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?

 

World Map of RCPD Patients

Marfan syndrome

A genetic connective tissue disorder caused by a defect in gene FBN1, which codes for abnormal structure of fibrillin-1, a protein crucial for formation of normal connective tissue. Most critical is Marfan syndrome’s effect on heart and blood vessels, which tend to dilate and be at risk of rupture. Connective tissue in bones, ligaments, and other parts of the body is also affected.

Laryngologists may encounter Marfan syndrome because parts or all of the aorta may need to be replaced over time, due to abnormal dilation of the weakened arterial wall, with risk of rupture. When such surgery is done, the left recurrent nerve is at risk of injury, and this would lead to left vocal cord paralysis. With Marfan syndrome, it is rare to live to age 70.


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Presbylarynx

Literally, “old age larynx.” The term presbylarynx is used to signify vocal cord changes (and, by extension, vocal limitations) that accompany aging. Typically, these vocal cord changes include bowing of the cords, atrophy, flaccidity, and sometimes reduced wetness and lubrication of the vocal cords. The symptoms of these changes include foggy or weak voice quality, difficulty being heard in noisy places, and decreased vocal endurance.

Such findings are by no means universal in older individuals, however, and some of these changes may be resisted with vocal conditioning exercises. Moreover, some “presbylarynx” changes can be seen in individuals who are only 40 or 50, due to disuse of the voice or familial predisposition. For these reasons, presbylarynx does not seem to be a very useful term; instead, a precise description of the patient’s vocal cords seems to be more useful.


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Bilateral Vocal Cord Fixation

Immobility of both vocal cords due to a scarring rather than paralytic cause. The scarring might manifest as a synechia that tethers the vocal cords to each other and prevents them from separating during breathing. Or it could mean that both cricoarytenoid joints are ankylosed, or “frozen.”

The most common cause of bilateral vocal cord fixation is prolonged endotracheal intubation, such as in gravely ill or injured persons, who may spend weeks in an intensive care unit and on a ventilator. Vocal cord fixation can rarely be caused by rheumatoid arthritis. It is also seen infrequently as a progressive, late complication of radiation therapy for larynx cancer.


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Bilateral vocal cord fixation: Series of 2 photos

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keyhole shaped glottis

Bilateral vocal cord fixation (1 of 2)

After bilateral posterior cordotomies, “keyhole” shaped glottis. Size of opening at posterior commissure is exaggerated by the wide-angle lens of the distal-chip video-endoscope.
Bilateral vocal cord fixation

Bilateral vocal cord fixation (2 of 2)

Persistent posterior opening, but musculomembranous cords come into good contact and have not been damaged by either the original endotracheal tube or the posterior cordotomies, and voice is very serviceable.

Necrosis

The death of cells or tissue. In laryngology, necrosis is seen most commonly after radiation therapy to the larynx for cancer treatment. Radiation kills the tumor but at the same time damages the blood supply of normal tissue on a permanent basis. Necrosis in this instance is called “radionecrosis.” Or, necrosis could result from trauma (a physical wound) that disrupts blood supply, or occasionally in the context of ulcerative laryngitis, which seems to necrose the superficial layers of the vocal cords. Necrotic tissue typically sloughs off down to viable (living) tissue.


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Phonatory insufficiency

When the vocal cords cannot close sufficiently or vibrate adequately to produce a serviceable voice. An inability to close is usually evidenced by air-wasting phenomenology.

This phonatory insufficiency could have one of several causes. It could be due to the loss of part or all of one or both vocal cords, such as after removal of a vocal cord cancer. Or it could follow prolonged intubation and resulting pressure necrosis of the posterior ends of the vocal cords 1. Another possibility might be scarring of the anterior joint capsule of the cricoarytenoid joints, also as a complication of prolonged endotracheal intubation due to grave illness. Yet another cause might be vocal cord paralysis or paresis. The latter problems not only interfere with the cords’ ability to close, but also make the affected cord flaccid, so that it blows out of the way too easily, further wasting the air stream.

When a person with any of these causes of poor vocal cord closure tries to produce voice, maximum phonation time is typically reduced, because only a fraction of the air pushed up from the lungs is converted to sound, with the remainder of the air quickly “wasted.”

