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Occult laryngomalacia resulting in obstructive sleep apnea in an infant
International Journal of Pediatric Otorhinolaryngology 77 (2013) 1617–1619
Contents lists available at SciVerse ScienceDirect
International Journal of Pediatric Otorhinolaryngology journal homepage: www.elsevier.com/locate/ijporl
Case report
Occult laryngomalacia resulting in obstructive sleep apnea in an infant Karin P.Q. Oomen, Vikash K. Modi * Department of Otolaryngology-Head & Neck Surgery, Pediatric Otolaryngology-Head & Neck Surgery, Weill Cornell Medical College, 428 East 72nd Street, Suite 100, New York, NY 10021, USA
A R T I C L E I N F O
A B S T R A C T
Article history: Received 12 April 2013 Received in revised form 2 July 2013 Accepted 3 July 2013 Available online 1 August 2013
Classic laryngomalacia presents in the awake infant with progressive stridor when agitated. Occult laryngomalacia usually presents with stridor in children older than 2 years and is limited to sleep or exercise. There have been no documented cases of occult laryngomalacia causing obstructive sleep apnea in infants. We report the youngest documented case of an infant with state-dependent laryngomalacia resulting in severe obstructive sleep apnea. This patient was successfully treated with supraglottoplasty, with resolution of symptoms. In conclusion, state-dependent laryngomalacia resulting in obstructive sleep apnea may present in children younger than 12 months of age. In these individuals, supraglottoplasty should be considered. ß 2013 Elsevier Ireland Ltd. All rights reserved.
Keywords: Laryngomalacia Occult laryngomalacia Obstructive sleep apnea Supraglottoplasty Sleep endoscopy
1. Introduction Obstructive sleep apnea (OSA) is a syndrome of partial or complete upper airway obstruction during sleep. Pediatric OSA is most commonly attributed to adenotonsillar hypertrophy, and adenotonsillectomy remains the mainstay of surgical treatment. A small proportion of pediatric OSA has been attributed to laryngomalacia [1]. Laryngomalacia is a disease entity characterized by collapse of supraglottic structures during inspiration, resulting in intermittent upper airway obstruction [2]. Its classic clinical picture is one of inspiratory stridor presenting within the first 2 weeks of life, increasing with agitation or with feeding. Upper airway obstruction can progress during the first 6 months, after which symptoms gradually resolve spontaneously. Approximately 5–10% of patients suffer from a severe form of classic laryngomalacia, requiring surgical intervention [3]. Occult laryngomalacia is an atypical form of laryngomalacia, characterized by stridor and symptoms of upper airway obstruction limited to exercise or sleep [4,5]. Laryngomalacia that is exclusively present during sleep has also been termed statedependent laryngomalacia, due to its variation of symptoms with level of consciousness [6]. Previous studies have described occult laryngomalacia as a cause of OSA, but only in children older than 2 years of age [1,4,5,7]. In this older age group, supraglottoplasty has been shown to be curative [5,7].
* Corresponding author. Tel.: +1 646 962 3017; fax: +1 212 746 8124. E-mail address: [email protected] (V.K. Modi). 0165-5876/$ – see front matter ß 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijporl.2013.07.006
We report the youngest documented case of pediatric OSA secondary to state-dependent laryngomalacia. 2. Case report A 5 month old male with a history of a high-pitched inspiratory sound during sleep for 2 months, was referred to Weill Cornell Medical College, Division of Pediatric Otolaryngology-Head & Neck Surgery. The patient was born full term at 38 weeks via a normal spontaneous vaginal delivery. He did not have a history of intubation or airway intervention. No stridor or other respiratory issues were reported when the infant was awake. The infant was feeding well and gaining weight appropriately. There were no dysmorphic features or developmental/neurologic issues. An inoffice awake exam, which included flexible fiberoptic laryngoscopy, revealed a small posterior cricoid cushion [8] but was otherwise normal. Polysomnography demonstrated an apnea-hypopnea index (AHI) of 10.2 and an arterial oxygen saturation (SaO2) nadir of 88%, consistent with severe OSA [9]. Normal end tidal carbon dioxide (ETCO2) measurements of 30.7 Torr at baseline and 45 Torr at maximum were present. A sleep endoscopy followed by a direct laryngoscopy and bronchoscopy were recommended to assess the level of airway obstruction during sleep and to rule out the presence of any airway lesions. For the sleep endoscopy, the infant was induced with inhalational anesthesia and propofol in the supine position, without the use of a shoulder roll. Appropriate time was allowed for the inhalational gasses to wear off, in order to ensure that the only mode of sedation was intravenous propofol. Upon initiation of
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K.P.Q. Oomen, V.K. Modi / International Journal of Pediatric Otorhinolaryngology 77 (2013) 1617–1619
Fig. 1. Inward prolapse of the arytenoids during inspiration on sleep endoscopy (type I laryngomalacia).
