Endoscopic correction of severe laryngomalacia
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《美国医学杂志》
1 Departments of Otorhinolaryngology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India
2 Departments of Pediatrics, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India
Abstract
Tracheostomy for management of severe laryngomalacia is associated with significant morbidity and mortality. Two cases are reported wherein the laryngeal abnormality was corrected by ary-epiglottic fold incision and CO2 laser supraglottoplasty. Stridor and respiratory obstruction were relieved and a long term tracheostomy avoided. Endoscopic correction of laryngomalacia offers significant benefits over conventional treatment with tracheostomy in terms of decreased morbidity and improved quality of life.
Keywords: Laryngomalacia; Tracheostomy; Morbidity and mortality; Endoscopic correction
Laryngomalacia is the most frequent cause (60 to 70%) of stridor in both newborns and infants.[1] Approximately 90% of reported cases are mild[2] and the symptoms resolve spontaneously by the age of two years. In 7 to 12% of children the condition is severe and potentially life threatening dyspnea may occur. In addition, there may be swallowing difficulties, failure to thrive, obstructive sleep apnea, cor pulmonale,[3] and even sudden death. The severity of the above symptoms may make it necessary to resort to tracheostomy till a spontaneous improvement occurs. Tracheostomy in young children, however, carries significant morbidity and mortality.[4],[5] Tracheostomy tube obstruction and accidental decannulation are common risks. The children are also prone to recurrent lower respiratory tract infections, subglottic stenosis, speech delay and a psychological dependence on the tracheostomy. These make its removal difficult even after improvement of the airway. The long term mortality from a pediatric tracheostomy, as reported from the US and Europe, ranges between 0.9% to 5%.[4],[5] Similar figures from India may well be higher. In addition, a tracheostomised child requires constant attention and supervision.
The above mentioned problems associated with tracheostomy , underline the unsatisfactory nature of this treatment option and the necessity of an alternate strategy. This report describes two young children with severe laryngomalacia wherein the upper airway obstruction has been treated by supraglottic surgery and a long- term tracheostomy avoided.
Case report
Case 1
A 20-day-old well-thriving female child was referred to the otolaryngology service with inspiratory stridor manifesting from the early neonatal period. The child was born at full term by vaginal delivery at hospital.
On examination, the child had inspiratory stridor, minimal suprasternal recession but no intercostal or subcostal recession. The stridor was exacerbated by crying, but was not significantly altered in the supine or prone position. The child weighed 3.5 kg. The respiratory rate was 42/min and heart rate 140/min. The oral cavity and oropharynx were normal. Laryngeal examination by a flexible nasopharyngoscope revealed the epiglottis to be omega-shaped and folded posteriorly so as to cap the anterior 2/3rd of the larynx. The arytenoids were tall and loose mucosal folds were prolapsing inwards with each inspiratory breath. The vocal folds were normal. These findings were suggestive of laryngomalacia. As the child did not have significant respiratory distress, it was decided to observe the child. Twenty-five days later, the child was brought to the clinic with worsening of stridor, significant chest retractions and two episodes of cyanosis. She had not been feeding well and weighed 2.45 kg. On examination, she had severe inspiratory stridor with suprasternal and intercostal retractions, a respiratory rate of 58/ min and a heart rate of 160/ min. Fibreoptic flexible laryngoscopic (FOL) examination showed increased supraglottic collapse, in addition to the findings at previous visit. The child was immediately scheduled for a rigid endoscopy and probable tracheostomy under general anesthesia.
The initial direct laryngoscopy and bronchoscopy, undertaken with the patient breathing spontaneously, confirmed the diagnosis of laryngomalacia Figure1a. This also excluded other abnormalities in the tracheo-bronchial tree, particularly vocal cord paralysis and interarytenoid cleft. The child was then intubated and microlaryngoscopy undertaken. The short aryepiglottic folds (AE folds) were divided by a sharp scissors at a point approximately midway between the arytenoid and the epiglottis. Following this incision, the epiglottis was found to immediately spring forward and the laryngeal inlet was rendered more visible and open.
