Laryngomalacia
Lawrence Simon, M.D.
August 18, 2005

We begin today with a three-month-old African-American female infant. She presented to TCH ER with a complaint of stridor. Further history revealed that this stridor began at approximately four weeks of age. It had also been associated with some sternal retractions. She also had some pretty severe gastroesophageal reflux disease and was unfortunately suffering from failure to thrive. In the Emergency Room, physical examination, including flexible fiberoptic laryngoscopy at the bedside, revealed inspiratory stridor and epiglottic prolapse with deep inspiration. There was also redundant arytenoid tissue, but her true vocal folds were normal. Given the severity of the patient's condition, direct laryngoscopy was performed in the operating room , revealing a tethering of the epiglottis, with shortening of the aryepiglottic folds and supraglottic laryngeal collapse with deep inspiration. Laryngoscopy was performed with a blade in the vallecula and with the patient on spontaneous respirations. She was given a diagnosis of laryngomalacia and admitted to the floor. She was initially treated conservatively with reflux precautions and observation, but she unfortunately ended up requiring a supraglottoplasty.

Laryngomalacia was first described in the 1850s by Drs. Rilliet and Barthez. In 1885, Dr. Lees first described the specific anatomic abnormality of inward curling of the epiglottis. Dr. Thomson in 1892 coined the term “congenital laryngeal stridor,” which was a fairly good term at that time. Jackson introduced the contemporary term “laryngomalacia” in 1942, a term that was popularized and solidified in contemporary laryngological nomenclature by Dr. Holinger in 1960.

To understand laryngomalacia, it is important to understand a little more about the mechanics of how we breathe. When we inspire, our diaphragm is depressed, and our thorax expands. This action generates a large degree of negative intrathoracic pressure. This negative intrathoracic pressure is, of course, transmitted to the upper airway including the trachea and larynx and wants to draw the supraglottic tissues inward. Now, this supraglottic collapse is prevented by two things: laryngeal musculature and the Bernoulli principle. The muscles of larynx that help in this situation include the intrinsic muscles of the larynx as well as some muscles of the upper neck, the hyoglossus, digastric, palatopharyngeus, and palatoglossus. These muscles actually respond to pressure sensors in the supraglottic area. When you inspire, they sense the negative pressure and reflexively dilate the supraglottis during inspiration to prevent supraglottic collapse. The second thing that helps is the Bernoulli principle, which is a physics principle describing the dynamics governing a fluid traveling through a pipe such as water through a hose or air through your larynx. There are three important tenets. The first one is that the velocity of the fluid traveling is inversely proportional to the cross sectional area of the tube. This means that a narrow tube produces very high flow velocities, and a large bore tube produces slower fluid velocities. For example, when a gardener places his thumb over the outlet of a hose, the water comes out a lot faster.

The second tenet of the Bernoulli principle is that the velocity and the pressure of the fluid in the pipe are inversely related. In this sense, “pressure” refers not to the pressure going in the forward direction or the water coming out of the hose, but the pressure the water puts against the wall of the hose, or in the case of breathing, the pressure that inspired air places against the walls of the larynx to keep it open and fight against the negative intrathoracic pressure drawing it inward and shut. Finally, the third tenet, which is based on the first two, is that pressure and cross sectional area are directly related. In other words, a more narrow pipe results in less pressure being exerted against the wall of the pipe to keep it open. In the case of laryngomalacia, the laryngeal inlet is narrowed. Therefore, the air traveling through it is traveling at a higher velocity and is exerting less pressure against the supraglottic tissues. It makes easier for them to collapse as a result of the negative intrathoracic pressure.

What this higher velocity also creates is turbulent flow, and this turbulence is what creates the harsh vibratory sound of stridor. There are three kinds of stridors; the first is an inspiratory stridor, which is the result of supraglottic obstruction. The second is biphasic, which results from extrathoracic tracheal obstruction. The final type is expiratory stridor, which is usually seen with intrathoracic tracheal obstruction. The differential diagnosis of stridor can be quite extensive and include infections like epiglottitis and croup, congenital acquired lesions like subglottic stenosis and respiratory papillomatosis, laryngoceles and laryngeal webs, even life threatening vallecular cysts and a small group of other conditions like esophageal reflux, foreign bodies, and turbinate hypertrophy.

