The Gasping Syndrome

By Dr. Bastian M.D.

A few times a year, distressed patients present from their internists or pulmonologists to see if I can explain their shortness of breath. The patient has already undergone numerous tests: e.g. chest x-ray, pulmonary function tests, EKG, stress test, echocardiogram, CT, blood tests, and even bronchoscopy. Everything has come back normal, or anything even slightly abnormal (the reader can fill in the blank) has been treated maximally without any reduction of the patient’s symptoms.

In short, the patient has complied with every test and treatment recommendation; yet there is still no apparent explanation for this difficulty breathing, and no relief provided by numerous treatment trials.

The patient seems weary of the problem. My “antennae” do not pick up any signals of la belle indifference (a peculiar lack of concern about symptoms that when present suggests that the problem may be non-organic). She tells me that her breathing is never noisy, and that her shortness of breath may or may not be associated with exercise. I apply my subjective but extremely useful “flow-volume loop” by asking her to exhale to “empty” and then rapidly breathe in until completely full, and there is no unusual noise, and no prolongation of the time required to fill.

My initial thought in this scenario? The gasping syndromeWhat is that? A recognizable but to my knowledge previously undescribed disorderHere is my composite description, meaning that individual patients may not fit every element of what follows:

  1. Either with exertion or at rest, the patient has an abrupt* sense of “smothering,” or air hunger. It happens almost from one second to the next. Like the abrupt shooting pain of neuralgia, the abrupt tickle of sensory neuropathic cough / throat clearing, or the abrupt laryngeal closure of laryngospasm. The patient says she can be engrossed in a movie or a book strolling with the dog when suddenly her consciousness is invaded by a need to “get more air.”
  2. She responds by taking a deep breath, but there is no relief and the sensation remains. So, she takes a series of deep breaths, all of them to no avail. The feeling is oppressive, anxiety-provoking, gaspingThis sensation may last for a few seconds, to several hours.* Unfortunately, it can happen again some time later, or maybe just a time or two per day or even per week.

Having seen many people who fit the gasping syndrome across the decades, though not usually more than a handful per year, I have speculated that this is a sensory disturbance. After all, I ponder, if it represents more than a primary neuropathic sensation, why is oxygen saturation measured by oximetry, including during exercise, always normal? Why are all the tests of heart and lung function normal? Why no mitral valve prolapse, or something to explain this? Why nothing on imaging? Why no noisy breathing?

My mind goes to patients who describe a similar sensation at the moment IV contrast is injected for a CT scan. In addition to “warmth,” “a sensation of needing to urinate,” etc., they can have a sensation of abrupt, quite compelling, and thankfully transient smothering.  Or to someone I know who in the middle of an IV infusion of a biologic modifier for cancer, (with prior warning) experienced profound air hunger that started abruptly and was completely gone 20 seconds later. In each of these cases, it seems like a primary sensory phenomenon more than an alerting and protective sensation in response to low oxygen or high carbon dioxide levels.

How would one conceptualize a mechanism? Here is one thought experiment: consider that we are all supplied with pulmonary stretch receptors. They send messages “in the background” several times across the day and night to the respiratory center: Excuse me… Take a deep breath; expand those alveoli; your surfactant is giving you some atelectasis. And so, without being aware of it, we sigh now and then. We roll over in our sleep, mutter, grind our teeth, and take a deep breath. While reading a book we subconsciously shift in our seat and inspire deeply as we turn a page. Again, we are unaware of this, but an observer watching us read or, equipped with night vision goggles and watching us sleep, will see it.

What if the pulmonary stretch receptors send a signal Hey! Time to take a deep breath! and despite our taking a deeper breath outside of conscious awareness, the respiratory center does not receive the return communication, Action completed. Even with normal O2 and CO2 levels, if the brain thinks that deep breath did not happen, would it not intrude on conscious thought to re-command more urgently: Hey! Deep breath please!

Where does one go to help the patient with this thought experiment diagnosis? Just give her this explanation and leave it there? Or, maybe punt back to the primary care or pulmonary or cardiology physician…? But what if the person has already seen 3 of each specialty—one who is local, another at a nearby university center, and a third at a national referral center? What if “every conceivable test” has already been done 3 times?

A follow-on thought experiment: to the patient, and via a summary letter to her doctors, explain the concept of dysesthesia or sensory disturbance. Give her analogies: at the dentist, after anesthesia is in place to allow that root canal or filling, your tongue/lip can feel swollen, but a look in the mirror shows them to be normal. When a leg goes to sleep, it can feel fatter and heavier than the other one, but it is not. When you suffer nerve damage from diabetes, it can feel like bees are stinging your feet, but none are present in the room.

And then explain scenarios where persons have to accommodate to or neglect the feeling of contact lenses. The sound of new tinnitus. The tickling of an indwelling tracheotomy tube. The dramatic sensation a sword swallower must ignore during the show. Or the sensation of air hunger the pearl diver must overcome to stay submerged for 2 minutes while swimming vigorously.

Perhaps point out that it appears there is no danger from this ominous-feeling sensation.  Remind her of the multiplicity of prior “normal” tests. Maybe suggest that she experiment with assuming “control” of her response to the sensation by saying to herself: It is just a feeling! Or, Stupid pulmonary stretch receptors! Maybe gently alter behavior to see if it has any impact. Introduce inspiratory resistance via “straw-breathing.” Or a gentle Valsalva maneuver. Or, exhale slowly through pursed lips whose opening is the size of a coffee-stirrer.

And if nothing else works, suggest trying to mentally shrug and “throw the sensation over the shoulder.” And then keep going. The very worried individual can purchase an oximeter. Or even a stethoscope as a “crutch” to allay anxiety.

All of this can be offered with a physician’s apologies that he or she has nothing better to offer. And also with encouragement that these ideas have “liberated” other patients struggling with the same problem.

A final thought: just as neuromodulators can help persons suffering from neuralgia or sensory neuropathic cough/throat clearing, and laryngospasm, consider a “sensory neuropathic cough” strategy of working one-by-one, from medication to medication such as amitriptyline, gabapentin, etc., hoping to find one that helps.

*Some describe a more continuous, lower-grade background sensation of difficulty breathing with abrupt “peaks”

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For more information on Dr. Bastian, go to our website at bastianvoice.com

Idiopathic Subglottic Stenosis

Idiopathic (unknown cause) inflammatory subglottic stenosis is a frustrating breathing problem seen mostly in women. It appears to be an autoimmune disorder that we have thought for many years to be an incomplete expression (forme fruste) of Wegener’s Granulomatosis, aka granulomatosis with polyangiitis (GPA). In a caseload of perhaps 125 patients, it appears that standard of care remains occasional outpatient dilation, steroid injection, and mitomycin C application. Most patients go a year or more between dilations. The rub: occasionally, dilations need to be done more frequently in an “active” case, or there may be reasons to avoid the brief general anesthesia required for dilation such as: morbid obesity, difficult jaw/tooth/neck anatomy, or even a phobia of general anesthesia.

“Office” Treatment Option for Inflammatory Subglottic Stenosis

In such situations, one naturally casts about for alternatives. Low dose methotrexate has not been very effective in our experience. And we work with a motivated rheumatologist open to considering rituximab, even with a negative ANCA study. Or the laryngologist might consider an office-based airway procedure as illustrated in the photos below. This particular person only requires dilation every 18 months or so, but it represents a major stressor for her given her fears, her size, and somewhat challenging anatomy. She is one of several offered the treatment shown below: steroid injection in the voice laboratory, followed by laser treatment.

Our thought is that in some, it may be the ridges and air turbulence that creates the feeling of airway restriction, or that these rings of stenosis “catch” mucus. In the case below, the clinician was almost dubious that what was accomplished would make that much difference to the person’s breathing. But upon calling her a week after the procedure below, and asking if the improvement was nil, subtle, small, medium, or large, she replied “large…a huge improvement.”

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60% Stenosis (1 of 5)

Estimated at a 60% stenosis, using the vocal cords as a reference.

Narrowing & erythema (2 of 5)

At closer range, the examiner sees concentric ridges of narrowing and erythema characteristic of this disorder.

Triamcinolone is injected (3 of 5)

With patient sitting in the chair with topical anesthesia, a needle is passed from anteriorly just below the cricoid. Here, triamcinolone is being injected into the posterior component of the stenosis.

