Inability to Burp or Belch

Inability to burp or belch occurs when the upper esophageal sphincter (cricopharyngeus muscle) cannot relax in order to release the “bubble” of air. The sphincter is a muscular valve that encircles the upper end of the esophagus just below the lower end of the throat passage. If looking from the front at a person’s neck, it is just below the “Adam’s / Eve’s apple,” directly behind the cricoid cartilage.

If you care to see this on a model, look at the photos below. That sphincter muscle relaxes for about a second every time we swallow saliva, food, or drink. All of the rest of the time it is contracted. Whenever a person belches, the same sphincter needs to let go for a split second in order for the excess air to escape upwards. In other words, just as it is necessary that the sphincter “let go” to admit food and drink downwards in the normal act swallowing, it is also necessary that the sphincter be able to “let go” to release air upwards for belching. The formal name for this disorder is retrograde cricopharyngeus dysfunction (R-CPD).

People who cannot release air upwards are miserable. They can feel the “bubble” sitting at the mid to low neck with nowhere to go. Or they experience gurgling when air comes up the esophagus only to find that the way of escape is blocked by a non-relaxing sphincter. It is as though the muscle of the esophagus continually churns and squeezes without success.

The person so wants and needs to burp, but continues to experience this inability to burp. Sometimes this can even be painful. Such people often experience chest pressure or abdominal bloating, and even abdominal distention. Flatulence is also severe in most persons with R-CPD. Other less universal symptoms are nausea after eating, painful hiccups, hypersalivation, or a feeling of difficulty breathing with exertion when “full of air.” Many persons with R-CPD have undergone extensive testing and treatment trials without benefit. R-CPD reduces quality of life, and is often socially disruptive and anxiety-provoking. Common (incorrect) diagnoses are “acid reflux” and “irritable bowel syndrome,” and therefore treatments for these conditions do not relieve symptoms significantly.

Approaches for treating the inability to burp:

For people who match the syndrome of:
1) Inability to belch
2) Gurgling noises
3) Chest/abdominal pressure and bloating
4) Flatulence

Here is the most efficient way forward: First, a consultation to determine whether or not the criteria for diagnosing R-CPD are met. Next, a simple office-based videoendoscopic swallow study which incorporates a neurological examination of tongue, pharynx (throat) and larynx muscles and often includes a mini-esophagoscopy. This establishes that the sphincter works normally in a forward (antegrade) swallowing direction, but not in a reverse (retrograde) burping or regurgitating fashion. Along with the symptoms described above, this straightforward office consultation and swallowing evaluation establishes the diagnosis of retrograde cricopharyngeus dysfunction (non-relaxation).

The second step is to place Botox into the malfunctioning sphincter muscle. The desired effect of Botox in muscle is to weaken it for at least several months. The person thus has many weeks to verify that the problem is solved or at least minimized.

The Botox injection could potentially be done in an office setting, but we recommend the first time (at least) placing it during a very brief general anesthetic in an outpatient operating room. That’s because the first time, it is important to answer the question definitively, that is, that the sphincter’s inability to relax when presented with a bubble of air from below, is the problem. Furthermore, based upon an experience with more than 190 patients as of August 2019, a single injection appears to “train” the patient how to burp. Approximately 80% of patients have maintained the ability to burp long after the effect of the Botox has dissipated. That is, long past 6 months from the time of injection.

Patients treated for R-CPD as just described should experience dramatic relief of their symptoms. And to repeat, our experience in treating more than 190 patients (and counting) suggests that this single Botox injection allows the system to “reset” and the person may never lose his or her ability to burp. Of course, if the problem returns, the individual could elect to pursue additional Botox treatments, or might even elect to undergo endoscopic laser cricopharyngeus myotomy. To learn more about this condition, see Dr. Bastian’s description of his experience with the first 51 of his much larger caseload.

Check out our list of resources containing peer-reviewed articles, patient stories and more!

Photos of the cricopharyngeus muscle:

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Location of the cricopharyngeus muscle

Cricopharyngeus Muscle (1 of 3)

The highlighted oval represents the location of the cricopharyngeus muscle.
Retrograde Cricopharyngeus Dysfunction (R-CPD)

Cricopharyngeus Muscle (2 of 3)

The cricopharyngeus muscles in the open position.
Contracted Cricopharyngeus Muscle

Contracted Cricopharyngeus Muscle (3 of 3)

The cricopharyngeus muscle in the contracted position.