sleep, inspiratory stridor developed, and the patient’s father was brought into the room to confirm this was the sound observed during sleep at home. A pediatric flexible fiberoptic laryngoscope was then introduced in the nasal cavity and advanced to assess the upper airway. The adenoid was normal in size, tonsillar size was 1+ (occupying less than 25% of the oropharynx), the soft palate was normal, and there was no lingual tonsil hypertrophy or base of tongue collapse. The arytenoids bilaterally were found to prolapse into the airway during inspiration (type I laryngomalacia) [10], reflecting a clinical picture consistent with state-dependent laryngomalacia (Fig. 1). Subsequently, a rigid microdirect laryngoscopy and bronchoscopy revealed no laryngeal cleft or other airway anomalies. Postoperatively, the parents were informed about the finding of state-dependent laryngomalacia. Medical management was implemented with reflux precautions and a twice daily proton pump inhibitor. No change was noted in the patient’s symptoms after 2 weeks, and supraglottoplasty was recommended. A supraglottoplasty was performed using microscissors to incise both aryepiglottic folds, and to excise redundant mucosa over the cuneiform cartilages. Hemostasis was achieved with oxymetazoline hydrochloride 0.05% soaked pledgelets. The patient had an uneventful overnight stay in the pediatric intensive care unit, and was discharged the next day tolerating an ageappropriate diet. There were no complications and the postoperative course was uneventful. A 4 week postoperative polysomnogram demonstrated an AHI of 2.4 and an SaO2 nadir of 89%, with normal ETCO2s of 28 Torr at baseline and 41 Torr at maximum. Only central apneas were present, no obstructive apneas or hypopneas were recorded. The parents have reported complete resolution of symptoms at consecutive postoperative visits. 3. Discussion Previous reports have described classic laryngomalacia resulting in OSA in infants and young children [11,12]. These children have had resolution of OSA after supraglottoplasty [5,7,13]. Sleep endoscopy for pediatric OSA, unexplained by tonsil or adenoid hypertrophy, has recently gained popularity and has led to the diagnosis of occult laryngomalacia as an etiology of OSA. Occult laryngomalacia has been described to have a later onset (>2 years old) and present with stridor and upper airway obstruction exclusively during sleep or exercise. Although the
laryngeal characteristics of occult laryngomalacia may be similar to those of its classic form, typical symptoms such as inspiratory stridor are usually absent while awake, which renders recognition of laryngomalacia difficult. Thevasagayam et al. [1] were the first to report a 3.9% prevalence of occult laryngomalacia in children over 2 years of age presenting with OSA. Our case is the first to report occult laryngomalacia resulting in severe OSA in an infant. Previously, Amin and Isaacson [6] described an inward prolapse of the arytenoids during anesthesia in 5 infants who presented with inspiratory stridor while asleep, but were found to have a normal appearing larynx when examined awake. The mean age in their patient group was 6 months. However, none of these patients were diagnosed with OSA or required surgical intervention. Smith et al. [14] reported state-dependent laryngomalacia in 5 patients between the ages of 3 and 4 years old, who were asymptomatic while awake, but experienced stridor and airway collapse during sleep. This symptomatic pattern was thought to be secondary to decreased neuromuscular tone during sleep. OSA was not demonstrated in their patient group and all patients underwent supraglottoplasty with complete resolution of symptoms. Richter et al. [3] described a late-onset laryngomalacia in 17 patients older than 2 years of age. He further divided his patients in groups having feeding-disordered, sleep-disordered and exercise-induced laryngomalacia. The sleep-disordered laryngomalacia group consisted of 7 patients with a mean age of 6.3 years old. The mean AHI in this group was 6, the mean SaO2 nadir was 86%. All 7 patients underwent supraglottoplasty and remained free of symptoms postoperatively, but postoperative polysomnography was not performed. Chan et al. [5] studied a group of 22 children with polysomnography – proven OSA, identified by sleep endoscopy to have occult laryngomalacia, and demonstrated a significant reduction in AHI after supraglottoplasty. All patients were over 2 years of age, with a mean age of 7.4 years. Our case highlights the importance of polysomnography in children younger than 12 months of age, who have normal awake upper airway exam combined with a strong clinical history of OSA. If polysomnography is positive for OSA, or if clinical suspicion for OSA and/or occult laryngomalacia is high, a sleep endoscopy in conjunction with microdirect laryngoscopy and bronchoscopy should be performed. In conclusion, occult or state-dependent laryngomalacia may present with severe OSA in infants younger than 12 months of age. When OSA of unknown etiology is suspected in infants, we recommend the use of polysomnography. If OSA is present, sleep endoscopy in conjunction with microdirect laryngoscopy and bronchoscopy should be performed. Occult or state-dependent laryngomalacia should be considered as part of the differential diagnosis and a supraglottoplasty may be considered.