The child was extubated after reversal of anesthesia. The stridor was significantly reduced and endoscopic examination confirmed decrease in the supraglottic collapse. Post-operatively she was nursed in the pediatric ICU wherein she received antibiotics, nebulized budesonide, adrenaline, and nasogastric feeds. The stridor progressively decreased and subsided completely by the 3rd post-operative day. Oral feeds were started on the 6th post-operative day and easily tolerated without aspiration. She was then discharged. At three weeks follow up, the child did not have stridor, was taking breast feeds adequately, and had gained weight. A repeat FOL evaluation Figure1b demonstrated no supraglottic collapse. At one year follow up, she is completely free of stridor.
Case 2
A 2-year-old male child presented with progressively increasing stridor since the first month of life which was now associated with respiratory distress. The child was born at full term in a hospital following an uneventful labor and was judged as normal at birth. The child had not been feeding well and had poor weight gain. Examination revealed inspiratory stridor with suprasternal recession, a respiratory rate of 40/min, and a heart rate of 132/min. The oral cavity and oropharynx. were normal. FOL examination revealed omega-shaped epiglottis and prominent arytenoids with loose mucosal folds. The loose supraglottic tissues obscured the glottis preventing assessment of vocal cord mobility.
Significant respiratory distress and incomplete clinic evaluation necessitated further endoscopic evaluation under general anesthesia. The initial evaluation undertaken without an endotracheal tube confirmed the diagnosis of laryngomalacia Figure2a. The cords were mobile, and the glottis, subglottis and trachea were normal. The endotracheal tube was then passed and microlaryngoscopy undertaken; the short AE folds were divided bilaterally. The child was extubated on the first postoperative day. However, there was recurrence of stridor and respiratory distress. Therefore, a tracheostomy had to be undertaken. A repeat FOL evaluation undertaken after a few weeks indicated the presence of persistent supraglottic collapse consequent to loose supraglottic tissues.
A second surgery was scheduled wherein a complete supraglottoplasty was undertaken with a CO2 laser so as to excise the loose mucosa at the base of the epiglottis, AE folds and false cord. Postoperative period was uneventful. The child was discharged with the tracheostomy, with detailed instructions to the parents regarding the care. Subsequent review at eight weeks with FOL, confirmed good healing, with a patent supraglottis devoid of any loose prolapsing tissues Figure2b. The child was then successfully decannulated.
Discussion
Severe stridor secondary to laryngomalacia has ominous implications and necessitates immediate diagnostic and therapeutic measures. A definitive diagnosis is best achieved by a rigid endoscopy under general anesthesia. The conventional treatment to relieve the stridor is a tracheostomy. Unfortunately these have significant morbidity and occasional mortality in infants and young children.[4],[5] The two cases reported here represent the current approach to the diagnosis and treatment of pediatric stridor and laryngomalacia. Most cases of laryngomalacia are self-limiting or may improve with age, making observation an established modality. Rigid endoscopy poses a risk of precipitating a tracheostomy in patients wherein it could otherwise have been avoided. Instrumentation in the airway may precipitate local edema and laryngospasm, and also the general anesthetic may cause respiratory depression. These changes can push a mildly compromised but compensated airway towards a situation wherein a tracheostomy may become imperative.
In our current practice we use FOL evaluation in outpatient clinic to select the cases wherein observation is persisted with and further rigid endoscopy deferred. Such an evaluation helps confirm supraglottic and glottic abnormalities and also facilitates a dynamic evaluation- this being especially relevant for laryngomalacia and vocal cord palsy. However, the evaluation of the subglottis and trachea is inadequate. This is important limitation as tracheobronchial anamolies are known to be multiple in 17.5 % of cases.[6]
Approximately 10% patients with laryngomalacia require surgery to secure the airway[7] although figures upto 22%[8] have been reported. Firm criteria for surgical intervention are difficult to define. Laryngoscopic appearance by itself is not used as the sole criterion to determine the need for surgery, though complete obstruction of laryngeal inlet by supraglottic collapse is certainly significant. Other features which are specifically relevant include respiratory distress, apneic attacks, feeding difficulty, failure to thrive and cor pulmonale. The conventional surgical option of a tracheostomy to relieve the obstruction is unsatisfactory, because of the reasons already cited. Techniques, which directly improve the airway, such as, reported in this communication, are preferable in terms of their immediate efficacy and the lack of any significant long-term morbidity.
