Mark Zafereo, M.D.
May 22, 2008
Disclaimer: The information contained within the Grand Rounds Archive is intended for use by physicians and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No warranties, either express or implied, are made with respect to accuracy, completeness or timeliness of this material. This material does not necessarily reflect the current or past opinions of the faculty of Baylor College of Medicine and should not be used as a basis for diagnosis or treatment, and is not a substitute for professional consultation and/or peer-reviewed medical literature.
KC is a 7-week-old boy with a history of “noisy breathing” with inspiration since 2 weeks of age. He was the product of a full-term, uncomplicated vaginal delivery without any respiratory distress at birth. His mother has taken him to the emergency room several times over the last six weeks for this noisy breathing, which she feels is worsening. The mother notes that the breathing is worse with feeding and when the baby is in the supine position. She reports no cyanosis, but has observed chest retractions associated with the noisy breathing. The child is finishing all of his feeds, and is gaining weight appropriately, and does not spit up with feeds. However the mother remains extremely anxious about her child’s breathing, noting that this anxiety often keep her awake at night.
On physical exam, KC appears healthy and well nourished. Intermittent inspiratory stridor and mild retractions are observed with the child in the supine position. Oxygen saturation is in the high 90’s on room air, and there is no appearance of distress. The nasal, oral cavity, oropharyngeal, and neck examination are normal.
Flexible fiberoptic laryngoscopy is performed. The omega shaped epiglottis is immediately apparent. This video is slowed down to 40% speed to allow better appreciation of the anatomy and the airway dynamics. On expiration, the glottis can be completely visualized; however on inspiration, the glottis cannot be visualized due to the supraglottic collapse, predominately posterolaterally. The short aryepiglottic folds tether the larynx in an anterior/posterior dimension, and redundant, floppy arytenoid tissue prolapses anteroinferiorly and obstructs the airway. The true vocal folds are mobile and symmetric.
Although this child was feeding and gaining weight appropriately, and having no acute distress, dyspnea, or desaturations, the mother raised the question of apneic spells at night. Therefore, a sleep study was obtained. Total sleep time was 8.2 hours with 40% REM, so there was adequate REM and non-REM sleep for a valid study. There were 20 obstructive apneic and hypopneic events per hour of sleep. These were associated with mild oxygen desaturations to a nadir of 86%. End tidal pCO2 values were mildly elevated with a maximum value of 50mmHg. This data is consistent with a moderate obstructive sleep apnea. The patient was also monitored during breast feeding, and mild hypoxemia was recorded with an oxygen saturation nadir of 85%.
Based on the history, physical examination, and results of the sleep study, microsuspension direct laryngoscopy and bronchoscopy with supraglottoplasty was scheduled, and we’ll follow up on this case later in the presentation.
Today I would like to discuss the historical perspective of laryngomalacia, the anatomic mechanism of obstruction, some associated pathology, management, and finally, briefly, a study I conducted retrospectively of patients at Memorial Hermann here in Houston, which is currently in press for Laryngoscope.
Before focusing specifically on laryngomalacia, it is important to recognize that there is a large differential for noisy breathing in infants to include nose and nasopharyngeal anomalies, oropharynx or hypopharynx, supraglottic, glottic, and subglottic larynx, and tracheobronchial abnormalities.
Laryngomalacia is the most common congenital laryngeal anomaly, accounting for about 60% of cases, and the most common cause of congenital stridor. It’s an inspiratory stridor, usually beginning several weeks after birth, and the history, type of stridor, whether inspiratory, expiratory, or biphasic, as well as findings on flexible fiberoptic laryngoscopy, allow the proper diagnosis.
Vocal cord paralysis is the second most common congenital laryngeal anomaly, and while unilateral paralysis may result in mild stridor and even go unnoticed, bilateral vocal fold paralysis causes a high-pitched inspiratory stridor. Congenital subglottic stenosis is the third most common laryngeal anomaly, and will result in a biphasic stridor. Subglottic hemangiomas are usually asymptomatic at birth but become symptomatic with biphasic stridor between 3 and 6 months. Laryngeal webs and atresias can occasionally present with stridor, especially if it is a posterior interarytenoid web. And congenital saccular cysts and laryngeal clefts also can occasionally cause stridor.