References [1] M. Thevasagayam, K. Rodger, D. Cave, M. Witmans, H. El-Hakim, Prevalence of laryngomalacia in children presenting with sleep-disordered breathing, Laryngoscope 120 (2010) 1662–1666. [2] L.D. Holinger, Etiology of stridor in neonate, infant and child, Ann. Otol. Rhinol. Laryngol. 89 (1980) 397–400. [3] F. Denoyelle, M. Mondain, N. Gresillon, G. Roger, F. Chaudre, E.N. Garabedian, Failures and complications of supraglottoplasty in children, Arch. Otolaryngol. Head Neck Surg. 129 (2003) 1077–1080. [4] G.T. Richter, M.J. Rutter, A. DeAlarcon, L.J. Orvidas, D.M. Thompson, Late-onset laryngomalacia: a variant of disease, Arch. Otolaryngol. Head Neck Surg. 134 (2008) 75–80. [5] D.K. Chan, M.T. Truong, P.J. Koltai, Supraglottoplasty for occult laryngomalacia to improve obstructive sleep apnea syndrome, Arch. Otolaryngol. Head Neck Surg. 138 (2012) 50–54. [6] M.R. Amin, G. Isaacson, State-dependent laryngomalacia, Ann. Otol. Rhinol. Laryngol. 106 (1997) 314–320.
K.P.Q. Oomen, V.K. Modi / International Journal of Pediatric Otorhinolaryngology 77 (2013) 1617–1619 [7] S.M. Revell, W.D. Clark, Late-onset laryngomalacia: a cause of pediatric obstructive sleep apnea, Int. J. Pediatr. Otorhinolaryngol. 75 (2011) 231–238. [8] P.J. Koltai, S.R. Hoff, The ‘‘postcricoid cushion’’: observations on the vascular anatomy of the posterior cricoid region, Arch. Otolaryngol. Head Neck Surg. 138 (2012) 562–571. [9] T.F. Hoban, R.D. Chervin, Sleep-related breathing disorders of childhood: description and clinical picture, diagnosis, and treatment approaches, Sleep Med. Clin. 2 (2007) 445–462. [10] L.D. Holinger, Congenital laryngeal anomalies, in: L.D. Holinger, R.P. Lusk, C.G. Green (Eds.), Pediatric Laryngology and Bronchoesophagology, Lippincott-Raven, Philadelphia/New York, 1997, pp. 139–142.
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[11] G.P. Digoy, M. Shukry, J.A. Stoner, Sleep apnea in children with laryngomalacia: diagnosis via sedated endoscopy and objective outcomes after supraglottoplasty, Otolaryngol. Head Neck Surg. 147 (2012) 544–550. [12] S. Goldberg, A. Shatz, E. Picard, I. Wexler, S. Schwartz, E. Swed, et al., Endoscopic findings in children with obstructive sleep apnea: effects of age and hypotonia, Pediatr. Pulmonol. 40 (2005) 205–210. [13] R. Powitzky, J. Stoner, T. Fisher, P. Digoy, Changes in sleep apnea after supraglottoplasty in infants with larygomalacia, Int. J. Pediatr. Otolaryngol. 75 (2011) 1234–2139. [14] J.L. Smith II., D.M. Seeney, B. Smallman, A. Mortelliti, State-dependent laryngomalacia in sleeping children, Ann. Otol. Rhinol. Laryngol. 114 (2005) 111–114.