Laser ablation (4 of 5)

The blue laser fiber (thulium laser) is seen just prior to beginning laser ablation. Note in particular the circular shape of the area of greatest stenosis, to compare with the next photo.

Stenosis is coagulated (5 of 5)

The anterior half of the ring of greater stenosis has been coagulated. Note that the shape of the opening is changed to more of an anterior-posteriorly oriented oval. Distal trachea is also more easily seen. Again, the patient reported that this improved her breathing to a large degree.

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Photos:

Idiopathic Subglottic Stenosis Has Different Levels

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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 (2 of 4)

At closer range, the inflammatory component appears more evident.

Rich vascular pattern (3 of 4)

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

"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

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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.

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.

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).


Subglottic Stenosis, after Treatment

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Subglottic stenosis, before treatment (1 of 2)

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

Subglottic stenosis, after treatment (2 of 2)

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

Subglottic Stenosis, before and after Dilation

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Subglottic stenosis, before dilation (1 of 2)

This individual has undergone at least a dozen prior dilations, each of which provides dramatic relief from noisy breathing and exercise intolerance. Here the patient is halfway to needing re-dilation, due to the typical inflammatory stenosis that is seen. Compare with photo 2.

Subglottic stenosis, after dilation (2 of 2)

One week after one of this patient's dilations (with Kenalog injection and topical Mitomycin C), showing a dramatic widening of her airway; compare with photo 1. After a number of years, inflammatory lesions such as this sometimes "burn out," and the interval between dilations increases.

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Subglottic stenosis (1 of 5)

Middle-aged woman with unexplained shortness of breath and noisy breathing, due to this idiopathic inflammatory and very high subglottic stenosis. The patient initially declined dilation due to her anxiety. She also had granularity of the nasal septum and a positive ANCA profile for Wegener’s granulomatosis.

Subglottic stenosis, worsened (2 of 5)

Five months later, the symptoms became intolerable, and the stenosis was noted to be slightly narrower and with a greater posterior component. The patient agreed to dilation.

Subglottic stenosis, worsened (3 of 5)

Same exam as photo 2; this close-up view shows more clearly the inflammatory nature of this stenosis.

Subglottic stenosis, after dilation (4 of 5)

Five days after outpatient dilation, triamcinolone injection, and topical mitomycin C application. The patient’s symptoms have vanished, the harsh inspiratory noise is no longer heard, and the size of the airway, though still not normal, is more than doubled. Compare with photo 2 of this series.

Subglottic stenosis, after dilation (5 of 5)

Same exam as photo 4, close-up view. Intensification of the inflammatory changes of this stenosis are expected so early after dilation. Compare size of the stenosis with photo 3 of this series.

Stenosis Before and After Dilation for Forme Fruste Wegener’s

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Subglottic stenosis (1 of 5)

High-grade subglottic stenosis in a woman diagnosed syndromically with forme fruste Wegener's granulomatosis-related subglottic stenosis. With a narrowing less than 50%, she is very symptomatic. Her breathing is noisy, and her forced inspiration time is about 3 seconds. Compare with photo 4.

Inflammation (2 of 5)

Closer visualization reveals the inflammatory nature of the stenosis.

Flexible scope (3 of 5)

Here the distal chip flexible scope has passed through the narrowing not only to see into distal trachea, but also as a breathing test. The patient becomes very aware of reduced space and this indicates a marginal airway.

Post-dilation (4 of 5)

A week after dilation, triamcinolone injection and mitomycin C application, the patient says breathing is now normal, and forced inspiration time is only a second in duration--normal. Compare with photo 1.

Post-operative bruising (5 of 5)

Closer visualization with early postoperative bruising. The trachea is now easily visible through the larger opening. Compare with photo 2.

Subglottic / Tracheal Stenosis

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Wegener's granulomatosis (1 of 4)

Inflammatory subglottic/tracheal stenosis, thought to be the result of an incomplete expression of Wegener's granulomatosis (no history of trauma).

Subglottic / Tracheal stenosis (2 of 4)

Close view, from vocal cord level.

Subglottic / Tracheal stenosis (3 of 4)

Close view, from just above vocal cords.

Inflammed Stenosis (4 of 4)

Close view, showing the inflammatory nature of the stenosis.

Subglottic Stenosis, Due to Wegener’s Granulomatosis

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Subglottic stenosis, due to Wegener's (1 of 2)

This person has Wegener’s granulomatosis, confirmed by anti-neutrophil cytoplasmic antibodies (ANCA) testing. Here, looking from above the vocal cords, one can see an estimated 50% narrowing of the subglottic and high tracheal passageway.

Subglottic stenosis, due to Wegener's (2 of 2)

Viewed from within the subglottis, one can see more clearly the inflammatory nature of this stenosis. A dotted oval estimates what the normal caliber or width of this airway would be. This patient has been managed with systemic medication, but also occasional dilation, steroid injection, and Mitomycin C application.

Supraglottic, Glottic, and Subglottic Endotracheal Tube Injury

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Breathing tube injury (1 of 4)

This 20-something individual was premature at birth and intubated for several weeks. Decades later, the evidence of breathing tube injury can be seen. Here, parallel lines outline likely trajectory of tube, taped at right corner of mouth. This fits as well with the left medial arytenoid divot at arrow. Dotted lines indicate aryepiglottic cord margins. Note deficit on right (left of photo) suggesting pressure necrosis from the endotracheal tube.

Aryepiglottic cord defect (2 of 4)

Aryepiglottic cord defect is better seen during phonation. The details of posterior commissure injury are obscured at this distance.

Phonation (3 of 4)

During phonation, low voice, note that the posterior vocal cords cannot come together, (even with cough or breath-holding) due to joint capsule injury from the endotracheal tube. Voice is intractably breathy.

Posterior subglottic thickening (4 of 4)

Posterior subglottic thickening surrounded by dotted lines, indicating a third level of old injury, here with no functional consequence.

Pinhole Opening in Near-Complete Subglottic Stenosis

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Narrowed space for breathing (1 of 4)

This man was gravely ill and intubated for several weeks. He is now well, but tracheotomy-dependent. The vocal cords do not abduct fully due to scarring of the cricoarytenoid joints. However, the narrowed space for breathing between the posterior vocal cords is not the main reason he is tracheotomy-dependent, as seen in the next photos.

Looking between the vocal cords (2 of 4)

At closer range, a deep erosion “divot” of the right posterior vocal cord (left of photo at dotted line) is the result of pressure necrosis of the endotracheal tube. Looking between the vocal cords into the subglottic airway, a small white oval is seen (arrow). This is the upper surface of the white plastic tracheotomy tube.

Closer view (3 of 4)

A closer view, again through the vocal cords.

Space between subglottis and trachea (4 of 4)

At yet closer range. The size of this pinhole between subglottis and trachea below cannot measure more than 3 mm. Crico-tracheal resection and re-anastomosis (planned for soon after this examination) is the best option to work towards decannulation.

Difficulty Breathing after a 3-day Intubation

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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).

Normal voice (2 of 5)

The vocal cords can come into contact as shown here, consistent with her normal-sounding voice.

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.

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.

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 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.)


Photos:

Vocal Cord Synechia: Before, During, and After Surgery

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Vocal Cord Synechia (1 of 9)

Post-intubation synechia tethers the arytenoid cartilages together. This patient is tracheotomy-dependent.

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.

Vocal cord synechia, during surgery (3 of 9)

Tiny forceps is separating the cords (arrows) and more clearly shows the extent of the synechia.

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, during surgery (5 of 9)

After division of the synechia and topical application of an anti-scarring agent.

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.

Vocal Cord Synechia, after surgery (7 of 9)

Completely healed larynx after release of synechia. Abduction completely restored.

Vocal cord synechia, after surgery (8 of 9)

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

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 (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.

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.

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 (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.

Ossified synechia, 4 months later (5 of 8)

Now, with the thulium laser, beginning a second attempt at dividing the 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 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".

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 (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 (2 of 4)

Same patient during phonation.

Vocal cord synechia (3 of 4)

Same patient at closer range.

Vocal cord synechia (4 of 4)

Same patient. Synechia in full view.

Intubation Injury, Including a Subglottic Synechia

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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.

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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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.

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.

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.

Nasal and Inter-arytenoid Synechiae, with Subglottic Stenosis in Forme Fruste Wegener’s

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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.

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 (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.

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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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.

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.

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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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.

Before laser removal (3 of 5)

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

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.

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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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).

