not 50% stenosis and grade 2 is 50–70% obstruction used in a single-stage LTR (ssLTR) and the child is (Figure 12). In grade 3 the stenosis is 71–99% and no left intubated with an age-appropriate endotracheal lumen is detected in grade 4 (Figure 13). tube for 5–7 days postoperatively, both stenting and The ‘gold standard’ technique for airway expan- safeguarding the airway. Although postoperative sion is LTR, whereby a cartilage graft, from either regimes will vary a further DLTB is usually per- the costal cartilages or the thyroid cartilage, is formed prior to extubating the child, and an interval inserted into a vertical laryngotracheal fissure in DLTB arranged dependant upon the condition of the order to expand a stenotic segment (Figure 14). Some larynx. All patients receive GERD prophylaxis post- stenoses will also require a posterior graft inserted operatively to negate the negative impact of gastric into a posterior cricoid chondrotomy. Prior to sur- contents on mucosal healing (30). gery the patient should have no untreated cardiore- Grade 1 SGS may be managed conservatively in spiratory compromise or respiratory infection and many cases; especially in congenital cases where should not be ventilated. In a double stage LTR expansion of the airway with growth of the child can (dsLTR) a tracheostomy is inserted (if not already in be anticipated. Grade 2 and 3 SGS usually requires situ) to safeguard the airway postoperatively and the surgical intervention with cartilage grafts inserted grafted area is stented for approximately 6 weeks. A anteriorly, and sometimes posteriorly, in order to further DLTB is then performed to remove the stent achieve sufficient airway expansion. Grade 4 SGS and assess the airway. Dependant upon the outcome necessitates either LTR or cricotracheal resection (32).

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Figure 10 Posterior view of the airway illustrating the Benjamin and Inglis classification of laryngeal clefts (Benjamin 1989). A, arytenoid cartilages; CC, cricoid cartilage; TC, tracheal cartilage; C, clavicle.

Success rates of 89–96% are reported for ssLTR (30,33) with success rates being generally lower for dsLTR (81–85%)(30,34).

Tracheomalacia

Tracheomalacia and tracheo- are Figure 11 characterized by airway collapse during expiration (a) and (b) Type 3 before and after endoscopic and are due to insufficient rigidity of the cartilagi- suture repair. nous framework (Figure 15). The condition usually presents within the first 12 months of life and loosely classified according to the underlying etiol- possible symptomology includes biphasic stridor, ogy into primary and secondary forms, although the expiratory wheeze, recurrent LRTI, chronic cough, exact pathogenic mechanisms are not fully under- cyanotic episodes, and ‘reflex apnoeas’. Chronic stood. In primary tracheomalacia the tracheal rings cough and recurrent infections are likely to be are considered to be of insufficient strength and this manifestations of inefficient clearance of secretions may be congenital, associated with prematurity or as and result airway inflammation. Tracheomalacia is a result of prolonged endotracheal intubation.

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Secondary tracheomalacia results from extrinsic pressure upon the airway or can be found in associ- ation with tracheo–esophageal fistula. Tracheo- malacia is usually self-limiting with resolution of symptoms by 2 years of age (35). The severity of symptoms is dependant upon the extent of airway involvement and collapse and may be compounded by co-existing airway pathology, such as laryngoma- lacia, laryngeal clefts and lower respiratory tract abnormalities, such as hyperplasia. Tracheomal- acia may be found in association with certain syn- dromes such as Down syndrome. Airway endoscope under general anesthesia with spontaneous ventila- tion is the principle method of diagnosis, but depen- dant upon the likely underling cause (e.g. vascular Figure 12 anomaly) additional radiological investigations will Myer and Cotton Grade 2 Subglottic stenosis. be indicated. The cardiovascular status of the child is critical when considering the requirement for, and nature of, any intervention. Noninvasive treatments include regular chest physiotherapy and splinting of the malacic segment with either Continuous positive airway pressure (CPAP) or Bi-level positive airway pressure (BiPAP) (36). Surgical options are dependant upon causation and include aortopexy to relieve external compression from an aberrant inominate artery and stenting (37). Tracheostomy may be indi- cated to splint the airway, while awaiting natural resolution of the cartilaginous weakness, especially when a significant length of the trachea is involved. A protocol for the investigation and management of tracheomalacia is given in Figure 16.