Esophageal Findings: Series of 3 photos

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A view of the mid-esophagus

Esophageal Findings (1 of 3)

A view of the mid-esophagus in a young person (early 30’s). The esophagus is kept open by the patient’s un-burped air. Note the “aortic shelf” at A, delineated by dotted lines.
A bony spur in the spine

Esophageal Findings (2 of 3)

A moment later, additional air is pushed upwards from the stomach to dilate the mid-esophagus even more. A bony “spur” in the spine is thrown into high relief by the stretched esophagus.
dilation of the upper esophagus

Esophageal Findings (3 of 3)

A view of the upper esophagus (from just below the cricopharyngeus muscle sphincter) shows what appears to be remarkable lateral dilation (arrows) caused over time by the patient’s unburpable air. Dilation can only occur laterally due to confinement of the esophagus by trachea (anteriorly) and spine (posteriorly), as marked.

Abdominal Distention of R-CPD: Series of 3 photos

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x-ray of Gastric Air Bubble

Gastric Air Bubble (1 of 3)

This abdominal xray of an individual with R-CPD shows a remarkably large gastric air bubble (dotted line), and also excessive air in transverse (T) and descending (D) colon. All of this extra air can cause abdominal distention that increases as the day progresses.

Bloated Abdomen (2 of 3)

Flatulence in the evening and even into the night returns the abdomen to normal, but the cycle repeats the next day. To ask patients their degree of abdominal distention, we use pregnancy as an analogy in both men and women. Not everyone describes this problem. Most, however, say that late in the day they appear to be “at least 3 months pregnant.” Some say “6 months” or even “full term.” In a different patient with untreated R-CPD, here is what her abdomen looked like late in every day. Her abdomen bulges due to all of the air in her GI tract, just as shown in Photo 1.

Non-bloated Abdomen (3 of 3)

The same patient, a few weeks after Botox injection. She is now able to burp. Bloating and flatulence are remarkably diminished, and her abdomen no longer balloons towards the end of every day.

Dramatic Lateral Dilation of the Upper Esophagus: Series of 3 photos

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lateral dilation of the throat at C6 of the spine

(1 of 3)

This photo is at the level of (estimated) C6 of the spine (at S). This person has known cervical arthritis, accounting for the prominence. Opposite the spine is the trachea (T). Note the remarkable lateral dilation (arrows) in this picture obtained with with no insufflated air using a 3.6mm ENF-VQ scope. It is the patient’s own air keeping the esophagus open for viewing.
air from below further dilates the upper esophagus

(2 of 3)

At a moment when air from below further dilates the upper esophagus, the tracheal outline is particularly well-seen (T) opposite the spine (S). The “width” of the trachea indicated further emphasizes the degree of lateral dilation, which is necessary because spine and trachea resist anteroposterior dilation.
aortic shelf at the mid-esophagus

(3 of 3)

Just for interest, at mid-esophagus, the familiar aortic “shelf” is seen. Again, this esophagus is being viewed with a 3.6 mm scope with only the patient own (un-burped) air allowing this view.

What the Esophagus Can Look Like “Below A Burp”: Series of 3 photos

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Mid-esophagus of a person with R-CPD

Baseline (1 of 3)

Mid-esophagus of a person with R-CPD who is now burping well after Botox injection into the cricopharyngeus muscle many months earlier. The esophagus remains somewhat open likely due to esophageal stretching from the years of being unable to burp and also a “coming burp.”
esophagus dilates abruptly

Pre-burp (2 of 3)

A split-second before a successful burp the esophagus dilates abruptly from baseline (photo 1) as the excess air briefly enlarges the esophagus. An audible burp occurs at this point.
burp in the esophagus

Post-burp (3 of 3)

The burp having just happened, the esophagus collapses to partially closed as the air that was “inflating it” has been released.

Where have no-burpers traveled from?


R-CPD patient across the U.S.A.