The exact pathophysiology of laryngomalacia remains obscure. It is however established that it leads to a dynamic supraglottic collapse in inspiration, and the following three anatomical abnormalities have been chiefly implicated.
a. short AE folds
b. a long curled epiglottis which prolapses posteriorly
c. bulky arytenoids with loose mucosa which prolapses forward on inspiration.
These features may be seen in combination or as separate entities.
Endoscopic surgical correction of laryngomalacia seeks to correct these anatomic anomalies. The most consistent of these structural abnormalities is the short aryepiglottic fold.[9] It is believed that the short AE folds are responsible for tethering the epiglottis posteriorly. Incision of the folds midway along its length serves to release the epiglottis and allows it to move forward. Hasslinger, in 1928, is credited with the first description of such a procedure, and several authors have described it since then[2],[9],[10],[11] Such division of the AE folds alone, is reported to be sufficient to relieve the airway obstruction in the vast majority of cases (90.6%).[12] We, therefore relied on AE fold division as the initial procedure in both our cases.
The alternate surgical option described for laryngomalacia is supraglottoplasty in which the obstructing supraglottic tissue is trimmed either with microlaryngeal instruments or vaporized with CO2 laser under suspension laryngoscopy.[13] This was required in one of the two cases reported here, wherein simple division of the AE folds proved inadequate.
Following such direct laryngeal manipulation, the resultant local inflammatory response to the surgical trauma may potentially cause transient compromise of the airway. Local edema and laryngospasm are ever-present dangers. The success of the procedure lies in limiting surgical trauma and in the availability of pediatric intensive care facilities in the post-operative period. In our cases, while we selected to use conventional instrumentation for the AE fold excision, a CO2 laser was used for more extensive supraglottoplasty. The CO2 laser allows for precise and atraumatic mucosal surgery and minimises surgical and thermal injury to the adjacent tissues.
Complications inherent to the procedure are minimal, provided adequate precautions are exercised. The improvement in airway took 2 to 3 days to be fully manifested. Presumably this was the result of local tissue edema consequent to both the anaesthesia and the surgical procedure. Also, AE fold incision alone proved inadequate in the second case and a second surgical procedure with laser supraglottoplasty was called for.
Our results with both the cases have been extremely gratifying, and the literature indicates that no further long term recurrence or morbidity is to be expected. As far as the review of literature from index journals is concerned, this is the first report of its kind in our country. The major benefit has been the avoidance of the potential morbidity and mortality of repeated intubation or tracheostomy. The relief in airway compromise has also helped in correcting for feeding difficulties and in facilitating normal growth.
Conclusion
We would like to emphasize the utility of an initial FOL examination in the outpatient setting for evaluation of children with stridor. Endoscopic correction of severe laryngomalacia is efficacious and serves to significantly limit the morbidity and mortality that is inherent with the conventional treatment of tracheostomy. The success of the technique hinges on limiting surgical injury by adequate instrumentation, and by expert post-operative intensive care in an intensive care unit. Close liason between the paediatric and otolaryngological teams is called for.
References
1. Holinger LD, Etiology of stridor in the neonate,infant ,and the child. Ann Otol Rhinol Laryngol 1980; 89: 397-400.
2. Lane RW, Weider DJ, Steinam C, Marin-Padilla, Laryngomalacia: A review and case report of surgical treatment with resolution of pectus excavatum. Arch otolaryngol 1984; 110: 546-551.