The second main category of phonatory insufficiency, in which the vocal cords cannot vibrate adequately, is seen in a person with stiff or scarred vocal cords. Such a person may not waste air, but just be unable to produce other than a harsh whispery sound, because the stiffened vocal cords (now more like thick leather rather than like, as is normal, plastic wrap overlying a thin layer of jello) cannot vibrate as freely or at all.


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  1. Bastian RW, Richardson BE. Postintubation phonatory insufficiency: an elusive diagnosis. Otolaryngol Head and Neck Surg. 2001; 124(6): 625-33. 

Arytenoid chondritis / perichondritis

An infectious or inflammatory response with ongoing ulceration or granulation on the superstructure of the arytenoid cartilage. Here we are talking of the arytenoid cartilage and/ or its thin “envelope” of fibrous tissue called perichondrium. The root chondr- refers to cartilage.

A similar and much more common disorder, contact granuloma or contact ulcer, occurs on the medial surface of the arytenoid cartilage, but low and at the level of the vocal process. When arytenoid chondritis or perichondritis occurs, it causes significant chronic pain (in contrast to contact granuloma, which can be pain-free or bring only minor discomfort). We have never diagnosed the underlying cause. Treatment tends to require definitive removal of the area of cartilage involved (not the entire arytenoid, of course), and then typically the area will heal, though often only after a time of re-granulation.


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Arytenoid chondritis, before and after removal: Series of 5 photos

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Festering arytenoid chondritis

Arytenoid chondritis (1 of 5)

Festering arytenoid chondritis of over a year's duration. Several biopsies done elsewhere showed only inflammation.
Arytenoid chondritis

Arytenoid chondritis, removed (2 of 5)

Two weeks after aggressive partial arytenoid superstructure excision, in an attempt to get down to healthy cartilage.
healed vocal cords

Arytenoid chondritis, removed and healed (3 of 5)

After complete healing. Note loss of anterior arytenoid prominence on the operated side as compared with the unoperated side.
resolution of the lesion and inflammation

Arytenoid chondritis, removed and healed (4 of 5)

At this point, patient is entirely symptom-free. Notice resolution of the lesion and inflammation. The arytenoid mound is a little lower on right (left of image) than on left (right of image), due to surgical removal of part of the superstructure of the arytenoid.
healed chondritis

Arytenoid chondritis, removed and healed (5 of 5)

The area of festering chondritis has completely healed. The arrow shows center of where the lesion was.

Arytenoid chondritis: Series of 3 photos

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arytenoid ulcer

Arytenoid chondritis (1 of 3)

This person has twinges of pain every time she swallows, like “ground glass” or “razor blades.” She locates the sensation by pointing precisely to the upper part of the thyroid cartilage on the left. The exam reveals an arytenoid ulcer (upper right of image), with surrounding erythema.
central depression of lesion

Arytenoid chondritis (2 of 3)

A closer view shows more clearly the central depression and rolled border of the lesion.
Arytenoid chondritis

Arytenoid chondritis (3 of 3)

Using narrow-band illumination at even closer range.

Arytenoid chondritis: Series of 1 photo

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Small ulcer with surrounding erythema

Arytenoid chondritis (1 of 1)

Small ulcer with surrounding erythema, right arytenoid superstructure.

Arytenoid chondritis at the glottic level NOT likely from reflux!: Series of 3 photos

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dilation of this inflammatory subglottic stenosis

2 weeks post dilation (1 of 3)

Two weeks after dilation of this inflammatory subglottic stenosis. Treatment elsewhere with esomeprazole for 2 years had not resolved this. This is likely forme fruste Wegener’s-type stenosis, which in this patient has required dilation every few years, with marked resolution of shortness of breath/ noisy breathing.
otted lines indicate where the ulcer would be if still present

3 months later, ulcer is gone (3 of 3)

Within a few weeks, the pain resolved. Here, 3 months later, the ulcer and erythema are gone. Dotted lines indicate where the ulcer would be if still present. Compare with photo 2.
flat ulcer with surrounding redness

Ulcer not caused by tube or reflux (2 of 3)

There was no postoperative pain at all until on the 4th postoperative day, when she developed left throat pain radiating to the left ear. Note within dotted line a flat ulcer with surrounding redness, resembling an apthous ulcer more than endotracheal tube injury or acid reflux. Observation was counseled, and even discontinuation or reduction of her esomeprazole.