Congenital stridor was reported as early as 1853 by two French physicians, Rilliet and Barthez, when they described a newborn with inspiratory stridor. Then in 1897, Sutherland and Lack described a series of 18 patients with “congenital laryngeal obstruction” in Lancet. They regarded the prognosis as good but highlighted that severe cases or upper respiratory tract infections in these patients could be dangerous and may warrant a tracheostomy. But it wasn’t until 1942 that the term laryngomalacia, derived from the Greek word “malakia,” which means morbid softening of an organ, was introduced by Chevalier Jackson.
The stridor occurs because of supraglottic collapse and narrowing on inspiration, which in turn creates high velocity, turbulent airflow that results in the characteristic high-pitched sound. In 1977, McSwiney and others studied 21 infants in London and described three classic laryngeal abnormalities associated with this disorder, but these do not all occur or occur to the same degree in every case.
This video is another dynamic view of a different infant with laryngomalacia. In this case, the epiglottis curls about its vertical axis, causing some obstruction anteriorly. The short aryepiglottic folds tether the larynx in the anterior/posterior dimension, contributing to the aforementioned anterior obstruction, as well as posterior obstruction with redundant arytenoid tissue. This picture represents an example of predominately anterior laryngomalacia, with the omega-shaped epiglottis curling about its vertical axis and obstructing the glottis anteriorly. This picture reveals a more posterolateral laryngomalacia demonstrating anteroinferior collapse of arytenoid mucosa and cuneiform cartilages on inspiration, and the short aryepiglottic folds that tether the supraglottic larynx in close anterior and posterior approximation, predisposing to inferomedial collapse of the supraglottic larynx.
Illustrated here is a predominately posterior laryngomalacia, with most of the obstruction caused by anteroinferior collapse of the arytenoid mucosa and cuneiforms. This is commonly associated with GERD, and it’s important to consider a barium swallow for assessment of gastroesophageal reflux with this type of laryngomalacia.
Up to 80% of patients with laryngomalacia have associated gastroesophageal reflux. This brings up an important study performed by Drs. Giannoni, Sulek, Friedman, and Duncan here at Texas Children’s Hospital. This was a prospective evaluation of 27 infants with laryngomalacia. Each patient had an initial history and physical examination, a barium swallow or pH probe, and then the course of their laryngomalacia was followed. For the barium swallow, borderline GERD was 3 or fewer episodes, all below the thoracic inlet, and high-grade GERD was greater than 3 episodes of reflux at or above the thoracic inlet. Severe laryngomalacia was defined as those patients with 2 or more emergency room visits or hospitalizations due to severe airway symptoms, failure to thrive, or those requiring surgical intervention for severe respiratory symptoms. Gastroesophageal reflux was observed in 64% of patients overall, and was significantly associated with severe symptoms and a complicated clinical course. From the graph here, 60% of mild laryngomalacia patients had no gastroesophageal reflux, while 65% of severe laryngomalacia patients had high-grade reflux. So, whether reflux represents a cause or an exacerbating factor in this disease, it is important to diagnose and treat associated reflux, as it is common and portends a more severe clinical course.
While 85%-90% of laryngomalacia is mild and resolves by two years of age without sequelae, 10%-15% of patients will have a more severe clinical course that can be complicated by life-threatening dyspnea, failure to thrive, obstructive sleep apnea, cor pulmonale, and sudden infant death syndrome. Various authors have characterized severe laryngomalacia and the need for surgical intervention. One that is frequently cited in the literature is a study of 115 patients by Roger and others at Trousseau Children’s Hospital in Paris. Their criteria for severe laryngomalacia and surgery included at least 3 of the listed criteria here, and they advocated close follow-up and treatment of gastroesophageal reflux if only one or two of these criteria were present.
For the 10%-15% of patients with a more severe clinical course, surgical management may be necessary. Tracheostomy was the standard of care for severe laryngomalacia for nearly a century, although as early as 1898, Variot suggested excision of the aryepiglottic folds for relief of obstruction , but he never actually performed the surgery. In 1922, Iglauer reported a case in Laryngoscope in which he successfully treated a severe case of laryngomalacia with suspension laryngoscopy without anesthesia using a nasal snare to resect a portion of the epiglottis. And in 1928, Hasslinger achieved excellent results in three endoscopic resections of the aryepiglottic folds. Then in the mid-80’s, there was renewed interest in endoscopic surgical management that led to the current standard of care for severe disease, which is the supraglottoplasty, initially performed with the microscissors and now, with some who prefer, the carbon dioxide laser or microdebrider.