Contents lists available at SciVerse ScienceDirect
International Journal of Pediatric Otorhinolaryngology journal homepage: www.elsevier.com/locate/ijporl
Case report
Occult laryngomalacia resulting in obstructive sleep apnea in an infant Karin P.Q. Oomen, Vikash K. Modi * Department of Otolaryngology-Head & Neck Surgery, Pediatric Otolaryngology-Head & Neck Surgery, Weill Cornell Medical College, 428 East 72nd Street, Suite 100, New York, NY 10021, USA
A R T I C L E I N F O
A B S T R A C T
Article history: Received 12 April 2013 Received in revised form 2 July 2013 Accepted 3 July 2013 Available online 1 August 2013
Classic laryngomalacia presents in the awake infant with progressive stridor when agitated. Occult laryngomalacia usually presents with stridor in children older than 2 years and is limited to sleep or exercise. There have been no documented cases of occult laryngomalacia causing obstructive sleep apnea in infants. We report the youngest documented case of an infant with state-dependent laryngomalacia resulting in severe obstructive sleep apnea. This patient was successfully treated with supraglottoplasty, with resolution of symptoms. In conclusion, state-dependent laryngomalacia resulting in obstructive sleep apnea may present in children younger than 12 months of age. In these individuals, supraglottoplasty should be considered. ß 2013 Elsevier Ireland Ltd. All rights reserved.
Keywords: Laryngomalacia Occult laryngomalacia Obstructive sleep apnea Supraglottoplasty Sleep endoscopy
1. Introduction Obstructive sleep apnea (OSA) is a syndrome of partial or complete upper airway obstruction during sleep. Pediatric OSA is most commonly attributed to adenotonsillar hypertrophy, and adenotonsillectomy remains the mainstay of surgical treatment. A small proportion of pediatric OSA has been attributed to laryngomalacia [1]. Laryngomalacia is a disease entity characterized by collapse of supraglottic structures during inspiration, resulting in intermittent upper airway obstruction [2]. Its classic clinical picture is one of inspiratory stridor presenting within the first 2 weeks of life, increasing with agitation or with feeding. Upper airway obstruction can progress during the first 6 months, after which symptoms gradually resolve spontaneously. Approximately 5–10% of patients suffer from a severe form of classic laryngomalacia, requiring surgical intervention [3]. Occult laryngomalacia is an atypical form of laryngomalacia, characterized by stridor and symptoms of upper airway obstruction limited to exercise or sleep [4,5]. Laryngomalacia that is exclusively present during sleep has also been termed statedependent laryngomalacia, due to its variation of symptoms with level of consciousness [6]. Previous studies have described occult laryngomalacia as a cause of OSA, but only in children older than 2 years of age [1,4,5,7]. In this older age group, supraglottoplasty has been shown to be curative [5,7].
* Corresponding author. Tel.: +1 646 962 3017; fax: +1 212 746 8124. E-mail address: [email protected] (V.K. Modi). 0165-5876/$ – see front matter ß 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijporl.2013.07.006
We report the youngest documented case of pediatric OSA secondary to state-dependent laryngomalacia. 2. Case report A 5 month old male with a history of a high-pitched inspiratory sound during sleep for 2 months, was referred to Weill Cornell Medical College, Division of Pediatric Otolaryngology-Head & Neck Surgery. The patient was born full term at 38 weeks via a normal spontaneous vaginal delivery. He did not have a history of intubation or airway intervention. No stridor or other respiratory issues were reported when the infant was awake. The infant was feeding well and gaining weight appropriately. There were no dysmorphic features or developmental/neurologic issues. An inoffice awake exam, which included flexible fiberoptic laryngoscopy, revealed a small posterior cricoid cushion [8] but was otherwise normal. Polysomnography demonstrated an apnea-hypopnea index (AHI) of 10.2 and an arterial oxygen saturation (SaO2) nadir of 88%, consistent with severe OSA [9]. Normal end tidal carbon dioxide (ETCO2) measurements of 30.7 Torr at baseline and 45 Torr at maximum were present. A sleep endoscopy followed by a direct laryngoscopy and bronchoscopy were recommended to assess the level of airway obstruction during sleep and to rule out the presence of any airway lesions. For the sleep endoscopy, the infant was induced with inhalational anesthesia and propofol in the supine position, without the use of a shoulder roll. Appropriate time was allowed for the inhalational gasses to wear off, in order to ensure that the only mode of sedation was intravenous propofol. Upon initiation of
1618
K.P.Q. Oomen, V.K. Modi / International Journal of Pediatric Otorhinolaryngology 77 (2013) 1617–1619
Fig. 1. Inward prolapse of the arytenoids during inspiration on sleep endoscopy (type I laryngomalacia).