Laryngomalacia accounts for 45-75% of all cases in inspiratory stridor in infants, depending on which study you want to cite. It is the result ofcollapse of supraglottic structures during inspiration, and the most important feature of laryngomalacia is that it is normally a very self-limited and benign disease. About 80% of these cases will resolve by 18 months and about 90% by two-years of age. Dr. Friedman did a study when she was in Boston where they investigated 60 patients with laryngeal stridor, 27 of them had laryngomalacia, and 80% of these children were fairly symptom free by 18 months of age. It is important to realize that almost 20% of these are going to have a synchronous lesion of the larynx, and this fact cannot be forgotten. Laryngomalacia can be either congenital or acquired and the most common form is definitely congenital. The classic presentation of laryngomalacia is an infant with an inspiratory stridor or noise that began at 4-6 weeks of age. The parents will usually tell you that they are having a normal cry and that they rarely experience severe upper respiratory distress at baseline. The inspiratory stridor may worsen when the patient is supine, as it is easier for the supraglottic larynx to collapse it this position, and it may worsen with activity. In fact there have actually been a few reports of exercise-induced laryngomalacia, in which patients only complained of symptoms when the child was exercising and under severe exertion. They may also state that the patient has some feeding difficulties if there is concomitant gastroesophageal reflux disease. On physical exam you will find that they do indeed have a normal cry and an inspiratory stridor that worsens when supine or with activity. They may have mild tachypnea, but they should have normal oxygen saturation. This is a problem of ventilation not of oxygenation, with an otherwise a normal physical exam. They should be meeting a normal height and weight requirements in the growth curve. They should have clear lung fields.

Now, you will deal with flexible fiberoptic laryngoscopy in the clinic on these patients probably. On the left of the slide is a normal larynx and on the right is a larynx with laryngomalacia with an omega-shaped epiglottis. It is a classic description that has shortened aryepiglottic folds. They may have enlarged or floppy arytenoid cartilages. They may have redundant arytenoid mucosa and these tissues are going to result in a collapse of this tissue during deep inspiration. When you do flexible laryngoscopy in the children you notice that they do indeed have supraglottic collapse, they do indeed have stridor with deep inspiration. You might also think about doing some other studies based on the patient’s history and if you have suspicion of these conditions, chest x-rays can help with foreign bodies. Lateral neck films can help with epiglottitis, for example if the infant is febrile or toxic. The barium swallow might also be indicated if you have suspicion of gastroesophageal reflux disease.

Once you have made a diagnosis and assessment of laryngomalacia, then the focus becomes managemen. Again, the important thing about the management of laryngomalacia is that about 80% do indeed resolve by 18 months of age. It usually a very benign disease, but you do want to closely monitor upper respiratory tract infections. Again, in Dr. Friedman’s study, they did note that patients with laryngomalacia do not have an increased incidence of upper respiratory tract infections. They do not have more than normal population, but when they do, they tend to have more problems. They have a harder time getting over them because they already have an inherent problem with inspiration. They need close monitoring and care during the upper respiratory infections of childhood. You can counsel parents about prone sitting position or possible supplemental oxygen if that becomes necessary. The child should be placed on maximum reflux precautions. Children with laryngomalacia can commonly have concomitant gastroesophageal reflux disease and they should be treated appropriately. Unfortunately, even with this treatment, about 10-20% of these patients are going to require some sort of surgical intervention.

Direct laryngoscopy for laryngomalacia is still argued about in literaturet. There are some physicians at Children’s Hospital of Cincinnati who advocate doing direct laryngoscopy in all patients with laryngomalacia, and then there are those, such as Dr. Smith and I, who advocate doing it only on patients that meet ceratin criteria. Universally accepted criteria for doing direct laryngoscopy includes patients with complications of laryngomalacia. For example, cor pulmonale, failure to thrive, severe respiratory distress, patients with prolonged symptoms that last longer than you would predict, or patients whose symptoms are more severe than you would expect. They are cyanotic, tachypneic or they are having sternal retractions, or if you think they may have any synchronous lesion of the larynx. Again these occur in an average of 20% of the patients with laryngomalacia. Finally, if you have a high suspicion that the patient is likely to require supraglottoplasty, then doing a direct laryngoscopy to get a better idea of precisely what anomalies exist would be a good idea. Now doing supraglottoplasty, surgical correction of laryngomalacia is going to be indicated only for the most complicated or refractory cases. As I said, complications that you may see include severe respiratory distress, cor pulmonale, failure to thrive, apneic events, and recurrent pneumonia. Apneic events can be quite scary. Actually, in 1991, a study was published describing a series of six patients that had near miss sudden infant death syndrome as a result of laryngomalacia, so apneic events can be quite severe.