Supraglottoplasty involves trimming redundant mucosa from the supraglottis, and has been variously termed supraglottoplasty, aryepiglottoplasty, and epiglottoplasty depending on the specific site of surgical excision. There are proponents for simple endoscopic division of the aryepiglottic folds. Loke and others described 32 patients with this method with a 90% success rate and no complications. Others advocate unilateral division of the aryepiglottic fold and unilateral resection of redundant tissue. Kelly and Gray described 18 patients with a 94% success rate and no complications. And, the most aggressive, bilateral division of the aryepiglottic folds and bilateral resection of redundant tissue, Denoyelle and others described 136 patients with this approach with a 91% success rate, but a 7% complication rate including 5 patients who developed some supraglottic stenosis. And, while supraglottoplasty is the current standard of care for severe disease, there are refractory cases where tracheostomy is still performed.
A common technique using the carbon dioxide laser is illustrated here, dividing the left aryepiglottic fold, excising redundant arytenoid mucosa, and then proceeding to do the same on the opposite side, avoiding cauterization of the interarytenoid tissue, which could lead to web formation.
So, back to our case presentation. This is a view upon microsuspension before supraglottoplasty. It is important to note that since laryngomalacia is a dynamic process, it is often difficult to appreciate when the larynx is suspended. But on a lateral view, the short aryepiglottic fold and redundant arytenoid mucosa can be better appreciated, even with suspension.
A bronchoscopy was performed prior to supraglottoplasty, which was normal in this case, but there is about a 20% incidence of synchronous airway lesions in patients with laryngomalacia, although Mancuso and others demonstrated in a study of 90 patients in 1996, that generally less than 5% of these are of any clinical significance. So, unless there is high clinical suspicion, a bronchoscopy is generally not indicated unless the patient is undergoing a supraglottoplasty for severe laryngomalacia.
This patient underwent a supraglottoplasty that was performed with the microdebrider, dividing the short aryepiglottic folds and unilaterally resecting redundant arytenoid mucosa on the right side, carefully preserving the interarytenoid region to prevent web formation. The patient recovered well from surgery, and is now several weeks postoperation with improved breathing, and both the mother and baby are sleeping much better.
So, while our patient today didn’t initially present with any criteria for severe laryngomalacia, the history, stridor, and retractions raised enough concern to order a polysomnogram, and prompted surgical management. In the last few minutes, I would like to present some data on patients with laryngomalacia and obstructive sleep apnea, which has been accepted for publication in Laryngoscope.
Despite obstructive sleep apnea being an indication for a supraglottoplasty in infants with laryngomalacia, there are no recommendations in the literature regarding the role of polysomnography in infants with laryngomalacia. There are children who do not have any of the severe sequelae of laryngomalacia, including either no history of sleep disordered breathing or a questionable history, as with our case presentation today, who may have obstructive sleep apnea. Obstructive sleep apnea has been associated with infant morbidity in terms of growth and developmental delay; and mortality in that there is evidence that it may play a role in sudden infant death syndrome. So, perhaps these patients with a moderate degree of laryngomalacia would benefit from a supraglottoplasty.
With that in mind, the objective of this study is to determine if supraglottoplasty is effective in ameliorating abnormal respiratory parameters in children with moderate laryngomalacia and obstructive sleep apnea. This is a retrospective review of 10 patients with laryngomalacia and obstructive sleep apnea as documented by polysomnography who underwent supraglottoplasty between 2005 and 2007. Inclusion criteria for the study included a diagnosis of moderate laryngomalacia, which was diagnosed by the degree of stridor, associated costal and sternal retractions, and findings on flexible endoscopy in the absence of failure to thrive, cyanotic spells, and signs of severe airway obstruction. All patients had preoperative polysomnographic confirmation of OSA and surgical intervention with supraglottoplasty, and a postoperative polysomnogram was generally scheduled at the first follow-up visit 4 weeks after the procedure. Mean age at presentation was 4 months with a range of 1-9 months. There were 6 males and 4 females. Comorbidities included 8 patients with gastroesophageal reflux, which is known to be significantly associated with laryngomalacia, as well as 2 patients with unilateral vocal fold paralysis, and one patient with mild subglottic stenosis.
Mean time between the preoperative polysomnogram and supraglottoplasty was 4 weeks with a range of 0-10 weeks, and mean time between supraglottoplasty and postoperative polysomnography was 11 weeks with a range of 2-29 weeks. So there was a mean 15-week period between the preoperative sleep study and the postoperative sleep study.