Intubation injury to the larynx

Figure 13 Significant postintubation injuries to the larynx are Myer and Cotton Grade 3 subglottic stenosis. rare. As alluded to earlier, endotracheal intubation is

Figure 14 Laryngotracheal reconstruction with anterior cartilage graft for subglottic stenosis.

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and cricoid cartilages with eventual mature scar formation (38). Whenever postintubation injury is suspected, often in the context of failed extubation, direct examination of the airway is mandatory. Laryngeal injury may also be suspected when airway symptoms develop following successful extubation. In such circumstances the severity and progression of symptomology will guide the timing of any formal airway evaluation. DLTB with spon- taneous ventilation is the investigation of choice and may demonstrate characteristic changes to the larynx, such as vocal cord edema, granulations and mucosal ulceration (Figure 17a,b). It is of critical Figure 15 importance to identify areas of superficial and deep Tracheomalacia resulting from external vascular compression. ulceration in the subglottis. Exposure of underlying implicated in the etiology of subglottic cysts and cartilage and circumferential ulceration risk the acquired SGS. Prolonged intubation may result in development of SGS and will often require trache- progressive ulceration of the subglottis, particularly ostomy insertion in order to ‘rest’ the subglottis. posteriorly, leading to chondritis of the arytenoid Exacerbating factors such as GERD and infection

Figure 16 A protocol for the management of Tracheomalacia. Based on Triglia J-M, Nicollas R & Roman S. Tracheomalacia in children. In: Graham JM, Scadding GK & Bull PD, Eds. Pediatric ENT. 1st Edn. Berlin: Springer, 2007: 241–244.

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treatment modality it is associated with significant morbidity and mortality. In children the mortality rate attributable to the tracheostomy has been reported to be as high as 3.4% (40). With the continuing evolution of endolaryngeal surgical tech- niques, greater demands will be placed on the anesthetist to achieve adequate anesthesia, often without endotracheal intubation, in the face of increasingly significant airway obstruction.

Acknowledgement Thanks to Sam Goddard from the Medical Illustra- tion department at the Manchester Royal Infirmary.

Supporting information Additional Supporting Information may be found in the online version of this article: Video Clip S1. This video represents Paediatric Anaesthesia, specifically upper airway obstruction. Please note: Wiley-Blackwell are not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article.

Conflicts of interest Figure 17 (a) Postintubation injury to the larynx demonstating extensive The authors have decalred no conflicts of interest. granulations. (b) Postintubation injury to the larynx demonstrat- ing vocal cord edema and ‘seal flipper’ granulations. References should also be managed appropriately. Repeat 1 Olney DR, Greinwald JH, Smith RJH et al. Laryngomalacia and its treatment. Laryngoscope 1999; 109: 1770–1775. DLTB 1–2 weeks later may confirm healing without 2 Freidman EM, Vastola AP, McGill TJI et al. Chronic pediatric scarring, facilitating early decannulation. Evolving stridor: etiology and outcome. Laryngoscope 1990; 100: 277– ‘soft’ subglottic scarring may be treated with balloon 280. 3 Yuen HW, Tan KK, Balakrishnan A. Synchronous airway dilatation using an appropriately sized angioplasty lesions and associated anomalies in children with laryngo- balloon (39). malacia evaluated with rigid endoscopy. Int J Pediatr Otorhi- nolaryngol 2006; 70: 1779–1784. 4 Mancuso RF, Choi SS, Zalzal GH et al. Laryngomalacia: the Summary search for the second lesion. Arch Otolaryngol Head Surg 1996; 122: 302–306. Rigid endoscopy remains the ‘gold standard’ inves- 5 Whymark AD, Clement WA, Kubba H et al. Laser epi- tigation for ‘fixed’ and dynamic childhood airway glottopexy for laryngomalacia: 10 years experience in the West of Scotland. Arch Otolaryngol Head Neck Surg 2006; 132: 978– pathologies. Assessment of the spontaneously 982. breathing child under general anesthesia is essential 6 O’Donnell SO, Murphy J, Bew S et al. Aryepiglottoplasty for if dynamic airway disorders such as laryngomalacia, laryngomalacia: results and recommendations following a case series of 84. Int J Pediatr Otorhinolaryngol 2007; 71: 1271– VCP and tracheomalacia are to be correctly identi- 1275. fied. Although, tracheostomy remains an important

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2009 The Authors Journal compilation 2009 Blackwell Publishing Ltd, Pediatric Anesthesia, 19 (Suppl. 1), 88–99