Normal voice (2 of 5)

The vocal cords can come into contact as shown here, consistent with her normal-sounding voice.

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.

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.

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.

Videos:

https://youtu.be/yF9pU_CncW4
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.

Stenosis

Abnormal narrowing of a passageway in the body. At our practice, stenosis typically refers to narrowing in the breathing passage, such as for narrowing in the glottic, subglottic, or tracheal areas.

Stenosis in the airway can be the result of prolonged endotracheal intubation, external trauma such as gunshot wound, crush injury, or tracheotomy, an inflammatory or auto-immune process, surgical resection of part of the airway for tumor, or other causes. Persons with airway stenosis will note a reduced capacity for exercise. Often the clinician hears noisy breathing on inhalation, especially when the patient is asked to fill the lungs quickly. Esophageal stenosis gives symptoms of difficulty swallowing solids more so than liquids.


Photos of Stenosis:

Tracheal Stenosis

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Tracheal stenosis (1 of 4)

Panoramic view showing normal larynx but, in the distance, narrowing of the trachea to an estimated 40% of normal diameter. Caused by long-term intubation and tracheotomy injury.

Tracheal stenosis (2 of 4)

View from just below the vocal cords.

Tracheal stenosis (3 of 4)

View at the stenosis showing more clearly its scarred, non-inflamed nature.

Just below the tracheal stenosis (4 of 4)

View of distal trachea after just passing the stenosis. Carina in the distance.

Subglottic Stenosis, before and after Dilation

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Subglottic stenosis, before dilation (1 of 2)

This individual has undergone at least a dozen prior dilations, each of which provides dramatic relief from noisy breathing and exercise intolerance. Here the patient is halfway to needing re-dilation, due to the typical inflammatory stenosis that is seen. Compare with photo 2.

Subglottic stenosis, after dilation (2 of 2)

One week after one of this patient's dilations (with Kenalog injection and topical Mitomycin C), showing a dramatic widening of her airway; compare with photo 1. After a number of years, inflammatory lesions such as this sometimes "burn out," and the interval between dilations increases.

Tracheal Stenosis

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Tracheal stenosis (1 of 3)

Tracheal stenosis due to combination of long-term intubation and tracheotomy. This view is from the level of the vocal cord. Patient has some functional collapse at the membranous tracheo-esophageal party wall (arrow) when she exhales.

Tracheal stenosis (2 of 3)

Closer view, just above the stenosis.

Just below the tracheal stenosis (3 of 3)

After just passing the stenosis, normal trachea seen distally.

Tracheal Stenosis and Collapse

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Tracheal stenosis and collapse (1 of 2)

Due to a life-threatening illness, this person had an endotracheal tube in place for a few weeks. When she got stronger, a tracheotomy tube (not seen as it is below this level of the trachea) was inserted. The result is severe scarring in the trachea. The expected diameter of the tracheal opening is indicated by the dotted line. The “X” marks the same location in each of the two photos.

Tracheal stenosis and collapse (2 of 2)

When this person exhales fully through her tracheotomy tube, or if she attempts to speak, the membranous tracheal wall also bulges forward, and obliterates the tiny residual opening. Dilation has been performed but helped minimally. The indicated procedure, if her severe medical condition will allow, is removal of the damaged segment of the trachea with reconstruction (aka tracheal resection, primary reanastomosis).

Tracheal Stenosis, Due to Forme Fruste Wegener’s Granulomatosis

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Tracheal stenosis (1 of 3)

View from level of vocal cords shows residual lumen of airway at only ~35% of normal. The dotted circle shows how big the lumen should be.

Tracheal stenosis (2 of 3)

Closer view shows the characteristic appearance of mucosa and the inflammatory nature of the stenosis (pinkness).

Just below the tracheal stenosis (3 of 3)

After just passing through the stenotic area, distal trachea is normal in caliber and color.

Subglottic / Tracheal Stenosis

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Wegener's granulomatosis (1 of 4)

Inflammatory subglottic/tracheal stenosis, thought to be the result of an incomplete expression of Wegener's granulomatosis (no history of trauma).

Subglottic / Tracheal stenosis (2 of 4)

Close view, from vocal cord level.

Subglottic / Tracheal stenosis (3 of 4)

Close view, from just above vocal cords.

Inflammed Stenosis (4 of 4)

Close view, showing the inflammatory nature of the stenosis.

Hypopharyngeal Stenosis

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Hypopharyngeal stenosis: not yet visible (1 of 2)

Panoramic view of the larynx, with the swallowing “crescent” in the middle of the view (indicated by the dotted lines). Several months prior, this patient had laser resection for hypopharyngeal cancer. Expected scarring from the surgery led to a stenosis (that is, a narrowing) at the entrance to the esophagus. The stenosis cannot be seen here, but is revealed in the next photo (for reference, an “X” marks the same point in the larynx in both photos).

Hypopharyngeal stenosis: revealed (2 of 2)

The patient performs the trumpet maneuver, which splays open the hypopharynx, revealing the stenosis; the dotted lines represent what would be a normal-sized opening. This stenosis affects swallowing of solid food, but the patient says this is no problem for him, if he eats a little more slowly and chews well.

Subglottic Stenosis, Due to Wegener’s Granulomatosis

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Subglottic stenosis, due to Wegener's (1 of 2)

This person has Wegener’s granulomatosis, confirmed by anti-neutrophil cytoplasmic antibodies (ANCA) testing. Here, looking from above the vocal cords, one can see an estimated 50% narrowing of the subglottic and high tracheal passageway.

Subglottic stenosis, due to Wegener's (2 of 2)

Viewed from within the subglottis, one can see more clearly the inflammatory nature of this stenosis. A dotted oval estimates what the normal caliber or width of this airway would be. This patient has been managed with systemic medication, but also occasional dilation, steroid injection, and Mitomycin C application.

Subglottic Stenosis, before and after Dilation

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Subglottic stenosis (1 of 5)

Middle-aged woman with unexplained shortness of breath and noisy breathing, due to this idiopathic inflammatory and very high subglottic stenosis. The patient initially declined dilation due to her anxiety. She also had granularity of the nasal septum and a positive ANCA profile for Wegener’s granulomatosis.

Subglottic stenosis, worsened (2 of 5)

Five months later, the symptoms became intolerable, and the stenosis was noted to be slightly narrower and with a greater posterior component. The patient agreed to dilation.

Subglottic stenosis, worsened (3 of 5)

Same exam as photo 2; this close-up view shows more clearly the inflammatory nature of this stenosis.

Subglottic stenosis, after dilation (4 of 5)

Five days after outpatient dilation, triamcinolone injection, and topical mitomycin C application. The patient’s symptoms have vanished, the harsh inspiratory noise is no longer heard, and the size of the airway, though still not normal, is more than doubled. Compare with photo 2 of this series.

Subglottic stenosis, after dilation (5 of 5)

Same exam as photo 4, close-up view. Intensification of the inflammatory changes of this stenosis are expected so early after dilation. Compare size of the stenosis with photo 3 of this series.

Airway Stenosis Caused By Wegener’s Granulomatosis, Before and After Dilations

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Airway stenosis (1 of 5)

Marked inflammatory narrowing in the immediate subglottis. Within the ring of arrows is the inflamed, reddened tissue, which is narrowing the airway into the shape of a slit. This man needs to be active for his work, but notices shortness of breath and noisy breathing with exertion.

Airway stenosis, after dilation (2 of 5)

Nine days after a dilation procedure, with local steroid injection and painting with Mitomycin C. The airway has widened, so that it is more oval-shaped and less slit-like. Compare with photo 1. Although a degree of stenosis remains, symptoms have subsided dramatically. For reference, asterisks mark the same points in the subglottis in this photo and the next photo.

Airway stenosis, after dilation (3 of 5)

Same exam, looking beyond the immediate subglottis. There is an inflammatory response that involves several centimeters of the upper trachea. Inflammatory areas often “trap” mucus, as seen here.

Airway stenosis, before another dilation (4 of 5)

Now five months after the dilation procedure mentioned in photos 2 and 3. The patient has been receiving systemic treatment with methotrexate and prednisone. General appearance of the inflammation has decreased. In spite of this, as expected, the stenosis has persisted (dotted oval shows the estimated caliber or width of a normal airway) and symptoms have gradually increased. Thus, another dilation was scheduled for the next day.