3. Zalzal GH, Anon JB, Cotton RT. Epiglottoplasty for the treatment of laryngomalacia. Ann Otol Rhinol Laryngol 1987; 96: 72-76.
4. Sichel J, Dangoor E, Eliashar R, Halperin D. Management of congenital laryngeal malformations. Am J Otolaryngol 2000; 21: 22-30.
5. Rogers JH.Tracheostomy and decannulation. In David A Adams and Michael J Cinnamond ed, Scott-Brown; 6th edn. Vol 6 page 15.
6. Gonzales C, Reilly JS, Bluestone CD. Synchronus airway lesions in infancy. Ann Otol Rhinol Laryngol 1987; 96: 77-80.
7. Fearon B, Ellis D. The management of long term airway problems in infants and children. Ann Otol Rhinol Laryngol 1971; 80: 669-71.
8. Friedman EM, Vastola P, McGill TJI et al. Chronic paediatric stridor: Etiology and Outcome. Laryngoscope 1990; 100: 277-280.
9. Seid AB, Park SM, Kearns MJ, Guhenheim S. Laser division of Aryepiglottic folds for severe laryngomalacia. Int J Pediatr Otorhinolaryngol 1985; 10: 153-158.
10. Polonovsky JM, Contencin P, Francois M, Viala P, Narcy P. Aryepiglottic fold excision for the treatment of severe laryngomalacia. Ann Otol Rhinol Laryngol 1990; 99: 625-627.
11. Templer J, Hast M, Thomas JR, Davis WE. Congenital laryngeal stridor secondary to flaccid epiglottis,anomalous accessory cartilages and redundant aryepiglottic fold. Laryngoscope 1981; 91: 394-397.
12. Loke D, Ghosh S, Panarese A, Bull PD. Endoscopic division of aryepiglottic folds in severe laryngomalacia Int JPediatr Otorhinolaryngol 2001; 60: 59-63.
13. McClurg EL, Evans DA. Laser laryngoplasty for laryngomalacia. Laryngoscope 1994; 104: 247-252.(Venkatakarthikeyan C, Tha)
2 Departments of Pediatrics, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India
Abstract
Tracheostomy for management of severe laryngomalacia is associated with significant morbidity and mortality. Two cases are reported wherein the laryngeal abnormality was corrected by ary-epiglottic fold incision and CO2 laser supraglottoplasty. Stridor and respiratory obstruction were relieved and a long term tracheostomy avoided. Endoscopic correction of laryngomalacia offers significant benefits over conventional treatment with tracheostomy in terms of decreased morbidity and improved quality of life.
Keywords: Laryngomalacia; Tracheostomy; Morbidity and mortality; Endoscopic correction
Laryngomalacia is the most frequent cause (60 to 70%) of stridor in both newborns and infants.[1] Approximately 90% of reported cases are mild[2] and the symptoms resolve spontaneously by the age of two years. In 7 to 12% of children the condition is severe and potentially life threatening dyspnea may occur. In addition, there may be swallowing difficulties, failure to thrive, obstructive sleep apnea, cor pulmonale,[3] and even sudden death. The severity of the above symptoms may make it necessary to resort to tracheostomy till a spontaneous improvement occurs. Tracheostomy in young children, however, carries significant morbidity and mortality.[4],[5] Tracheostomy tube obstruction and accidental decannulation are common risks. The children are also prone to recurrent lower respiratory tract infections, subglottic stenosis, speech delay and a psychological dependence on the tracheostomy. These make its removal difficult even after improvement of the airway. The long term mortality from a pediatric tracheostomy, as reported from the US and Europe, ranges between 0.9% to 5%.[4],[5] Similar figures from India may well be higher. In addition, a tracheostomised child requires constant attention and supervision.
The above mentioned problems associated with tracheostomy , underline the unsatisfactory nature of this treatment option and the necessity of an alternate strategy. This report describes two young children with severe laryngomalacia wherein the upper airway obstruction has been treated by supraglottic surgery and a long- term tracheostomy avoided.