World Map of RCPD Patients

Swelling Checks to Detect Vibratory (Overuse) Injury to the Surface Tissue (Mucosa) of the Vocal Cords



Definition: Vocal tasks (swelling checks) that detect acute or chronic vocal fold mucosal injury reliably; Secondarily, they can also detect gaps between otherwise normal folds.
Purpose /rationale: To provide persons with a way to detect mucosal trouble for themselves. We are in effect “taking all of the clothes off the mucosa.”
Who they are for: Anyone who uses the voice extensively or vigorously—particularly vocal overdoers.*
What they are not for: Voice training or performance.
When they should be done: When first learning the tasks, they should be done often until the concept of one’s mucosal ceiling is understood (see below). Once both proficiency and ceiling are established, the tests require 20 seconds or less both morning and evening.


  1. In your upper voice range, sing the first phrase of “Happy Birthday” as softly as you can, using a “boy soprano pianissimo.” Resist the temptation to “make it work” by getting louder!
  2. Repeat the phrase at progressively higher pitches.
  3. Verify carefully the pitch at which you falter (onset delays or air escape) or can’t go higher without getting louder. THIS IS YOUR MUCOSAL CEILING PITCH, FOR THIS TASK.
  4. If your mucosa is normal, the “soft voice” and “loud voice” ceilings should be about the same.
  5. If your mucosa is abnormal, the “loud” ceiling should be higher than the “soft.”


  1. Sing again “boy soprano pianissimo” using the descending staccato figure so so so so so fa mi re do
    (5-5-5-5-5-4-3-2-1; e.g. G-G-G-G-G-F-E-D-C) Attack each note precisely in the middle of the continuum
    between an aspirated ho and a coupe de glotte. In other words, lightly, precisely, and with a little bounce.
  2. As for “Happy Birthday,” repeat at progressively higher pitches.
  3. Again carefully verify the pitch at which you experience onset delays or air escape or can’t go higher without getting louder. THIS IS YOUR MUCOSAL CEILING PITCH, FOR THIS TASK.


My mucosal ceiling is higher when I do the staccato exercise than it is when I do “Happy Birthday.” What does that mean?

Though needing verification via careful laryngeal examination, this phenomenon suggests that a small gap between the folds, rather than swelling, is the problem.

My mucosal ceiling is higher when I do the “Happy Birthday” exercise than it is when I do staccato. What does that mean?

Again needing verification, this phenomenon suggests a mucosal disturbance rather than a gap as the explanation.

I can figure out my mucosal ceiling easily enough, but how do I know if it is normal?

This can be answered best at the outset by individuals who can compare your performance with that of hundreds of others to whom they have applied these tests (e.g. laryngologist, speech pathologist, voice teacher). It is also helpful at the beginning to correlate your mucosal ceiling with high quality visualization of the vocal folds.

What if my ceiling isn’t normal as compared to others?

The swelling tests are nevertheless just as valuable! Here’s how: Suppose an individual’s initial mucosal ceiling is abnormal because of small vocal nodules, but the person is happy with the voice’s capabilities. Here, the swelling tests can be monitored to help the individual prevent additional mucosal injury, by not allowing the ceiling to descend any further. A different person whose initial ceiling is abnormal might be unhappy with
perceived limitations due to mucosal injury. Now, ongoing use of the swelling tests can confirm the benefits of medical, behavioral (voice therapy) or, eventually, surgical treatments, because the ceiling will rise with successful treatment. Furthermore, these tests can help to avoid recurrent injury.

What if I notice that my ceiling is abnormal (lower) as compared to my usual?

First, consider recent voice use for the possibility that it was “too much.” If so, and/or if the ceiling
remains lowered on subsequent trials of the tests later in the day, “back off” by reducing voice use
until the ceiling returns to your usual pitch, whether “normal” as compared to other persons or not.
Women: Some may find that the ceiling lowers routinely during pre-menstrual days, but returns to normal in a few days.

Do I need to cancel everything until the ceiling recovers?

This depends on the severity of the lowering of the ceiling. Generally, however, careful strategy concerning amount and manner of voice use during this time will allow the mucosa to recover while you continue to work or perform.

Are there common pitfalls in use of the swelling tests?

First and foremost, is the tendency to adjust how the voice is produced when the voice begins to falter. A singer will, for example, unconsciously get a bit louder or use a slight glottal attack to “make it work,” thereby reducing the sensitivity of the tasks. Another might be to perform them without a pitch reference at hand, so that the value of comparing with one’s known “ceiling” pitch is lost. A third might be to become a bit too obsessive and easily “spooked” with any ceiling change. And finally, comes the tendency to “lose the habit!”