Airway stenosis, after another dilation (5 of 5)

A week after photo 4, following the most recent dilation. There is expected immediate postoperative inflammation and an increase in the airway’s caliber or width by an estimated 30% (dotted oval again shows the estimated caliber or width of a normal airway; compare with photo 4). Symptoms are again abolished.

Tracheal Stenosis, before and after Tracheal Resection and Primary Reanastomosis

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Tracheal stenosis (1 of 8)

This view from the level of the vocal cords shows high-grade tracheal stenosis, involving rings two, three, and four; the airway here is an estimated 30% of its normal diameter. For reference, a dotted line marks the level of the cricoid cartilage.

Tracheal stenosis (2 of 8)

Slightly closer view. This patient is very short of breath with minimal activity and, even at rest, has audible stridor. Elsewhere, across a span of several prior weeks, she had undergone three dilation procedures with only minimal, transient benefit.

Close up view (3 of 8)

Close-up view shows scarring, collapse of tracheal walls, and some granulation tissue.

Just below the tracheal stenosis (4 of 8)

The trachea just beyond the stenosis is normal.

Tracheal stenosis, 5 days after surgery (5 of 8)

Five days after tracheal resection and primary reanastomosis. Compare with photo 1. Note that the airway’s diameter has at least tripled (part of the opening is obscured by tenacious mucus). The patient’s shortness of breath is now gone, as is the stridor.

Tracheal stenosis, 5 days after surgery (6 of 8)

Close-up of the line of anastomosis, with a couple of sutures visible. Compare with photo 3. Again, tenacious mucus in the upper part of the photo is obscuring part of the view.

Tracheal stenosis, 2 months after surgery (7 of 8)

Another eight weeks later. The airway is wide-open and has also now healed since the surgery. Compare this view with photo 1 (pre-surgery) and photo 5 (early follow-up).

Tracheal stenosis, 2 months after surgery (8 of 8)

Compare this view with photo 2.

Dilation for Post-Radiation Hypopharyngeal Stenosis

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Dilation for post-radiation hypopharyngeal stenosis (1 of 4)

Early after radiotherapy for left vocal cord cancer (indicated by arrow), tumor seems to have responded, but it has become difficult to swallow solid foods due to a radiation-induced stricture (indicated by solid oval) with expected lumen (indicated by the dotted lines).

Dilation for post-radiation hypopharyngeal stenosis (2 of 4)

Closer-range view of the stricture at opening to the esophagus.

Dilation for post-radiation hypopharyngeal stenosis (3 of 4)

A tapered device used for dilation (bougie) is now inserted into the stricture and down into the upper esophagus in order to enlarge the entrance to the esophagus.

Dilation for post-radiation hypopharyngeal stenosis (4 of 4)

Immediately following dilation, the opening is enlarged (compare with photo 2). The patient’s ability to swallow food improved noticeably, but not to normal.

Tracheal Deformity and Stenosis, before and after Repair

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Upper tracheal stenosis, before repair (1 of 6)

View from above the level of the vocal cords, showing severe narrowing and deformity of the upper trachea, caused by a “difficult” tracheotomy many years earlier. This man is frustrated by activity limitations, and difficulty coughing up accumulated mucus.

Upper tracheal stenosis, before repair (2 of 6)

View from just below the level of the vocal cords, showing the deformity and stenosis more clearly.

Looking from below the stenosis (3 of 6)

The trachea below the area of stenosis is normal.

After tracheal repair (4 of 6)

View from just above the level of the vocal cords, six weeks after tracheal resection and primary anastomosis, showing final result. Patient feels he breathes completely normally. Compare with photo 1.

After tracheal repair (5 of 6)

View from just below the level of the vocal cords. The tracheal caliber is now virtually normal. A broken, absorbable suture is seen at 2 o’clock, and a tiny remaining unhealed area is at 11 o'clock. Compare with photo 2.

After tracheal repair (6 of 6)

A close-up view shows the circular line of the anastomosis more clearly.

Post-Intubation Stenosis

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Endotrachel tube injury (1 of 4)

View of larynx of an individual in critical condition who was ventilated for 2 weeks via an endotracheal tube. See the erosion of the posterior right cord (left of photo) from pressure necrosis of the endotracheal tube, indicated by the white, semi-circle markings.

Closer view, between the posterior vocal cords (2 of 4)

With tip of endoscope positioned deeper within the larynx, between the posterior vocal cords, a small opening is visible several centimeters distally. Diameter of the opening is an estimated 20% of normal, which is below the level of the patient's tolerance, and explains why a (white) tracheotomy tube has been placed.

Even closer view, showing upper surface of the tube (3 of 4)

Closer view, showing more clearly the curved upper surface of the tracheotomy tube entering just below the stenosis and serving as a “back door” for breathing.

Non-inflammatory stenosis, caused purely by injury (4 of 4)

Note in this close-range view that this is a non-inflamed kind of stenosis caused purely by injury. Compare this with stenosis from presumed forme fruste Wegener’s granulomatosis.

Sickle Cell Disease and Laryngeal Stenosis

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Sickle cell disease and subglottic swelling (1 of 4)

Distant view of vocal cords and immediate subglottic swelling in a man in early 30’s with sickle cell disease (SCD). During a SCD crisis, he was intubated for approximately 10 days, and then due to inability to extubate, a tracheotomy was performed

At closer range (2 of 4)

At closer range, the dotted line again indicates the margin of the true cords. Is this stenosis a complication of intubation only, or was the endotracheal tube injury exacerbated by sickling/ hypoxia in the area?

Maturing granuloma (3 of 4)

The greatest point of narrowing is estimated to be only 30% of normal lumen size. Some of that space is taken by a maturing granuloma (G).

High-grade stenosis ( 4 of 4)

A view from within this high-grade stenosis shows no additional stenosis at the level of tracheotomy tube entry.

Subglottic Granulation and Curving Airstream

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Intubation injury (1 of 4)

After a 9-day intubation for serious illness, the patient has difficulty breathing due to this “proud flesh” response to injury within the cricoid ring, posteriorly. Breathing has improved in the past week, leading to a decision to await further maturation, rather than proceeding to microlaryngoscopic removal.

Lobules (2 of 4)

Close-up view of the lobules of granulation tissue. Air can easily pass around the obstruction as indicated by the arrows.

2 months later (3 of 4)

As predicted, breathing continued to improve to the point of seeming normal to the patient, and 2 months later, the granulation tissue has matured and detached, leaving behind a subglottic scar band (parallel lines).

Scar band (4 of 4)

Here is a close-up of the scar band. A solid line denotes the anterior border of the scar band for reference in all 4 photos, but compare especially to photo 2.

Office-Based Surgery When General Anesthesia Is too Risky

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Involuntary inspiratory voice (1 of 6)

This elderly man is tracheotomy-dependent due to inability to open the vocal cords. Here while breathing in, there is a posterior “keyhole” from the divots caused by pressure necrosis of the breathing tube. Still, due to inspiratory airstream, he produces involuntary inspiratory voice. General anesthesia for laser widening of the airway (posterior commissuroplasty) would be very risky due to his diabetes and many other medical problems. Hence, the decision to attempt this with patient awake and sitting in a chair.

Laser posterior commissuroplasty (2 of 6)

The posterior right vocal cord is injected with lidocaine with epinephrine, in preparation for office laser posterior commissuroplasty. F = false vocal cord. T = true vocal cord, near its posterior end. The left vocal cord is injected similarly prior to the procedure that follows.

During the commissuroplasty (3 of 6)

The thulium laser fiber is being used to excavate the posterior commissure. Note the existing divot of the opposite (right) vocal cord (dotted lines) which will also be enlarged (next photos).

Deepening divot (4 of 6)

With view rotated clockwise approximately 45 degrees, work is commencing to deepen the right vocal cord divot.

Inspiratory indrawing decreased (5 of 6)

At the conclusion of the procedure. Not only is the ‘keyhole’ seen in photo 1 larger, but inspiratory indrawing of the rest of the vocal cords is greatly diminished.

Phonation (6 of 6)

Now phonating, voice is similar to the beginning of the procedure, because the vibrating part of the vocal cord was not disturbed. Of course, number of words per breath is slightly lower, due to increased use of air through the keyhole—air wasting.

The Adult Result of Infant Cricoid Split

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Cricoid split procedure (1 of 6)

This man spent considerable time intubated in a neonatal ICU at his birth 30 years before this examination. To avoid tracheotomy, doctors performed a cricoid split procedure. Vertical lines depict the cuts between the anterior vocal cords and posterior cricoid plate. Due to lateral expansion of the larynx lumen, vocal cords cannot fully approximate, explaining his lifelong extremely weak, breathy, and air-wasting voice.