Arytenoid perichondritis: Series of 5 photos

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Arytenoid perichondritis

Arytenoid perichondritis (1 of 5)

Singer with constant right throat pain and vocal impairment, worsened by singing and speaking. Examination finding: arytenoid perichondritis. Note the erosion exposing the arytenoid cartilage, and the associated swelling.
pseudopolyp

Pseudopolyp (2 of 5)

Swelling creates a “pseudopolyp” (at arrow) that interferes with vocal cord closure and vibration.
Phonatory view under strobe light.

Phonation (3 of 5)

Phonatory view under strobe light.
Minimal residual erosion

Two weeks post treatment (4 of 5)

Two weeks after antibiotic treatment. He has intermittent mild discomfort only when singing, and his voice is much improved. Minimal residual erosion (see arrow), with mild inflammatory changes.
voice is entirely normal

Normal voice (5 of 5)

Pseudopolyp has resolved and no longer interferes with voice. At follow-up 6 weeks later, his voice is entirely normal and he has no pain.

Arytenoid perichondritis awaiting surgery: Series of 2 photos

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inflamed, rolled border

Inflammation (1 of 2)

Spontaneous onset of sore throat, laryngitis, without any other URI symptoms approximately 6 months earlier. Biopsy elsewhere showed 'acute and chronic inflammation.' Note the inflamed, rolled border outlined by dotted line, and a sense of central excavation.
lesion

Surgery likely (2 of 2)

At closer range. The solution here will likely be to remove the lesion to include a central "festering" area of perichondrium, as for the other cases on this page. Cause of this kind of lesion is always unknown.

Arytenoid perichondritis going…coming…gone!: Series of 4 photos

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lesion on the left vocal cord

Throat pain (1 of 4)

Very localized throat pain, left mid-neck, has been present for about 5 months with no sign of improvement despite trials of antibiotics, and fluconazole elsewhere. The location of pain correlates well to the lesion (bold arrow). The pain is very troublesome, fluctuating between 5 and 7 on a ten-point scale, worse with talking and tending to increase as the day progresses. The patient was also experiencing frequent laryngospasm. The patient was offered further observation vs. excision at her option.
festering point of lesion

1 week post removal (2 of 4)

After waiting an additional month, the patient became motivated to have the lesion removed. This examination is one week after excision of perichondrium and a small amount of cartilage, seeking to remove the “festering point.” The surgical wound is indicated by small dotted line on the left (right of photo). The patient’s pain is already much reduced, in spite of this wound, but peculiarly, she now has just a slight similar pain on the right. Note the small lesion indicated by the arrow, and visible in retrospect, in photo 1.
Five weeks after surgical removal

5 weeks post removal (3 of 4)

Five weeks after surgical removal, left-sided pain is still gone, and after a course of antibiotics and steroids, right sided lesion (arrow) and pain are nearly gone. It is not known whether healing was spontaneous or the result of steroid and antibiotic. This is because treatment of longstanding lesions often fails, and early, minimal lesions like this one sometimes heal without treatment.
larynx is entirely healed

3 months post removal (4 of 4)

Now 3 months after surgical excision, the larynx is entirely healed; pain and laryngospasm are gone.

Flaccidity of the Vocal Cords

Vocal cord flaccidity correlates to some degree with atrophy of the muscle comprising them. Bowing also accompanies flaccidity most of the time. It is possible to have bowed/slender vocal cords that are not particularly flaccid—they still vibrate with good firmness and resilience. Similarly, vocal cords that appear to have good bulk (and are not atrophied) can nevertheless have a flaccid vibratory pattern. Photos below show the visual findings of flaccidity as distinct from bowing and atrophy. Voice manifestations of flaccid vocal cords are similar to bowing in cases such as:

  • Loss of “edge”
  • Reduced ability to be heard in noisy places
  • Reduced vocal endurance (The voice becomes fuzzier or raspier and more air-wasting as the day progresses and the atrophied muscles tire).









Voice Building:

Voice Building (shorter version):

Vocal cord scissoring

Mismatching of the levels of the vocal cords. Vocal cord scissoring may in some cases be asymptomatic, but more often it introduces a rough quality to the voice, because the desired mirror-image bilateral symmetry of oscillation will be lost.


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