Case report
Case 1
A 20-day-old well-thriving female child was referred to the otolaryngology service with inspiratory stridor manifesting from the early neonatal period. The child was born at full term by vaginal delivery at hospital.
On examination, the child had inspiratory stridor, minimal suprasternal recession but no intercostal or subcostal recession. The stridor was exacerbated by crying, but was not significantly altered in the supine or prone position. The child weighed 3.5 kg. The respiratory rate was 42/min and heart rate 140/min. The oral cavity and oropharynx were normal. Laryngeal examination by a flexible nasopharyngoscope revealed the epiglottis to be omega-shaped and folded posteriorly so as to cap the anterior 2/3rd of the larynx. The arytenoids were tall and loose mucosal folds were prolapsing inwards with each inspiratory breath. The vocal folds were normal. These findings were suggestive of laryngomalacia. As the child did not have significant respiratory distress, it was decided to observe the child. Twenty-five days later, the child was brought to the clinic with worsening of stridor, significant chest retractions and two episodes of cyanosis. She had not been feeding well and weighed 2.45 kg. On examination, she had severe inspiratory stridor with suprasternal and intercostal retractions, a respiratory rate of 58/ min and a heart rate of 160/ min. Fibreoptic flexible laryngoscopic (FOL) examination showed increased supraglottic collapse, in addition to the findings at previous visit. The child was immediately scheduled for a rigid endoscopy and probable tracheostomy under general anesthesia.
The initial direct laryngoscopy and bronchoscopy, undertaken with the patient breathing spontaneously, confirmed the diagnosis of laryngomalacia Figure1a. This also excluded other abnormalities in the tracheo-bronchial tree, particularly vocal cord paralysis and interarytenoid cleft. The child was then intubated and microlaryngoscopy undertaken. The short aryepiglottic folds (AE folds) were divided by a sharp scissors at a point approximately midway between the arytenoid and the epiglottis. Following this incision, the epiglottis was found to immediately spring forward and the laryngeal inlet was rendered more visible and open.
The child was extubated after reversal of anesthesia. The stridor was significantly reduced and endoscopic examination confirmed decrease in the supraglottic collapse. Post-operatively she was nursed in the pediatric ICU wherein she received antibiotics, nebulized budesonide, adrenaline, and nasogastric feeds. The stridor progressively decreased and subsided completely by the 3rd post-operative day. Oral feeds were started on the 6th post-operative day and easily tolerated without aspiration. She was then discharged. At three weeks follow up, the child did not have stridor, was taking breast feeds adequately, and had gained weight. A repeat FOL evaluation Figure1b demonstrated no supraglottic collapse. At one year follow up, she is completely free of stridor.
Case 2
A 2-year-old male child presented with progressively increasing stridor since the first month of life which was now associated with respiratory distress. The child was born at full term in a hospital following an uneventful labor and was judged as normal at birth. The child had not been feeding well and had poor weight gain. Examination revealed inspiratory stridor with suprasternal recession, a respiratory rate of 40/min, and a heart rate of 132/min. The oral cavity and oropharynx. were normal. FOL examination revealed omega-shaped epiglottis and prominent arytenoids with loose mucosal folds. The loose supraglottic tissues obscured the glottis preventing assessment of vocal cord mobility.
Significant respiratory distress and incomplete clinic evaluation necessitated further endoscopic evaluation under general anesthesia. The initial evaluation undertaken without an endotracheal tube confirmed the diagnosis of laryngomalacia Figure2a. The cords were mobile, and the glottis, subglottis and trachea were normal. The endotracheal tube was then passed and microlaryngoscopy undertaken; the short AE folds were divided bilaterally. The child was extubated on the first postoperative day. However, there was recurrence of stridor and respiratory distress. Therefore, a tracheostomy had to be undertaken. A repeat FOL evaluation undertaken after a few weeks indicated the presence of persistent supraglottic collapse consequent to loose supraglottic tissues.