Actual surgical treatment of laryngomalacia should be tailored to the specific side of the lesion: redundant or flat arytenoid cartilages need to be trimmed; short aryepiglottic folds need to be ligated; or an overhanging epiglottis that needs to be pexed or resected. Tthere are two different classification scans that helps us understand this. The first was proposed by Dr. Hollinger in 1989, and described six different types. Type I is the inward collapse of the cuneiform cartilages. Type II is inward curling of the epiglottis. Type III is usually seen in conjunction with type II and involves an anterior and medial displacement of the cuneiform cartilages similar to type I. Type IV is prolapse of the epiglottis with inspiration. Type V is the shortened aryepiglottic fold, and type VI is an overly acute angle of the epiglottis at the laryngeal limit. In 1989, an alternate classification system was introduced that reduces those six down to three. These three are: type I, the prolapse of the mucosa overlying the arytenoid cartilages, similar to types I and III proposed by Dr. Hollinger; type II, the shortened aryepiglottic folds; and, type III, the prolapse of the epiglottis. You can use this classification to directly predict the kind of operation needed to correct the anomaly. If the patient has type I, you want to excise the redundant arachnoid mucosa. If they have type II, you are going to want to ligate the aryepiglottic folds. If they have type III, you are going to want a procedure to spin the epiglottis or to resect a part of that.

It is important to remember that surgical treatment needs to be tailored to the specific lesion. The good news about it is you can achieve a greater than 90% success rate for all respiratory symptoms. There have been a number of studies that have investigated the effect of supraglottoplasty on laryngomalacia. The largest one involved over 100 patients, and there was a greater than 90% success rate. Of course, you get a very low complication rate, usually less than 5%. The most common severe complication is supraglottic stenosis. It is also possible to attempt a unilateral procedure first. Uunilateral supraglottoplasty has been found to be effective in about 94% of the cases. Then, if it does not work, proceed to a bilateral supraglottoplasty. The use of instrumentation is surgeon preference. There have been studies indicating that there is no difference in results with the CO2 laser or microdebrider or microlaryngeal instruments, or any combination of the above.