Rotated view (2 of 6)

Rotated view of the subglottis again showing the line of the cuts created to expand the lumen of the airway as depicted by the arrows.

Open phase (3 of 6)

Open phase of vibration under strobe light during voice. The tips of vocal processes (dots) should be directly opposite each other. Instead, the right side (lower dot) is displaced anteriorly, likely because the right half of the posterior plate of the cricoid shifted anteriorly on the left.

Cricoarytenoid joints (4 of 6)

This photo is a repeat of photo three and shows that the cricoarytenoid joints have also been medial-to-lateral in order to widen the airway posteriorly, explaining why the vocal processes also cannot come fully together.

Lateral excursion (5 of 6)

A second repeat of photo three: With an anteriorly shifted right arytenoid, the right vocal cord is shortened and made more flaccid. This explains the greater lateral excursion from indicated midline of the right cord as compared with the left.

Closed phase (6 of 6)

"Closed" phase of vibration is not truly closed due to the separation of the arytenoid cartilages and the spreading of the anterior commissure. Dots continue to indicate tips of vocal processes, though mucosa has moved medially on the right vocal process to make the gap seem smaller. As depicted in a separate series, bilateral medialization laryngoplasty is planned to strengthen voice.

A Fenestrated Trach Tube Allows Voicing when there Is Stenosis

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Tracheotomy (1 of 4)

This woman was gravely ill and intubated longterm. A tracheotomy was required. Now she wants the tube removed.

View below vocal cords (2 of 4)

The tip of the scope has been taken below the vocal cords. Note the fenestrated tracheotomy tube within the high trachea.

Fenestra (3 of 4)

When the patient plugs her trach tube with a finger, air comes into the distal tip of the tube (dark circle within the tube), passes up and out of the fenestra (window) and can power the vocal cords which are above our view. The trachea surrounds the tube as a whole without any "blow-by". If there were no fenestra, the patient would be unable to speak.

Patient post-trach (4 of 4)

After tracheal resection and re-anastomosis, the tracheotomy is no longer needed. The circular scar is at the dotted line. The M denotes overlying mucus. The patient now breathes normally.

Stenosis of Larynx and Trachea before and after Cricotracheal Resection and Reanastomosis

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Post intubation and tracheotomy (1 of 8)

Panoramic (distant) view of larynx in a middle-aged man recovered from near-death due to post-viral cardiomyopathy. After longterm intubation, and tracheotomy, he remains tracheotomy-dependent. Salivary pooling in the subglottis suggests stenosis.

Confirmed stenosis (2 of 8)

Closeup at the level of the vocal cords. This degree of salivary pooling, inability to breathe at all or to talk with trach plugged, confirms total stenosis.

Tracheotomy tract (3 of 8)

Looking down the tracheotomy tract, there should be an opening upward into the larynx as depicted by the dotted cylinder. Total stenosis is again proven.

Cricoid cartilage (4 of 8)

CT image at the beginning of the total stenosis, is about 5 mm superior to the inferior border of the cricoid cartilage.

Resection needed (5 of 8)

Approximately 3.25 cm below, the trachea begins to open around the tracheotomy tube. But to get to good quality tissue, 5cm of the airway (approximately 2 inches) must be resected, and the ends sutured back together.

Post surgery (6 of 8)

17 days after surgical repair. Because the cricoid cartilage was resected and airtight closure is occasionally not possible due to poor “match” of cricoid and trachea, a “safety trach” was placed 3 rings below the anastomosis at the conclusion of the repair.

Trach removed (7 of 8)

At close range, the circular line of the anastomosis is indicated by the dotted line. The trach was removed on this day.

Patient's sentiment (8 of 8)

Patient's sentiment about his removed tracheotomy tube.

Stenosis Before and After Dilation for Forme Fruste Wegener’s

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Subglottic stenosis (1 of 5)

High-grade subglottic stenosis in a woman diagnosed syndromically with forme fruste Wegener's granulomatosis-related subglottic stenosis. With a narrowing less than 50%, she is very symptomatic. Her breathing is noisy, and her forced inspiration time is about 3 seconds. Compare with photo 4.

Inflammation (2 of 5)

Closer visualization reveals the inflammatory nature of the stenosis.

Flexible scope (3 of 5)

Here the distal chip flexible scope has passed through the narrowing not only to see into distal trachea, but also as a breathing test. The patient becomes very aware of reduced space and this indicates a marginal airway.

Post-dilation (4 of 5)

A week after dilation, triamcinolone injection and mitomycin C application, the patient says breathing is now normal, and forced inspiration time is only a second in duration--normal. Compare with photo 1.

Post-operative bruising (5 of 5)

Closer visualization with early postoperative bruising. The trachea is now easily visible through the larger opening. Compare with photo 2.

Sometimes “low-tech” Is Best for Stenosis

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Esophageal bougie (1 of 4)

This is an esophageal bougie. With the patient sitting in a chair and after gargling topical anesthetic, this tapered and flexible dilator is passed through the mouth and into the upper esophagus to dilate (stretch) an area narrowed by radiation therapy for a larynx cancer.

Swallowing crescent (2 of 4)

The area of stenosis is just below the swallowing crescent (dotted outline). Arytenoid mounds are permanently swollen due to (expected, typical) radiation damage. The arrow shows the trajectory of the bougie that is about to be inserted.

Post-arytenoid area (3 of 4)

The tapered tip is arriving at and just beginning to enter the post-arytenoid area. As it is inserted farther, its diameter will increase.

Maximum diameter (4 of 4)

Here, the bougie is at its maximum diameter. The real goal is to stretch the stenosis, but it also pulls the larynx forward, creating space (bracket) between posterior surface of arytenoid (A) and the posterior pharyngeal wall (PPW)

Who knew…? Many Such Injuries Are Never Found

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Coughing evaluation (1 of 6)

An octogenarian is being evaluated for recent coughing of months duration. To evaluate her complaint of major mucus production, an “exam of opportunity” mini-bronchoscopy was done. Salivary pooling (see bubbles) is seen, likely due to interference with swallowing caused by topical anesthesia.

Intubation scars (2 of 6)

Just barely through the vocal cords, two circumferential scars are seen at 1 and 2. This prompted a conversation during which the patient noted that decades earlier, she had been intubated for 11 days during a grave illness.

Stenosis (3 of 6)

At closer range, the zone of stenosis is seen better. This is an incidental finding at this time, and is not responsible for her sensory neuropathic cough. She has no shortness of breath or sense of exercise limitation.

Further down trachea (4 of 6)

The trachea beyond the lower edge of the scarred segment is of normal caliber but turns to the patient’s left, giving the illusion of distal narrowing.

Below stenosis (5 of 6)

Just below the stenosis, the normalcy of the distal trachea is better seen. The carina is at C.

Carina (6 of 6)

Right at the carina, and looking into both mainstem bronchi. Many persons who have been intubated for a long period of time likely have asymptomatic and therefore undetected and inconsequential scars like those seen in photos 2, 3, and 4.

Stenosis at Two Levels: Supraglottic and Glottic

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Laryngeal stenosis post intubation (1 of 7)

4 months after prolonged intubation during a severe illness, this person experienced initial mild post-intubation breathing difficulty which subsequently progressed considerably. At this first consultation, in spite of this marked laryngeal stenosis, she says she sleeps well, has had no frightening episodes, and breathing has been the same (no further deterioration) for 3 weeks. She is exercise-intolerant and breathing is noisy. This is maximum abduction, and at least one explanation is the inter-arytenoid synechium at "S."

Closer range (2 of 7)

At closer range, looking below the supraglottic synechium, a second, posterior commissure synechium is also seen.

Posterior commissure (3 of 7)

A very close view of the posterior commissure. The question is whether the injury is a synechium alone, or whether there is fixation (ankylosis) of the cricoarytenoid joint(s) as well.

View into trachea (4 of 7)

With laryngeal injury from a breathing tube, a search is always made for injury within the trachea. Here, none is found.

Post laser release (5 of 7)

A few days after laser release of the adhesion between the arytenoid superstructure (X's used for reference with the next photo).