* Vocal overdoer: Defined as an individual with both of the following:
  1. A high propensity to use the voice. Generally, “sixes and sevens” on a 7-point (maximum) intrinsic talkativeness scale.
  2. A high extrinsic opportunity or invitation to use voice, based on family, social, vocational, and avocational considerations.

Foreign Content in the Throat


Closeup, magnified examination finds barbecue brush bristle base of tongue: Series of 4 photos

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Pain in throat

Pain in throat (1 of 4)

While eating barbecued steak, this person felt a sharp pain deep in her throat. At this visit the next day, she continued to feel a sharp sensation, especially when swallowing. Note the faint dark line at the arrow.
abnormality in the throat

Closer view (2 of 4)

From a slightly closer vantage, the abnormality is seen better.
bristle in the throat

Bristle identified (3 of 4)

At even closer range, the bristle is identified.
bristle stuck in the esophagus

Bristle to be removed (4 of 4)

At this final view, the metallic nature of the foreign body and stuck-on carbonaceous debris can be appreciated. This bristle was removed with cup forceps through a channel scope in an office setting.

Idiopathic Subglottic Stenosis

A subtype of subglottic stenosis that is inflammatory. One view is that this entity is actually a limited expression of Wegener’s Granulomatosis (aka Granulomatosis with polyangiitis).



Idiopathic subglottic stenosis has different levels: Series of 4 photos

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dilation of idiopathic subglottic stenosis

Post dilation (1 of 4)

Six months after dilation of idiopathic (inflammatory) subglottic stenosis, the patient has noted only slight deterioration, and breathing ability remains acceptable to her.
closer view of idiopathic subglottic stenosis

Closer view (2 of 4)

At closer range, the inflammatory component appears more evident.
vascular pattern

Rich vascular pattern (3 of 4)

The rich vascular pattern accompanying the lesion is seen better and is a visual finding of inflammation.
congested capillaries

"Sharing" the airway (4 of 4)

Here, the scope has been passed through the area of maximal narrowing and the patient becomes acutely aware of greater difficulty breathing. "Sharing the airway" is a way of 'measuring' it functionally. Note again the congested capillaries.

Another way to inject idiopathic subglottic stenosis: Series of 3 photos

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idiopathic inflammatory subglottic stenosis

Idiopathic inflammatory subglottic stenosis (1 of 3)

This patient is about to receive a triamcinolone (steroid) injection into her idiopathic inflammatory subglottic stenosis, while sitting in a chair under topical anesthesia. Dotted circle is for reference with Photo 2.
infused medication into cricoid

Priot to injection (2 of 3)

A needle has been passed through anterior neck skin and its tip rests out of sight, submucosally just inferior to the anterior cricoid ring. Note that the milky white medication has been infused submucosally within the dotted ring.
needle in tracheal wall

Injection (3 of 3)

Here, the 27-gauge needle traverses the trachea in order to inject the posterior tracheal wall. The submucosal white medication appears at the *.

Subglottic stenosis

Subglottic stenosis is narrowing just below the vocal cords, in the lowest part of the larynx and immediately above the first tracheal ring. Examples of causes include scarring from a breathing tube used during a long ICU stay, Wegener’s Granulomatosis (aka Granulomatosis with polyangiitis), and idiopathic subglottic stenosis (aka limited Wegener’s Granulomatosis).

Photos of subglottic stenosis:

Subglottic stenosis, after treatment

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Subglottic stenosis

Subglottic stenosis, before treatment (1 of 2)

Subglottic and high tracheal stenosis, inflammatory, idiopathic (Lab).
Subglottic stenosis

Subglottic stenosis, after treatment (2 of 2)

Same patient, a few days after dilation and steroid injection (Lab).

Open Epidermoid Cyst

An open epidermoid cyst occurs when it spontaneously ruptures, but yet not empty all of its contents (keratin). The outline of the partially-emptied cyst may still be very evident, but it usually assumes an oval shape with the long axis oriented anteriorly and posteriorly. If the cyst empties nearly completely, the white oval is no longer seen, but the vocal cord may have a mottled appearance. If the cyst empties completely, a sulcus lined by epithelium remains.