In the last few minutes, I will talk about the pathophysiology of laryngomalacia. The pathophysiology remains controversial in literature and no one really understands exactly where it comes from, but there are three dominant hypotheses. The first involves laryngeal hypertonia and this is proposed by Drs. Thompson and Turner in 1990. The argument was that tone is important in keeping the supraglottic larynx open during inspiration and weakening of this musculature can lead to supraglottic collapse. Proponents of this theory cite two things. One, there is a known association between both congenital and acquired laryngomalacia and other neurological disorders such as cerebral palsy, memory retardation, central apnea, and severe CNS injury. There have even been studies of acquired laryngomalacia that have documented its resolution after recovery of neurological deficits. There is a study of 24 patients in 1984 who showed the association of laryngomalacia with other neuromuscular conditions such as central and obstructive sleep apneas, gastroesophageal reflux disease, and hyperthermia. So there is an association, but there is also another school of thought regarding abnormal laryngeal structure. The proponents argue that the larynx is actually born malformed. Their argument is that the true mechanism is the narrowing of the larynx, altering airflow velocity. Eevidence for this theory cites an association of laryngomalacia with other structural abnormalities and changes in the head and neck, such as in patients who get an acquired laryngomalacia after floor of mouth surgery. There have been a couple of case repots of laryngomalacia associated with adenotonsillar hypertrophy and, of course, with laryngeal trauma. They also argue that mucosal and histological studies of supraglottoplasty specimens demonstrate this edema of the supraglottic tissues but no chondropathy, and otherwise, the cartilage taken out is normal cartilage. It is just wrongly shaped in a patient, but histologically, the cartilage is normal. The final theory is that of gastroesophageal reflux disease. There have been a few studies investigating the histology of specimens from supraglottic tissue. One of them, in 1989, demonstrated that there is an inflammatory infiltrate in the subepithelial tissues from supraglottoplasty specimens. This inflammatory infiltrate is not present in all the specimens, but it is present in fair number of them. Intrinsic inflammatory cell infiltrate and these inflammatory infiltrates are a hallmark of acid damage. They cite this as evidence that esophageal reflux is leading to acidic damage to the supraglottic tissues, damage to the mucosa and resulting in laryngomalacia. Further evidence for the correlation between esophageal reflux disease and laryngomalacia comes from several studies. One of which was done by Dr. Matthews in 1999. He investigated 24 patients that had laryngomalacia and gave them double pH probe studies and versus patients with nonrespiratory complaints. He found that there was a much larger prevalence of reflux in those patients with laryngomalacia than in the patients without laryngomalacia. There is also a study done by Dr. Hadfield in 2003 where she compared three patients with reflux without laryngomalacia and three patients with laryngomalacia and reflux. She found that the reflux improved with supraglottoplasty, which was very interesting. Dr. Giannoni, Dr. Sulek, Dr. Friedman, and Dr. Duncan did a study here in 1998 where they showed that there was a correlation between the severity of a patient’s laryngomalacia and the presence of gastroesophageal reflux disease. On the rightof the chart, in the severe laryngomalacia category, an overwhelming majority of patients had high-grade gastroesophageal reflux disease whereas the patients with mild laryngomalacia had either normal or borderline gastroesophageal reflux disease.

Dr. Giannoni’s study also pointed out a couple of other contributing facts that I want to mention. One is that having a smoker in the household can increase the complications in severity, so when you have patients with laryngomalacia, it is important to counsel the parents about smoking cessation. Their continued smoking can result in worsening of the patient course and, if the patient has other concomitant medical problems (mainly cardiovascular, pulmonary, or neurological medical problems), this can also worsen the course of the laryngomalacia.

The key points of this presentation include: Llaryngomalacia is indeed the most common cause of congenital stridor. Remember that it has a benign course in about 80-98% of cases, which resolve spontaneously by the time that patient is 18-months or two-years-old with no long term sequela and no need for further treatment. The mainstay is going to be observation and parental reassurance. One should maintain a low threshold direct laryngoscopy. Supraglottoplasty and surgical correction can be very effective for complicated cases and have drastically reduced the need for tracheotomy in these patients. Lastly, you should treat the esophageal reflux disease, treat their upper respiratory infections aggressively, and treat any associated illnesses, such as heart or lung disease or neurological disease, aggressively as well in order to maximize the good outcomes in these patients.

Case Presentation:

The patient is a two-month-old African-American female born a full term. She presented to the Texas Children’s Hospital Emergency Room with an upper respiratory tract infection. She was noted to have significant inspiratory stridor with a small expiratory phase, and mom reported a history of “noisy breathing” since near birth.

Further history found that the patient also suffered from severe reflux symptoms, including frequent regurgitation and difficulty tolerating any oral feedings. The combination of respiratory difficulty and poor oral intake has resulted in failure to thrive.

Physical examination revealed a child in mild respiratory distress with fever to 101 degrees F. She was noted to have biphasic stridor, with the inspiratory phase being much worse that the expiratory phase, and sternal retractions. Flexible fiberoptic laryngoscopy revealed tethering of the epiglottis consistent with laryngomalacia.

Given the severity of her condition, the patient was admitted to the hospital and taken to the OR for DL&B with a shortened, tethered epiglottis, and redundant aryepiglottic mucosa. She was given maximum medical therapy for her gastroesophageal reflux, but did not respond to this treatment. At three months of age, she was taken back to the operating room where the otolaryngology service performed a cold supraglottoplasty, and the pediatric surgery service performed a fundoplication and gastrostomy tube placement.

The patient responded well to these treatments. Her respiratory distress has improved, and she is gaining weight.

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