Surgical procedure consisted of a telescopic laryngoscopy, bronchoscopy, and microlaryngoscopy with division of the aryepiglottic folds either alone in four patients, or in combination with unilateral excision of redundant arytenoid mucosa in 6 patients. All ten patients were successfully extubated following supraglottoplasty, there were no peri- or postoperative complications including no subsequent airway procedures and no positive pressure ventilation required following surgery.
At four weeks after surgery, 1 caregiver reported only mild improvement in the stridor, 7 reported significant improvement, and 2 reported complete resolution of the stridor. Thus, 90% of patients had subjective significant improvement of symptoms according to the caregiver.
Listed here are the pre- and postoperative means for the obstructive apnea index, which is obstructive apneas per hour of sleep; the obstructive apnea/hypopnea index, which includes both obstructive and hypopneic events per hour of sleep; the respiratory disturbance index, which includes both obstructive and central events, and the low arterial oxygen saturation during the course of the study.
According to a classification system for obstructive sleep apnea in children proposed by Dr. Katz and others at John Hopkins in 2002, 9 of 10 of these children would be preoperatively classified as either moderate or severe obstructive sleep apnea based on their obstructive apnea index and low oxygen saturations.
The differences between the pre- and postoperative data were statistically significant for all the indices, as well as the low oxygen saturation. There was a 72% decrease in the obstructive apnea index, a 66% decrease in the obstructive apnea, and a 53% decrease in the respiratory disturbance index following supraglottoplasty.
So, despite several limitations of the study including a retrospective design, small sample size, and absence of a control group, we feel that several conclusions can be drawn from this data. Although better studied in adults, there is increasing concern that pediatric OSA may be linked to cardiovascular health, as well as metabolic, behavioral, growth, and learning impairment. While infants with laryngomalacia have varying degrees of obstruction, some of which may require active intervention, there are currently no definitive recommendations regarding the role of polysomnographies in children with laryngomalacia. If a child is having cyanotic spells or significant feeding difficulties causing failure to thrive, this represents severe laryngomalacia, and a supraglottoplasty should be performed without waiting for a sleep study. Similarly, if the mother is a good historian, and this is her third child, and she tells you that the child is having significant noisy breathing and breath-holding spells at night, you may not want to wait several weeks for a sleep study. But there are many infants with laryngomalacia with signs and symptoms of sleep disordered breathing, stridor, and retractions without significant desaturations or overt failure to thrive. The polysomnogram is just another tool to help in the decision-making process in borderline cases, and it certainly does not replace clinical judgment. So, based on the results of this study, we recommended that polysomnography be considered in the diagnostic workup of cases of moderate laryngomalacia, and if there is evidence of obstructive sleep apnea, a supraglottoplasty should be considered. If the infant then has significant improvement or no stridor a month after surgery, no further studies are indicated. If the symptoms persist, a subsequent polysomnogram and close follow-up would be warranted.
KC is a 7-week-old boy with a history of “noisy breathing” with inspiration since 2 weeks of age. He was the product of a full-term, uncomplicated vaginal delivery without any respiratory distress at birth. His mother has taken him to the emergency room several times over the last six weeks for this noisy breathing, which she feels is worsening. The mother notes that the breathing is worse with feeding and when the baby is in the supine position. She reports no cyanosis, but has observed chest retractions associated with the noisy breathing. The child is finishing all of his feeds, and is gaining weight appropriately, but the mother remains extremely anxious about her child’s breathing, noting that this anxiety often keep her awake at night.
On physical exam, KC appears healthy and well nourished. Intermittent inspiratory stridor and mild retractions are observed with the child in the supine position. Oxygen saturation is in the high 90’s on room air, and there is no appearance of distress. The nasal, oral cavity, oropharyngeal, and neck examination are normal. A flexible fiberoptic laryngoscopy reveals short aryepiglottic folds and anterior collapse of the arytenoid mucosa. The vocal folds could be visualized well on expiration, and were mobile bilaterally, but could not be well visualized on inspiration.
A sleep study revealed 20 obstructive apneic and hypopneic events per hour of sleep, and an oxygen saturation nadir of 86%. End tidal pCO2 values were mildly elevated with a maximum value of 50mmHg. During breast feeding, oxygen saturation nadir was 85%.
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