Scarring (6 of 7)

The dense adhesions at the posterior vocal cords have been released (compare with photos 2 and 3). It appeared intraoperatively that the cricoarytenoid joints were scarred, and so "cookie bites" were also taken to increase space. At this first postoperative examination, it is surprising to the surgeon that this degree of abduction of the cords has been achieved.

Closer view (7 of 7)

Closer visualization of the area of surgery. Time will tell if the mobility of the vocal cords is sufficient to counteract the tendency of these raw surfaces to scar back together.

Progressive Radiation Fibrosis Effects on the Larynx and a Solution to some of it

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Forty years post-radiation (1 of 8)

This photo is taken forty years after curative radiation for a vocal cord cancer. Four decades of progressive radiation fibrosis (“leatherization”) has taken away arytenoid movement so that this is the maximum opening. The patient is exercise-intolerant and makes loud inspiratory breathing noises while sleeping. Her voice is also very poor.

Involuntary inspiratory voice (2 of 8)

With sudden inspiration, the darker mucosa (at the arrows) indraws and vibrates, making an involuntary inspiratory voice.

Only capable of high pitch (3 of 8)

Other than a stage whisper, she can only make a very high pitch, because the only mucosa capable of vibration is the small segment indicated by the arrows.

Open phase vibration (4 of 8)

Again under strobe light, this is the open phase of vibration, with arrows again indicating the short segment of mucosa that can oscillate.

One week post-commissuroplasty (5 of 8)

A week after posterior commissuroplasty, the patient’s breathing is much improved. Despite the distant view, the “cookie bites” taken from the posterior cords are visible.

Rapid inhalation, closer view (6 of 8)

In a much closer view, the posterior vocal cord divots are seen well. The segment of flexible mucosa is indrawing here as the patient inhales rapidly (at arrows).

Three months post-surgery (7 of 8)

Three months after the laser surgery, the patient continues to say the improvement of breathing is “large.” In this distant view the full reason why is not seen.

Closer view, post-surgery (8 of 8)

In a closer view, as is always the case after complete healing, the divots are smaller than just after surgery.

Tracheal Red Herring; the Real Culprit is Cricopharyngeus Spasm

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Tracheal stenosis? (1 of 4)

During a grave illness, this woman eventually underwent tracheotomy. Though she wore the tube for several months, it was removed 3 years ago. Only six months prior to this examination, due to a feeling of choking, she underwent a CT scan that revealed tracheal stenosis. The patient does have mildly noisy breathing but has no sense of exercise intolerance.

Narrowing at trachea (2 of 4)

Viewing from just below the vocal cords, there is narrowing and deformity of the trachea at the site of prior tracheotomy.

Closer view (3 of 4)

A closer view shows normal trachea beyond.

No significant change in breathing (4 of 4)

Now with the scope through the area of greatest narrowing, the patient doesn’t experience any significant change in her breathing. Her symptoms are those of cricopharyngeus spasm, not tracheal stenosis.

A Different Approach to Inflammatory Tracheal Stenosis

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Planning on periodical injections (1 of 4)

Three months after successful dilation, the patient says breathing is still normal. We are planning an injection of triamcinolone every 3 or 4 months, attempting to lengthen the interval between dilation procedures. Please note that the *s (right of photo) are for comparison with photo 2.

Long-acting steroid (2 of 4)

A needle has been passed into the anterior neck to place submucosal long-acting steroid. Note the bulging and blanching at the *s and compare with photo 1.

Needle going into the posterior of stenosis (3 of 4)

Here the needle has been passed translumenally and into the posterior portion of the stenosis.

Posterior tracheal wall (4 of 4)

The posterior tracheal wall has flattened as compared with photo 3, due to the infiltrated medication.

Motivated Airway Examination Avoids Further Surgery

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Marginal airway (1 of 4)

This woman underwent radiotherapy for larynx cancer several decades earlier. Some years ago, progressive post-radiation fibrosis had nearly fixed the vocal cords in the midline and airway was marginal. A laser posterior commissuroplasty was done as an alternative to tracheotomy. During a recent hospitalization for pneumonia elsewhere, she was told that her airway was inadequate; she returned for examination for this reason. During this kind of distant view, her airway does indeed look marginal.

Airway at close range (2 of 4)

At close range using topical anesthesia, with the patient exhaling, her airway appears adequate. The dotted line is where the margin of the cords would be if the divots had not been removed.

Forced inspiration (3 of 4)

Forced inspiration draws the vocal cord mucosa medially to narrow the airway, and inspiratory noise is heard, but the posterior divots maintain a small but adequate airway and time to fill is only mildly prolonged.

Alternative to tracheotomy (4 of 4)

During phonation, the divots removed from the posterior vocal cords are more clearly seen. Voice is air-wasting, airway is of course suboptimal, but no tracheotomy or additional laser commissuroplasty is needed.
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Supraglottic Scarring (1 of 4)

This man was treated with radiotherapy for an early vocal cord cancer, approximately 35 years prior to this examination. For those 35 years, his breathing has been slightly noisy, and he feels mild restriction of exercise tolerance. Here, you see an arch-like scar above the posterior end of the vocal cords (dotted line).

Radiation causes hoarseness (2 of 4)

The vocal cords can come together fully when he makes voice; his mild hoarseness is therefore not due not to the scar band, but instead to reduction of vibratory flexibility of the surface tissue of the vocal cords due to radiation effects.

Cords don't close completely (3 of 4)

In this closer view, one can also appreciate that the vocal cords do not separate to as wide a “V” as would be normal, and this is the main explanation of the harsh inspiratory noise and slight prolongation of time to fill his lungs with forced inspiration. Note as well additional evidence of radiation damage (scar band) at the arrow.

Trachea (4 of 4)

A view is obtained of his (normal caliber) trachea, to make certain that there is not an additional reason for his noisy breathing.

Glottic Web Management Without A Keel

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Glottic Web (1 of 7)

More than a year after laser excision elsewhere of a small vocal cord cancer, this man has a web joining the anterior half of the vocal cords. Voice is a whisper. A simple division with a microscissor is worthwhile before contemplating something more invasive, such as insertion of a keel.

Glottic Web (2 of 7)

A closer view. The dotted line indicates the proposed division. The tag of extra tissue at * in all photos is not to be disturbed, preferring to preserve all tissue until the mucosa’s vibratory ability could be assessed.

Glottic Web (3 of 7)

A week after that simple endoscopic division of the web, steroid injection, and topical mitomycin C application. The anterior vocal cords have not yet re-mucosalized. Voice is remarkably functional.

Glottic Web (4 of 7)

Approximately 3 weeks after division, voice remains very good. Compare with photo 1.

Glottic Web (5 of 7)

Only a small part of the cut surface is not yet covered with new mucosa. This photo is illuminated with narrow band (blue-green) light to accentuate capillaries on re-grown mucosa.

Glottic Web (6 of 7)

Under strobe light, the closed phase of vibration.

Glottic Web (7 of 7)

Open phase of vibration, showing restoration of oscillatory ability on both cords. Voice remains rough but highly functional without syllable dropouts or “effort” in the quality.

Nuances of Endotracheal Tube Injury

This woman with high-risk comorbidities of diabetes and obesity, was in ventilated in ICU more than a month for pulmonary complications of Covid-19 infection. She had an orotracheal tube in place for 3.5 weeks, and then a tracheotomy tube was placed. Now at her first visit a year later, she remains tracheotomy-dependent, and is told she has bilateral vocal cord paralysis (disproven in the following photo series).

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Maximum glottic opening (1 of 8)

Is it paralysis, as diagnosed elsewhere? At a fairly distant view, the maximum opening between the vocal cords at any phase of breathing appears to be approximately a 4mm glottic opening.

Undersurface mucosa indraws (2 of 8)

When the patient inspires rapidly with tracheotomy tube plugged, the vocal cord undersurface mucosa indraws (grey bands at dotted lines), further narrowing the glottic chink. One sees a faint suggestion of breathing tube injury (divot) at the arrow. Notably, there is a very low pitched rumbling sound heard that does not come from the glottis.

Phonation (3 of 8)

During phonation, the cords approximate fully, and in fact the voice is remarkably normal-sounding and she even has an excellent upper range.

Posterior commissure divot (4 of 8)

At close range while breathing with trach plugged, the posterior commissure divot subtly visible in Photo 2 is confirmed. A divot in the right posterior cord “always” indicates that the tube was taped to the left corner of the mouth. The patient’s mother confirmed that this was so.