Photos of open epidermoid cyst:

Indicator Lesions

Indicator lesions are visual findings of vibratory injury in a person who has no current voice complaints, and whose “swelling checks” are normal.


Individuals who fit the “vocal overdoer profile” may only notice vocal limitations caused by vibratory injury on an occasional and transient basis. These episodes may be brushed off as insignificant, because they are so brief, and recovery so complete. Even while asymptomatic, however, such individuals may have subtle visual findings of vibratory injury—“Indicator lesions.” Unless discovered during a screening examination for entry to music studies, the individual may be unaware of these findings. What if indicator lesions are found? Suggested responses:

1. Make sure the individual understands that these are indicator lesions and as such constitute a “yellow flag” suggesting at least occasional overuse of voice.

2. Define the “vocal overdoer syndrome” for the person as the combination of and interaction between an expressive, talkative, extroverted personality and a “vocally busy” life. Said another way, there may be both intrinsic, personality-based and extrinsic, vocal commitment based reasons that amount and forcefulness of voice may be excessive. A 7-point talkativeness scale can be used to estimate the intrinsic risk, where “1” represents Clint Eastwood, “4” the averagely talkative person, and “7” the life of the party. The extrinsic risk is addressed by making a list of vocal commitments such as for occupation, childcare, hobbies, social activities, religious practice, athletics/ sports, and rehearsal and performance.

3. Discuss the symptom complex of mucosal injury: a) loss/ impairment of high, pianissimo singing; b) day-to-day variability of vocal clarity and capability; c) a sense of increased effort to produce voice; d) reduced mucosal endurance, or becoming “tired” vocally from amount/ manner of voice use that does not seem to induce this in others; and e) phonatory onset delays—the slight hiss of air that precedes the beginning of the sound, especially if high and soft. Speaking voice hoarseness can be a fairly late and gross symptom of mucosal injury.

4. Talk about managing the amount, manner, and spacing of voice use to reduce unnecessary wear and tear on the vocal cord mucosa.

5. Teach vocal cord swelling checks as a means of detecting even subtle injury. Respond to what they tell you!

Singers are understandably distressed when they discover even the tiniest mucosal swelling such as indicator lesions. That is because for true singers, singing is not just what they do; the term “singer” also defines who they are. So injury threatens both activity and identity. Consequently, discuss indicator lesions with great care and sensitivity. Keep in mind that some doctors speak of “small vocal nodules that do not interfere with singing.” Small nodules that are but a tiny step above indicator lesions, especially when spicule-shaped rather than fusiform, always exact a penalty to the singing voice (see #3 above), but limitations can often be concealed by warming up, and singing more loudly. Singers often say “I have a big voice that doesn’t do pianissimo.” That is, pp becomes p; mp becomes p; mf becomes f; and so forth. Alternatively, the singer considers the missing pianissimo to be a technical fault.

Photos of Indicator Lesions:

Vocal Cord Synechia

Vocal cord synechia is a strand of scar tissue that tethers the vocal cords to each other. It can prevent the vocal cords from opening fully for breathing.

A synechia can also form in other parts of the body. (Note the subglottic synechia shown below.)


Vocal Cord Synechia: before, during, and after surgery

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Post-intubation synechia

Vocal Cord Synechia (1 of 9)

Post-intubation synechia tethers the arytenoid cartilages together. This patient is tracheotomy-dependent.
Vocal cord synechia during surgery

Vocal cord synechia, during surgery (2 of 9)

Operative view of synechia ("v" of the vocal cords is inverted). Notice that the vocal cords are completely approximated because the synechia has bound them together.
Tiny forceps are separating the cords

Vocal cord synechia, during surgery (3 of 9)

Tiny forceps is separating the cords (arrows) and more clearly shows the extent of the synechia.
Micro-scissors in position to divide the synechia cleanly

Vocal cord synechia, during surgery (4 of 9)

Micro-scissors in position to divide the synechia cleanly. For perspective, the blade of the scissors is only a few millimeters long.
Vocal cord synechia

Vocal cord synechia, during surgery (5 of 9)

After division of the synechia and topical application of an anti-scarring agent.
Vocal cord synechia after surgery