A second surgery was scheduled wherein a complete supraglottoplasty was undertaken with a CO2 laser so as to excise the loose mucosa at the base of the epiglottis, AE folds and false cord. Postoperative period was uneventful. The child was discharged with the tracheostomy, with detailed instructions to the parents regarding the care. Subsequent review at eight weeks with FOL, confirmed good healing, with a patent supraglottis devoid of any loose prolapsing tissues Figure2b. The child was then successfully decannulated.
Discussion
Severe stridor secondary to laryngomalacia has ominous implications and necessitates immediate diagnostic and therapeutic measures. A definitive diagnosis is best achieved by a rigid endoscopy under general anesthesia. The conventional treatment to relieve the stridor is a tracheostomy. Unfortunately these have significant morbidity and occasional mortality in infants and young children.[4],[5] The two cases reported here represent the current approach to the diagnosis and treatment of pediatric stridor and laryngomalacia. Most cases of laryngomalacia are self-limiting or may improve with age, making observation an established modality. Rigid endoscopy poses a risk of precipitating a tracheostomy in patients wherein it could otherwise have been avoided. Instrumentation in the airway may precipitate local edema and laryngospasm, and also the general anesthetic may cause respiratory depression. These changes can push a mildly compromised but compensated airway towards a situation wherein a tracheostomy may become imperative.
In our current practice we use FOL evaluation in outpatient clinic to select the cases wherein observation is persisted with and further rigid endoscopy deferred. Such an evaluation helps confirm supraglottic and glottic abnormalities and also facilitates a dynamic evaluation- this being especially relevant for laryngomalacia and vocal cord palsy. However, the evaluation of the subglottis and trachea is inadequate. This is important limitation as tracheobronchial anamolies are known to be multiple in 17.5 % of cases.[6]
Approximately 10% patients with laryngomalacia require surgery to secure the airway[7] although figures upto 22%[8] have been reported. Firm criteria for surgical intervention are difficult to define. Laryngoscopic appearance by itself is not used as the sole criterion to determine the need for surgery, though complete obstruction of laryngeal inlet by supraglottic collapse is certainly significant. Other features which are specifically relevant include respiratory distress, apneic attacks, feeding difficulty, failure to thrive and cor pulmonale. The conventional surgical option of a tracheostomy to relieve the obstruction is unsatisfactory, because of the reasons already cited. Techniques, which directly improve the airway, such as, reported in this communication, are preferable in terms of their immediate efficacy and the lack of any significant long-term morbidity.
The exact pathophysiology of laryngomalacia remains obscure. It is however established that it leads to a dynamic supraglottic collapse in inspiration, and the following three anatomical abnormalities have been chiefly implicated.
a. short AE folds
b. a long curled epiglottis which prolapses posteriorly
c. bulky arytenoids with loose mucosa which prolapses forward on inspiration.
These features may be seen in combination or as separate entities.
Endoscopic surgical correction of laryngomalacia seeks to correct these anatomic anomalies. The most consistent of these structural abnormalities is the short aryepiglottic fold.[9] It is believed that the short AE folds are responsible for tethering the epiglottis posteriorly. Incision of the folds midway along its length serves to release the epiglottis and allows it to move forward. Hasslinger, in 1928, is credited with the first description of such a procedure, and several authors have described it since then[2],[9],[10],[11] Such division of the AE folds alone, is reported to be sufficient to relieve the airway obstruction in the vast majority of cases (90.6%).[12] We, therefore relied on AE fold division as the initial procedure in both our cases.
The alternate surgical option described for laryngomalacia is supraglottoplasty in which the obstructing supraglottic tissue is trimmed either with microlaryngeal instruments or vaporized with CO2 laser under suspension laryngoscopy.[13] This was required in one of the two cases reported here, wherein simple division of the AE folds proved inadequate.