Further evidence of scarring (5 of 8)

Angling farther posteriorly, additional evidence of inter-arytenoid and possible joint capsule injury is seen. Faint dotted lines outline this area. The problem is not bilateral vocal cord paralysis but posterior commissure scarring, tethering the arytenoids together.

View into trachea (6 of 8)

Looking now into the subglottis and trachea, there is narrowing only at trach entry site, accentuated functionally because the membranous trachea (MT) moves in and out with respiratory phase.

Vibration of trachea (7 of 8)

When the patient plugs the trach tube and inspires rapidly, the deep rumbling sound is again heard, and comes from vibration of the membranous trachea indrawing (arrows) and vibrating (zigzag line).

Open trachea beyond the tube (8 of 8)

A view past the tip of the trach tube shows no secondary area of tracheal stenosis.

The plan here is posterior commissuroplasty, followed by placement of a smaller trach tube and a trial of plugging. If plugging is tolerated during the day, she will need a sleep study with it plugged at night, given the tracheomalacia and her obesity.

Breathing Tube Injury, not Vocal Cord Paralysis

This middle-aged woman was injured severely in an auto accident as a teenager. Recovery involved a long stay in ICU, and ventilation via a breathing (endotracheal) tube for a few weeks prior to tracheotomy. Fifteen years earlier, a posterior commissuroplasty was done by me on the left side.  Severely short of breath before that procedure, she said the improvement was such that she was able to do most activities of daily living remarkably well for many years. While still much better than prior to the posterior commissuroplasty, she has felt a little more limited in the past few years and wants now another similar airway-widening procedure. Speaking voice can easily pass for normal, though she thinks it is occasionally a little rough.
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Aperture is very narrow (1 of 6)

Seen from a distance, during exhalation, the vocal cord aperture is perhaps 30% of normal.

Involuntary inspiratory phonation (2 of 6)

When asked to inspire rapidly, even in this distant view, the vocal cords can be seen to in-draw and vibrate (see blur), creating involuntary inspiratory phonation. Inspiratory phonation time is estimated at 2.5 seconds, rather than the normal 1 second or less.

Divot on left vocal cord (3 of 6)

The shallow “divot” of the left cord (right of photo) is all that remains of what would have been a much deeper divot created at the time of posterior commissuroplasty, 15 years earlier. The dashed line indicates the likely magnitude of laser excision.

Endotracheal tube injury (4 of 6)

The full extent of the original endotracheal tube injury is seen best in this view of the extreme posterior commissure. One can almost see the upper surface of the cricoid cartilage marked with “C” showing also a scar band between arytenoid and cricoid cartilages, especially on the right (at S).

Laser cookie bite (5 of 6)

The posterior commissure during phonation shows the divot on the left cord (right of photo). The dashed line shows the approximate magnitude of the laser “cookie bite” to be created at the time of surgery. But the lighter dotted line is a typical remaining divot after full healing. Interestingly, (as explained by Charles’ Law) if even this small area is added to the size of the glottic aperture while breathing, the patient will notice a significant improvement of exercise tolerance.

Surface scarring in the tracheotomy (6 of 6)

When there is a scar anywhere in the airway, the clinician must make sure there isn’t another causing narrowing. In this case there is no narrowing, but the tracheotomy site shows surface scarring at the arrow.

Videos of Stenosis:

Tracheal Stenosis: Before and After
In this video, trachea (windpipe) blockage causes shortness of breath until the narrowed segment is removed. You will see views of the trachea before and after surgical repair.
Post-Radiation Hypopharyngeal Stenosis
People with larynx or pharynx (voice box or throat) cancer often undergo radiation therapy as part of their treatment regimen. An uncommon complication is stenosis (narrowing, scarring) of the entrance to the upper esophagus at the junction of the throat and esophagus. This video provides an example of this disorder.

Pharyngocele

Pharyngocele is a dilated outpouching from the normal contour of the pharynx.


Photos:

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Pharyngocele: view at vocal cord level (1 of 6)

A 20-year-old man complains that his neck expands and that he has pain while playing the trumpet. This radiographic image is at the level of the vocal cords, during quiet breathing; at this point, the pharyngeal dilation and pharyngocele are not yet seen. Compare with image 2.

Pharyngocele: view at vocal cord level (2 of 6)

Same view as in image 1, except that the patient is performing a Valsalva maneuver, to simulate trumpet playing. Whereas in image 1 the pharynx is completely collapsed, here it is inflated with air. A true pharyngocele, seen on the right side of the image, is beginning to develop. Also, compare the neck’s surface contour between this image and image 1.

Pharyngocele: view at supraglottic level (3 of 6)

This view is at the supraglottic level, during quiet breathing, and already shows mildly dilated pyriform sinuses. Compare with image 4.

Pharyngocele: view at supraglottic level (4 of 6)

The patient again performs a Valsalva maneuver, during which the pharynx dilates dramatically. Compare with image 3.

Pharyngocele: view at base of tongue level (5 of 6)

Higher view yet, at the base of the tongue opposite the tip of the epiglottis, during quiet breathing. Compare with image 6.

Pharyngocele: view at base of tongue level (6 of 6)

The patient again performs a Valsalva maneuver, during which the hypopharynx expands dramatically; the beginning of a true pharyngocele can be seen again, this time on the left of image. If this young man were to continue playing trumpet, one would expect the pharynx to expand more and more over time.

Redundant Supraglottic Mucosa

An excess of mucosa overlying one or more structures in the larynx above the vocal cords. Mucosa in this area should “fit” snugly, like leggings, but in the case of redundant supraglottic mucosa, the fit becomes more like baggy pants.

Symptoms and treatment:

This redundant supraglottic mucosa most commonly develops on the apex and posterior surface of the arytenoid cartilage. Such mucosa sometimes draws inward during breathing and fills the laryngeal vestibule. In a severe case, inspiration can become noisy (stridor) or even effortful. When symptoms like these become troublesome, the excess mucosal tissue can be removed with endoscopic laser surgery.

Redundant supraglottic mucosa vs. laryngomalacia:

Redundant supraglottic mucosa is similar to the disorder laryngomalacia. In both disorders, supraglottic tissue is pulled into the laryngeal vestibule during breathing and can cause stridor. However, the causes of these symptoms are different. In the case of redundant supraglottic mucosa, the main problem is an excess of overlying mucosa, but in the case of laryngomalacia, the main problem is that the underlying structural tissue, such as that which comprises the aryepiglottic cord and epiglottic cartilage, is abnormally weak or soft.


Redundant Supraglottic Mucosa, before and after Surgery

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Redundant supraglottic mucosa (1 of 8)

This patient said that, when she breathes in (inspires), she hears noise and feels a sense of obstruction, especially if she inspires rapidly or with her chin down. She had found it necessary to use CPAP while reading with chin down, for example. Here, the patient is breathing quietly, with chin in neutral position, “looking at the horizon.” The vocal cords are abducted, the laryngeal vestibule is open, and there is no breathing noise.

Supraglottic tissue (2 of 8)

Upon request, with her head position unchanged, the patient begins to inspire rapidly. As she inspires, supraglottic tissue (of the arytenoids and aryepiglottic cords) is drawn into the laryngeal vestibule, and harsh breathing noise is heard. This indrawn tissue, which is redundant mucosa, partially obscures the view of the still-abducted vocal cords (dotted lines).

Vibrating mucosal margin (3 of 8)

At the peak of rapid inspiration. The vocal cords are still fully abducted (dotted lines) but almost completely obscured by the indrawn mucosa. In addition to the rushing sound, there is also a low-pitched fluttering or rumbling sound, caused by vibration of the leading edge of the indrawn supraglottic mucosa. “B” marks this blurred, vibrating mucosal margin.

1 week after surgery (4 of 8)

Same patient, one week after laser peeling of the redundant mucosa. The areas which were addressed include: the upper face of the arytenoid, apical mucosa, aryepiglottic mucosa adjacent to the arytenoid, mucosa from the postarytenoid surface, and even some postcricoid mucosa.

1 week after surgery (5 of 8)

At the peak of rapid inspiration. The aryepiglottic cords are drawn in slightly, but the laryngeal vestibule remains widely open. Compare with photo 3.

1 week after surgery (6 of 8)

Closer view of surgical details, showing that the entire posterior surface of the arytenoids has been denuded. An asterisk marks the edema at the cut edge of the postcricoid mucosa.