Vocal cord synechia, after surgery (6 of 9)

Five days after surgery. Vocal cords are able to separate for breathing, and the tracheotomy tube can be removed. Compare with photo 1.
healed larynx after release of synechia

Vocal Cord Synechia, after surgery (7 of 9)

Completely healed larynx after release of synechia. Abduction completely restored.
vocal cords are coming together for phonation

Vocal cord synechia, after surgery (8 of 9)

As the vocal cords are coming together for phonation (not yet completely adducted).
Vocal cord synechia

Vocal cord synechia, after surgery (9 of 9)

Closer view. Can hardly see where the synechia was. Compare again with photo 1.

Ossified synechia resists thulium laser

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Ossified synechia

Ossified synechia (1 of 8)

This 75-year-old woman suffered complications after open heart surgery, and was intubated for three weeks. Nearly two years later, she remains short of breath and bothered by difficulty mobilizing secretions. On initial examination, a synechia was identified; at patient request, microlaryngoscopy was scheduled both to divide the synechia and to inject voice gel into the deficient posterior commissure. At surgery, a view sufficient to divide the synechia was not possible. The patient was rescheduled for office-based thulium laser division of the synechia.
Tip of glass fiber near the Ossified Synechia

Ossified Synechia, during first laser treatment (2 of 8)

Close-range view of the synechia. The tip of the glass fiber through which laser energy will be delivered is seen just inferior to the synechia.
Laser energy reveals bone underneath

Ossified synechia, during first laser treatment (3 of 8)

As the synechia is divided, a core of bone formation is exposed. More than half of the laser energy has been delivered to this spar of bone, yet it will not yield. The tip of the scope has also been flexed against the synechia to no avail. A second attempt with higher energy laser has been scheduled.
Ossified synechia 4 months later

Ossified synechia, 4 months later (4 of 8)

Four months later. The synechia remains, and there is residual granulation tissue on its undersurface. It's not yet known whether the spar of bone is still present. Compare with photo 2.
Second surgery attempt of thulium laser

Ossified synechia, 4 months later (5 of 8)

Now, with the thulium laser, beginning a second attempt at dividing the synechia.
Thulim laser reveals no bone remaining in ossified synechia

Ossified synechia, 4 months later (6 of 8)

The spar of bone is not found within the synechia (apparently turned to ash during the original procedure four months earlier), and now the scar band is divided. The patient could feel the difference in her breathing immediately.
synechia is now gone 6 months later

Synechia gone, 6 months later (7 of 8)

Six months after the initial laser treatment for this patient's bone-containing synechia. The synechia is now gone, with only a small residual projection remaining, left of photo. The vocal cords also separate more widely, to a wider "V".
divots from pressure necrosis of the endotracheal tube remain evident

Synechia gone, 6 months later (8 of 8)

During phonation. The divots from pressure necrosis of the endotracheal tube remain evident. In spite of them, the patient's voice is excellent.

Vocal cord synechia

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Vocal cord synechia

Vocal cord synechia (1 of 4)

Note that the vocal cords cannot fully abduct, due to the presence of a synechia, which tethers them to each other posteriorly.
Vocal cord synechia

Vocal cord synechia (2 of 4)

Same patient during phonation.
Vocal cord synechia

Vocal cord synechia (3 of 4)

Same patient at closer range.
Vocal cord synechia

Vocal cord synechia (4 of 4)

Same patient. Synechia in full view.

Intubation injury, including a subglottic synechia

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View of the vocal cords in abducted position

Intubation injury, including a subglottic synechia (1 of 2)

View of the vocal cords, in abducted position, in a patient with voice change after long-term intubation due to brain injury. Injury of the left posterior vocal cord (right of image) can be seen, where pressure from the breathing tube caused an erosion or divot (arrow). The synechia is not yet visible from this viewing perspective.
posterior synechia

Intubation injury, including a subglottic synechia (2 of 2)

Same patient, just below the level of the cords. This synechia, located posteriorly, is additional evidence of breathing tube injury.