sleep, inspiratory stridor developed, and the patient’s father was brought into the room to confirm this was the sound observed during sleep at home. A pediatric flexible fiberoptic laryngoscope was then introduced in the nasal cavity and advanced to assess the upper airway. The adenoid was normal in size, tonsillar size was 1+ (occupying less than 25% of the oropharynx), the soft palate was normal, and there was no lingual tonsil hypertrophy or base of tongue collapse. The arytenoids bilaterally were found to prolapse into the airway during inspiration (type I laryngomalacia) [10], reflecting a clinical picture consistent with state-dependent laryngomalacia (Fig. 1). Subsequently, a rigid microdirect laryngoscopy and bronchoscopy revealed no laryngeal cleft or other airway anomalies. Postoperatively, the parents were informed about the finding of state-dependent laryngomalacia. Medical management was implemented with reflux precautions and a twice daily proton pump inhibitor. No change was noted in the patient’s symptoms after 2 weeks, and supraglottoplasty was recommended. A supraglottoplasty was performed using microscissors to incise both aryepiglottic folds, and to excise redundant mucosa over the cuneiform cartilages. Hemostasis was achieved with oxymetazoline hydrochloride 0.05% soaked pledgelets. The patient had an uneventful overnight stay in the pediatric intensive care unit, and was discharged the next day tolerating an ageappropriate diet. There were no complications and the postoperative course was uneventful. A 4 week postoperative polysomnogram demonstrated an AHI of 2.4 and an SaO2 nadir of 89%, with normal ETCO2s of 28 Torr at baseline and 41 Torr at maximum. Only central apneas were present, no obstructive apneas or hypopneas were recorded. The parents have reported complete resolution of symptoms at consecutive postoperative visits. 3. Discussion Previous reports have described classic laryngomalacia resulting in OSA in infants and young children [11,12]. These children have had resolution of OSA after supraglottoplasty [5,7,13]. Sleep endoscopy for pediatric OSA, unexplained by tonsil or adenoid hypertrophy, has recently gained popularity and has led to the diagnosis of occult laryngomalacia as an etiology of OSA. Occult laryngomalacia has been described to have a later onset (>2 years old) and present with stridor and upper airway obstruction exclusively during sleep or exercise. Although the
laryngeal characteristics of occult laryngomalacia may be similar to those of its classic form, typical symptoms such as inspiratory stridor are usually absent while awake, which renders recognition of laryngomalacia difficult. Thevasagayam et al. [1] were the first to report a 3.9% prevalence of occult laryngomalacia in children over 2 years of age presenting with OSA. Our case is the first to report occult laryngomalacia resulting in severe OSA in an infant. Previously, Amin and Isaacson [6] described an inward prolapse of the arytenoids during anesthesia in 5 infants who presented with inspiratory stridor while asleep, but were found to have a normal appearing larynx when examined awake. The mean age in their patient group was 6 months. However, none of these patients were diagnosed with OSA or required surgical intervention. Smith et al. [14] reported state-dependent laryngomalacia in 5 patients between the ages of 3 and 4 years old, who were asymptomatic while awake, but experienced stridor and airway collapse during sleep. This symptomatic pattern was thought to be secondary to decreased neuromuscular tone during sleep. OSA was not demonstrated in their patient group and all patients underwent supraglottoplasty with complete resolution of symptoms. Richter et al. [3] described a late-onset laryngomalacia in 17 patients older than 2 years of age. He further divided his patients in groups having feeding-disordered, sleep-disordered and exercise-induced laryngomalacia. The sleep-disordered laryngomalacia group consisted of 7 patients with a mean age of 6.3 years old. The mean AHI in this group was 6, the mean SaO2 nadir was 86%. All 7 patients underwent supraglottoplasty and remained free of symptoms postoperatively, but postoperative polysomnography was not performed. Chan et al. [5] studied a group of 22 children with polysomnography – proven OSA, identified by sleep endoscopy to have occult laryngomalacia, and demonstrated a significant reduction in AHI after supraglottoplasty. All patients were over 2 years of age, with a mean age of 7.4 years. Our case highlights the importance of polysomnography in children younger than 12 months of age, who have normal awake upper airway exam combined with a strong clinical history of OSA. If polysomnography is positive for OSA, or if clinical suspicion for OSA and/or occult laryngomalacia is high, a sleep endoscopy in conjunction with microdirect laryngoscopy and bronchoscopy should be performed. In conclusion, occult or state-dependent laryngomalacia may present with severe OSA in infants younger than 12 months of age. When OSA of unknown etiology is suspected in infants, we recommend the use of polysomnography. If OSA is present, sleep endoscopy in conjunction with microdirect laryngoscopy and bronchoscopy should be performed. Occult or state-dependent laryngomalacia should be considered as part of the differential diagnosis and a supraglottoplasty may be considered.