7 weeks after surgery (7 of 8)

Same patient, now seven weeks since laser peeling of the redundant mucosa. As the patient rapidly inspires here, the laryngeal vestibule remains widely open. The patient says that she no longer feels a sense of obstruction or hears noise when breathing, even with her chin down. Compare with photos 2 and 3.

7 weeks after surgery (8 of 8)

The areas that were operated on have healed. Compare with photo 6.

Nonorganic Breathing Disorder, Laryngeal

Laryngeal nonorganic breathing disorder is when a person’s vocal cords partially or fully close during breathing, which causes noisy breathing. Also called vocal cord dysfunction (VFD) or vocal cord dysfunction (VCD).

The fundamental disorder is not in the mechanism itself, but rather in the patient’s “use” of the mechanism. Consciously or sub-consciously, the patient inappropriately narrows the space between the vocal cords, usually for secondary gain. Unlike with asthma or nonorganic breathing disorder of the trachea, the noisy breathing is mostly heard when the person breathes in (inspiration). Still, on occasion, individuals with this disorder are treated for years as having asthma before this diagnosis is finally made.


Photos:

Nonorganic Breathing Disorder, Laryngeal

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Nonorganic breathing disorder, laryngeal (1 of 4)

Normal quiet breathing with vocal cords widely abducted.

Nonorganic breathing disorder, laryngeal (2 of 4)

Typical posture of vocal cord dysfunction, with vocal cords only slightly abducted.

Breathing (3 of 4)

If air is drawn into the lungs in this posture, the vocal cords are brought into vibration and make inspiratory phonation (see blurring of the margins).

Nonorganic breathing disorder, laryngeal (4 of 4)

For comparison, same patient, normal (expiratory) phonation.
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Nonorganic breathing disorder, laryngeal (1 of 3)

Nonorganic breathing disorder in a patient who makes loud inspiratory noise with athletic exertion. Images shows functional partial closure during inspiration as a nonorganic phenomenon.

Nonorganic breathing disorder, laryngeal (2 of 3)

Normal abduction of vocal cords with elicited sniffing.

Nonorganic breathing disorder, laryngeal (3 of 3)

Note the convexity and vibratory blurring of the free margins, correlating with inspiratory phonation.

Videos:

Nonorganic Breathing
This video portrays a breathing abnormality that is non-organic / functional.

Nonorganic Breathing Disorder, Tracheal

A breathing disorder, often mistaken for asthma, in which a person induces his or her trachea to narrow, causing wheezing or apparent shortness of breath. The person’s oxygen saturation remains normal, but his or her description of the problem and apparent breathing distress may be quite dramatic; in severe instances, the person may have been intubated and placed in intensive care, based purely upon the “drama”—that is, the person’s distressed appearance and audible noises. The extent of medical intervention prompted by this pseudo-asthma can be remarkable.

How it happens:

The person’s trachea momentarily narrows or collapses, but unlike with tracheomalacia, this narrowing or collapse is not due to any anatomical or physiological disorder of the person’s trachea. Instead, it can be seen as an added capability of the trachea: an unusual, heightened capability of the membranous tracheal wall to flex inward and decrease the caliber of the “pipe.” A person whose trachea has this added capability may figure out how, with inconspicuous excessive expiratory effort—a sort of semi-Valsalva maneuver that isn’t evident to observers—to induce this tracheal or tracheobronchial collapse that creates the wheezing heard by family, friends, or co-workers.

The nonorganic element:

Often, this upper airway wheezing ability can be just a personal quirk (like double-jointedness) that has no particular significance to the person’s life; think of a “wheezy laugh.” Such a case would not be a nonorganic breathing disorder case. In extreme cases, however, a person may begin to use this wheezing ability to masquerade (perhaps sub-consciously) as having asthma, in order to achieve some kind of “secondary gain”; this added element puts a case into the category of a nonorganic breathing disorder. Sometimes, the person does have asthma, but is able to markedly amplify the asthma’s apparent severity by overlaying on it this dramatic nonorganic upper airway wheezing ability.

How it is diagnosed:

If a clinician listens to this person’s breathing with a stethoscope placed over the lung fields, the wheezing can indeed sound exactly like asthma. However, there are some key diagnostic criteria that help the discerning clinician to recognize a case of nonorganic breathing:

  • The wheezing is louder over the manubrium (uppermost part of the sternum) than over the peripheral lung fields.
  • There is a surprising incongruity between, on the one hand, the person’s apparent distress and, on the other hand, his or her objective findings, such as oxygen saturation, pulmonary function tests, blood gas measurement, and so forth.
  • Potent treatments for asthma do not seem to diminish or abolish the wheezing.
  • There appears to be some kind of “secondary gain” (mentioned above). Examples of secondary gain might be simple increased attention from family, healthcare workers, and so forth, or else avoidance of school or work, or an enhancement of the chance of winning a lawsuit, or release from responsibility for losing a competitive race, or the ability to manipulate others who have high levels of empathy combined with low levels of discernment of others’ motivations.

Nonorganic Breathing Disorder, Tracheal

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Nonorganic breathing disorder, tracheal (1 of 2)

Distal trachea, showing the carina (middle arrow), where the trachea (or windpipe) divides into the two mainstem bronchi. The membranous tracheal wall is flexible, and beginning to bulge forward functionally (under patient control).

Nonorganic breathing disorder, tracheal (2 of 2)

On expiration, there is anterior bulging (arrows) of the tracheoesophageal party wall, to the point of largely obstructing the mainstem bronchi. Air moving through this functionally narrowed space can cause wheezing on a non-organic basis. Wheezing will be much louder with auscultation over the manubrium, than on listening in the peripheral lung fields.
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Nonorganic breathing disorder, tracheal (1 of 2)

View of the distal trachea in a patient with nonorganic “asthma.” An arrow marks the location of the carina; note how, at this moment, the mainstem bronchi to each side are widely opened.

Nonorganic breathing disorder, tracheal (2 of 2)

Wheezing. (Arrow still at the carina.) One can see that the cause of the wheezing is functional manipulation of the distal trachea, in this case mainly the left mainstem bronchus (right of image); hence, the wheezing is louder over the lung on that side than the other side. Also, unlike with true asthma, the wheezing is much louder over the manubrium than either of the peripheral lung fields.
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distal trachea at the carina

Nonorganic breathing disorder, tracheal (1 of 2)

View of the distal trachea at the carina (where the windpipe divides into the right and left mainstem bronchi). Orienting arrow at the base of the carina.
tracheoesophageal party wall bulges inward

Nonorganic breathing disorder, tracheal (2 of 2)

With exhalation, the tracheoesophageal party wall bulges inward to largely obstruct the right mainstem bronchus. The result is convincing, but nonorganic, wheezing. This is suspected from the patient's affect (e.g., surprising nonchalance and distractibility) and because the wheezes auscultate more loudly over the central chest than in the periphery. (In this slightly closer view, an arrow again indicates the base of the carina.)

“Functional” Mainstem Bronchial Wheezing Is Easier to Mistakenly Diagnose as Asthma than Tracheal Wheezing

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View of trachea during inspiration (1 of 6)

This man has expiratory wheezing but the question of vocal cord dysfunction (which usually causes inspiratory noise) has been raised. The actual problem is not laryngeal, but instead functional/ non-organic large airway wheezing. Here is a view of most of trachea during inspiration. “M” designates membranous portion in all photos of this series.

Exhaling forcibly (2 of 6)

When asked to exhale forcibly, marked wheezing is heard. The membranous trachea invaginates but does not appreciably narrow the lumen caliber. Wheezing is NOT from this level of the trachea.

Carina (3 of 6)

Deeper in, with carina in clear view during inspiration (marked with “C” in this and subsequent photos).

Trachea bulges inward (4 of 6)

With forced expiration, the membranous trachea bulges inward and mostly obscures the carina, but the degree of luminal narrowing is still not sufficient to create significant wheezing at this level.

Right mainstem bronchus during inspiration (5 of 6)

Now viewing even farther down, into the right mainstem bronchus, with base of the carina still barely in view (again at “C”).

Wheezing origin (6 of 6)

The membranous right mainstem bronchus bulges inward and leaves only a small dark crescent of space for out-rushing air. THIS is where the wheezing is originating. Wheezing noises from distal trachea and mainstem bronchi will be transmitted to the lungfields better and more closely mimic asthma, as compared with wheezing that originates in the trachea; which is much louder on auscultation at the sternal notch than in the peripheral lungfields.