Synechia hidden by overhanging arytenoid superstructure

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Maximum possible abduction of the vocal cords

Synechia hidden by overhanging arytenoid superstructure (1 of 4)

Maximum possible abduction of the vocal cords, as seen a few months after an illness that required endotracheal intubation for 3 weeks. This person experienced noisy breathing with any significant exertion.
involuntary inspiratory phonation

Synechia hidden by overhanging arytenoid superstructure (2 of 4)

With elicited sudden inhalation the inspiratory air draws the vocal cords together, and the result is involuntary inspiratory phonation.
overhanging arytenoid superstructure

Synechia hidden by overhanging arytenoid superstructure (3 of 4)

Close-up view of the posterior vocal cords reveal a synechia or scar band tethering the vocal cords to each other and preventing their abduction. This kind of injury can exist in isolation; it can also occur together with cricoarytenoid joint ankylosis.
Synechia hidden by overhanging arytenoid superstructure

Synechia hidden by overhanging arytenoid superstructure (4 of 4)

An even closer view of the synechia.

Nasal and inter-arytenoid synechiae, with subglottic stenosis in forme fruste Wegener’s

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inflammatory adhesion in left nasal cavity

Nasal cavity (1 of 4)

View in left nasal cavity, showing inflammatory adhesion between septum and turbinate/ lateral wall of nose. Note intense erythema at “e.” Dotted line shows where normal separation would be seen.
adhesion of septum and turbinates

Closer view (2 of 4)

Closer, brighter view, again with dotted line where there should be no tissue bridge, but instead separation between septum and turbinates. This adhesion is asymptomatic, and therefore does not need to be treated.
Panoramic view of larynx

Panoramic view (3 of 4)

Panoramic view of larynx, showing adhesion between arytenoid cartilages indicated by vertical hashed lines. Horizontal dashed line is for reference with the next photo.
interarytenoid synechia is no longer seen after dilation

Post dilation (4 of 4)

After dilation, the interarytenoid synechia is no longer seen. Subglottic stenosis is present but not shown in this series.

Ulcerative laryngitis and resulting synechia – fixed!

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a synechia attaching the cords together

Synechia (1 of 3)

This woman developed a sore throat and lost her voice a week after a chemotherapy treatment for her metastatic breast cancer. Here, 6 weeks later, note the hazy area representing resolving “ulcerative” laryngitis (surrounded by tiny dotted line). There is a synechia attaching the cords together.
slight separation of attached vocal cords

Attempted to detach (2 of 3)

The flexible scope has been used once to “twang upwards” from below in order to detach the cords from each other. At the arrow, slight separation can be seen.
adhesion has been released

Successfully detached (3 of 3)

Just after the second attempt. That is, for the second time, the scope was passed below the cords, angulated sharply underneath the synechia, and then pulled upwards. The adhesion has been released. Voice is instantly and dramatically restored (though still hoarse, of course).

Posterior Commissure Synechiae

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tissue band tethers the vocal cords closer together

Tethered vocal cords (1 of 5)

This man has right vocal cord paralysis and a history decades ago of Teflon injection into the right vocal cord, resulting in posterior commissure synechiae. He is short of breath, partly due to the tissue band and partly because it tethers the vocal cords closer together than they would otherwise need to be as seen in photo 4 after the band is removed. See also photo 5.
Tethered vocal cords

Tethered vocal cords (2 of 5)

At closer range.
thulium laser fiber is touching the synechiae

Before laser removal (3 of 5)

The thulium laser fiber (F) is touching the synechiae, with laser energy about to be delivered.
thulium laser division of the band

Immediately after laser (4 of 5)

This is just after the thulium laser division of the band using topical anesthesia only, with patient sitting in a chair.
Vocal cords free of synechiae

One month post-op (5 of 5)

A month later, no residue of the synechiae is seen, and the vocal cords can spring farther apart than in photo 1.