Following such direct laryngeal manipulation, the resultant local inflammatory response to the surgical trauma may potentially cause transient compromise of the airway. Local edema and laryngospasm are ever-present dangers. The success of the procedure lies in limiting surgical trauma and in the availability of pediatric intensive care facilities in the post-operative period. In our cases, while we selected to use conventional instrumentation for the AE fold excision, a CO2 laser was used for more extensive supraglottoplasty. The CO2 laser allows for precise and atraumatic mucosal surgery and minimises surgical and thermal injury to the adjacent tissues.
Complications inherent to the procedure are minimal, provided adequate precautions are exercised. The improvement in airway took 2 to 3 days to be fully manifested. Presumably this was the result of local tissue edema consequent to both the anaesthesia and the surgical procedure. Also, AE fold incision alone proved inadequate in the second case and a second surgical procedure with laser supraglottoplasty was called for.
Our results with both the cases have been extremely gratifying, and the literature indicates that no further long term recurrence or morbidity is to be expected. As far as the review of literature from index journals is concerned, this is the first report of its kind in our country. The major benefit has been the avoidance of the potential morbidity and mortality of repeated intubation or tracheostomy. The relief in airway compromise has also helped in correcting for feeding difficulties and in facilitating normal growth.
Conclusion
We would like to emphasize the utility of an initial FOL examination in the outpatient setting for evaluation of children with stridor. Endoscopic correction of severe laryngomalacia is efficacious and serves to significantly limit the morbidity and mortality that is inherent with the conventional treatment of tracheostomy. The success of the technique hinges on limiting surgical injury by adequate instrumentation, and by expert post-operative intensive care in an intensive care unit. Close liason between the paediatric and otolaryngological teams is called for.
References
1. Holinger LD, Etiology of stridor in the neonate,infant ,and the child. Ann Otol Rhinol Laryngol 1980; 89: 397-400.
2. Lane RW, Weider DJ, Steinam C, Marin-Padilla, Laryngomalacia: A review and case report of surgical treatment with resolution of pectus excavatum. Arch otolaryngol 1984; 110: 546-551.
3. Zalzal GH, Anon JB, Cotton RT. Epiglottoplasty for the treatment of laryngomalacia. Ann Otol Rhinol Laryngol 1987; 96: 72-76.
4. Sichel J, Dangoor E, Eliashar R, Halperin D. Management of congenital laryngeal malformations. Am J Otolaryngol 2000; 21: 22-30.
5. Rogers JH.Tracheostomy and decannulation. In David A Adams and Michael J Cinnamond ed, Scott-Brown; 6th edn. Vol 6 page 15.
6. Gonzales C, Reilly JS, Bluestone CD. Synchronus airway lesions in infancy. Ann Otol Rhinol Laryngol 1987; 96: 77-80.
7. Fearon B, Ellis D. The management of long term airway problems in infants and children. Ann Otol Rhinol Laryngol 1971; 80: 669-71.
8. Friedman EM, Vastola P, McGill TJI et al. Chronic paediatric stridor: Etiology and Outcome. Laryngoscope 1990; 100: 277-280.
9. Seid AB, Park SM, Kearns MJ, Guhenheim S. Laser division of Aryepiglottic folds for severe laryngomalacia. Int J Pediatr Otorhinolaryngol 1985; 10: 153-158.
10. Polonovsky JM, Contencin P, Francois M, Viala P, Narcy P. Aryepiglottic fold excision for the treatment of severe laryngomalacia. Ann Otol Rhinol Laryngol 1990; 99: 625-627.
11. Templer J, Hast M, Thomas JR, Davis WE. Congenital laryngeal stridor secondary to flaccid epiglottis,anomalous accessory cartilages and redundant aryepiglottic fold. Laryngoscope 1981; 91: 394-397.
12. Loke D, Ghosh S, Panarese A, Bull PD. Endoscopic division of aryepiglottic folds in severe laryngomalacia Int JPediatr Otorhinolaryngol 2001; 60: 59-63.
13. McClurg EL, Evans DA. Laser laryngoplasty for laryngomalacia. Laryngoscope 1994; 104: 247-252.(Venkatakarthikeyan C, Tha)