References [1] M. Thevasagayam, K. Rodger, D. Cave, M. Witmans, H. El-Hakim, Prevalence of laryngomalacia in children presenting with sleep-disordered breathing, Laryngoscope 120 (2010) 1662–1666. [2] L.D. Holinger, Etiology of stridor in neonate, infant and child, Ann. Otol. Rhinol. Laryngol. 89 (1980) 397–400. [3] F. Denoyelle, M. Mondain, N. Gresillon, G. Roger, F. Chaudre, E.N. Garabedian, Failures and complications of supraglottoplasty in children, Arch. Otolaryngol. Head Neck Surg. 129 (2003) 1077–1080. [4] G.T. Richter, M.J. Rutter, A. DeAlarcon, L.J. Orvidas, D.M. Thompson, Late-onset laryngomalacia: a variant of disease, Arch. Otolaryngol. Head Neck Surg. 134 (2008) 75–80. [5] D.K. Chan, M.T. Truong, P.J. Koltai, Supraglottoplasty for occult laryngomalacia to improve obstructive sleep apnea syndrome, Arch. Otolaryngol. Head Neck Surg. 138 (2012) 50–54. [6] M.R. Amin, G. Isaacson, State-dependent laryngomalacia, Ann. Otol. Rhinol. Laryngol. 106 (1997) 314–320.
K.P.Q. Oomen, V.K. Modi / International Journal of Pediatric Otorhinolaryngology 77 (2013) 1617–1619 [7] S.M. Revell, W.D. Clark, Late-onset laryngomalacia: a cause of pediatric obstructive sleep apnea, Int. J. Pediatr. Otorhinolaryngol. 75 (2011) 231–238. [8] P.J. Koltai, S.R. Hoff, The ‘‘postcricoid cushion’’: observations on the vascular anatomy of the posterior cricoid region, Arch. Otolaryngol. Head Neck Surg. 138 (2012) 562–571. [9] T.F. Hoban, R.D. Chervin, Sleep-related breathing disorders of childhood: description and clinical picture, diagnosis, and treatment approaches, Sleep Med. Clin. 2 (2007) 445–462. [10] L.D. Holinger, Congenital laryngeal anomalies, in: L.D. Holinger, R.P. Lusk, C.G. Green (Eds.), Pediatric Laryngology and Bronchoesophagology, Lippincott-Raven, Philadelphia/New York, 1997, pp. 139–142.
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[11] G.P. Digoy, M. Shukry, J.A. Stoner, Sleep apnea in children with laryngomalacia: diagnosis via sedated endoscopy and objective outcomes after supraglottoplasty, Otolaryngol. Head Neck Surg. 147 (2012) 544–550. [12] S. Goldberg, A. Shatz, E. Picard, I. Wexler, S. Schwartz, E. Swed, et al., Endoscopic findings in children with obstructive sleep apnea: effects of age and hypotonia, Pediatr. Pulmonol. 40 (2005) 205–210. [13] R. Powitzky, J. Stoner, T. Fisher, P. Digoy, Changes in sleep apnea after supraglottoplasty in infants with larygomalacia, Int. J. Pediatr. Otolaryngol. 75 (2011) 1234–2139. [14] J.L. Smith II., D.M. Seeney, B. Smallman, A. Mortelliti, State-dependent laryngomalacia in sleeping children, Ann. Otol. Rhinol. Laryngol. 114 (2005) 111–114.