Difficulty Breathing After A 3-day Intubation

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granulation tissue at the posterior commissure

Noisy, restricted breathing following intubation (1 of 5)

This teenager was intubated for 3 days due to tongue swelling. Breathing became noisy and restricted approximately 6 weeks later. Note that the vocal cords do not abduct fully and there is what appears to be granulation tissue at the posterior commissure (anterior asterisk).
vocal cords come into contact

Normal voice (2 of 5)

The vocal cords can come into contact as shown here, consistent with her normal-sounding voice.
small tract is seen posterior to the granulation

At close range (3 of 5)

At very close range within the posterior commissure, a small tract is seen posterior to the "granulation" which is now seen more clearly to be a broad-based synechiae with asterisks marking anterior and posterior limits.
posterior tract

At even closer range (4 of 5)

An even closer view verifies a posterior tract, and this makes it less likely that the cricoarytenoid joints are also injured.
small superficial-looking scar

Mucosa-only scar (5 of 5)

This view is taken with the scope passed just between the vocal cords and just anterior to the synechiae and angled directly posteriorly. A small superficial-looking "mucosa-only" scar is seen bilaterally, surrounded by dotted line. It can be confidently predicted that when the synechiae is released, the arytenoid cartilages will likely be able to abduct fully.

Vocal Cord Synechia
Vocal cord synechia is a condition wherein a scar band tethers the vocal cords to each other. Therefore, the vocal cords cannot fully open for breathing. This video provides a clear example — using laryngeal videostroboscopy — of a vocal cord synechia.

Recurrent Respiratory Papillomatosis (RRP) and Other HPV-Induced Lesions

A disorder in which wart-like tumors or other lesions grow recurrently within a person’s airway. These growths are caused by the human papillomavirus (HPV), and they may occur anywhere in a person’s airway, such as on the vocal cords (by far the most common site), in the supraglottic larynx, or in the trachea. If these growths are removed, they will almost always grow back, or recur; hence, “recurrent respiratory papillomatosis.”

Symptoms and risks of recurrent respiratory papillomatosis:

RRP can be life-threatening in young children, if not carefully followed and treated, since a child’s airway is relatively narrow and can potentially be obstructed completely by the disease’s proliferative growths; moreover, RRP in children tends to grow and recur more aggressively. In adults, RRP will usually only impair voice function (when the growths occur on the vocal cords), though it can also impair breathing in severe cases. Occasionally, RRP can also progress to cancer, and therefore patients found to be at high risk for this (see below) need to be monitored carefully.

Characteristics of the growths:

The growths usually associated with RRP are wart-like tumors, or papillomas, that protrude conspicuously from the surface on which they grow, often in grape-like clusters. These kinds of papillomas are usually seen in patients who have HPV subtypes 6 or 11, which are both lower-risk subtypes for incurring cancer. There are some HPV patients, however, who manifest their HPV infection with subtler, velvety growths within the airway—“carpet-variant” growths, so to speak. Although these “carpet-variant” growths do not have the wart-like appearance of the papillomas typically associated with RRP, there at least a few key points of similarity:

  1. Both the “carpet-variant” and wart-like growths are lesions that sometimes appear, either independently or together, in patients who have HPV;
  2. Both the “carpet-variant” and wart-like growths are stippled with polka-dot vascular markings, because each “loop” in the “carpet” or each “grape” in the wart-like cluster has its own fibrovascular core, seen as a red dot;
  3. Both the “carpet-variant” and wart-like growths can disrupt voice function;
  4. Both the “carpet-variant” and wart-like growths usually recur if they are removed.

Because of these similarities, we consider these “carpet-variant” growths, even when the sole expression of the infection, to be at least a cousin to RRP, within the family of HPV-induced lesions. Many patients with this “carpet-variant” condition have HPV subtypes such as 16 or 18 that are higher-risk for cancer; such patients need to be monitored with particular care.

Treatment for recurrent respiratory papillomatosis:

The primary treatment for RRP and other HPV-induced lesions is careful, conservative surgical removal of the growths. Because these growths almost always recur, surgery must usually be performed on a repeated basis, as frequently as every few weeks in children, but on average much less often in adults. A common interval between surgeries for adult patients is between every six months and every two years, depending on how quickly the RRP or other HPV-related lesion recurs and impairs the patient’s voice function again. There are also a few medical treatments that have been used in addition to surgery, including, among others, interferon, indole-3-carbinol, intralesional mumps or MMR (measles-mumps-rubella) vaccine, cidofovir, and bevacizumab.



Papillomas of the Larynx and Trachea
This video shows wart-like growths in the voicebox and windpipe (larynx and trachea) caused by chronic infection with the human papillomavirus (HPV).
Pulsed-KTP Laser Coagulation of Vocal Cord Papillomas
See a video demonstration of laser coagulation of vocal cord papillomas.