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Laryngopedia By Bastian Medical Media

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Saccular Cyst

A closed sac originating from a formerly open and functioning laryngeal saccule. An analogy for a saccular cyst is a velvet bag used to hold coins which has its opening cinched shut by a drawstring. The mouth of the saccule becomes blocked, and mucus secreted within the saccule cannot escape through the normal opening in the anterior ventricle. This closed sac gradually expands, causing the false cord and aryepiglottic cord to bulge; the sac can further expand over the top of the thyroid cartilage and into the neck.


Anterior Saccular Cyst, before and after Removal

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Anterior saccular cyst (1 of 4)

Phonation, open phase of vibration, under strobe light. Left-sided cyst (right of image) causes mildly rough voice quality.

Anterior saccular cyst (2 of 4)

Four years later. Phonation, open phase of vibration, under strobe light. The cyst has enlarged, and voice quality has deteriorated. The patient wants this removed.

Anterior saccular cyst, removed (3 of 4)

Ten days after laser dissection of the complete cyst (not simple unroofing). At close range, looking into the left ventricle. The raw area (at arrows) is the bed of excision.

Anterior saccular cyst, removed (4 of 4)

Phonation, standard light. Some residual bruising of the left vocal cord (right of image), but voice quality and capabilities are normal.

20 Years after Saccular Cyst Removal!

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Saccular cyst (1 of 3)

Saccular cyst on the left was removed ~ 20 years ago. In this panoramic view, notice that the left false cord is surgically absent.

Phonation (2 of 3)

Voice is normal during this view of phonation. Dotted line indicates the outline of the original cyst, as much was delivered from within the aryepiglottic cord.

Respiration (3 of 3)

A closer view during respiration.

Anterior Saccular Cyst

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Anterior saccular cyst (1 of 4)

Breathing position, with a saccular cyst protruding from the right anterior ventricle (left of image). The cyst’s location, color, and superficial vessels indicate that it is neither a polyp nor granuloma.

Closer view (2 of 4)

Still closer view (under strobe light), breathing position, showing that the cyst does not arise from the cord, but appears to be depressing the anterior end of the right cord (left of image) slightly. On the left cord is an incidental finding of margin swelling, which is unsurprising in this very talkative individual.

Cyst vibrates when speaking (3 of 4)

Phonation, strobe light, open phase of vibration. The laryngeal vestibule between the false cords is partially blocked. The cyst occasionally participates in vibration, making an extra sound.

Anterior saccular cyst (4 of 4)

Phonation, strobe light, closed phase of vibration.

Bilateral Anterior Saccular Cysts

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Bilateral anterior saccular cysts (1 of 6)

Bilateral anterior saccular cysts (faint dotted lines), with vocal cords in open, breathing position. The right cyst (left of image) is larger than the left. These present only into the ventricle, and not significantly upwards into the false cords, nor downwards to press down on the true cords.

Phonation (2 of 6)

Phonation, at a high pitch, so that the laryngeal vestibule (the “airspace” above the vocal cords) is mostly open. Voice sounds normal.

Bilateral anterior saccular cysts (3 of 6)

Phonation at a high pitch again, but under strobe lighting, and at the closed phase of vibration. Note that there is good vibratory closure and that neither cord is pushed down by the cysts; again, the voice sounds normal at this pitch.

Bilateral anterior saccular cysts (4 of 6)

Phonation at a high pitch again, under strobe lighting, but at the open phase of vibration. Note that the cords aren’t impaired from oscillating laterally; again, the voice sounds normal.

Bilateral anterior saccular cysts (5 of 6)

Phonation at a mid-range pitch. The vocal cords shorten at this pitch, which constricts the laryngeal vestibule (up-down pairs of arrows) and brings the saccular cysts further over the cord (left-right arrows). Voice is still fairly normal.

Bilateral anterior saccular cysts (6 of 6)

Phonation at a low pitch. The laryngeal vestibule constricts even further (up-down pairs of arrows), bringing the cysts, especially the larger one, further yet over the cords ( left-right arrows), so that they interfere more with vibration. Voice at this pitch sounds congested or bottled up.

Removal of Lateral Saccular Cyst, Endoscopic Approach

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Lateral saccular cyst removal, endoscopic approach (1 of 4)

Note margin of false cord, at line of arrows.

Lateral saccular cyst removal, endoscopic approach (2 of 4)

Removal begins by excising the false cord margin in order to dissect downward to the lining of the saccule.

Lateral saccular cyst removal, endoscopic approach (3 of 4)

After removal, see upper border of inner surface of thyroid cartilage, at dotted line (distal end of laryngoscope aimed laterally towards neck contents).

Lateral saccular cyst removal, endoscopic approach (4 of 4)

In-line view of vocal cords at conclusion of surgery.

Removal of Lateral Saccular Cyst, External Approach

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Lateral saccular cyst removal, external approach (1 of 3)

Right of photo is superior, at chin. Note dome of cyst at arrow.

Lateral saccular cyst removal, external approach (2 of 3)

Near completion of dissection, cyst has ruptured and spilled its contents.

Lateral saccular cyst, external approach: Series of 1 photo

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Lateral saccular cyst external approach

Lateral saccular cyst, external approach (1 of 1)

The hemostat in the lower photo points to the upper part of the thyroid cartilage. The neck of the sack is being followed over the top of the cartilage and between the thyroid cartilage and soft tissue, to its origin at the ventricle.

Saccular Cyst with Extensive Oncocytic Metaplasia

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Spherical submucosal mass (1 of 7)

Spherical submucosal mass fills the left supraglottis (right of photo) and bulges into the medial left pyriform sinus, best seen using a “trumpet maneuver”.

Closer view (2 of 7)

Close range endoscopy shows that although the mass obscures the left true vocal cord (right of photo), it is clearly separate.

Preoperative CT (3 of 7)

On preoperative CT, the homogeneous, smoothly-marginated mass pushes superiorly into the preepiglottic space.3

Post laser resection (4 of 7)

Two months after endoscopic transoral laser resection. The normal contours of the supraglottis and medial pyriform have been restored, and the left vocal cord (right of photo) is now fully visible. Her voice has returned to normal.

Postoperative CT (5 of 7)

3 month postoperative CT shows complete excision of mass.

Pathology diagnosis (6 of 7)

Saccular cyst with extensive oncocytic metaplasia. Note the presence of both respiratory ciliated mucosa and granular oncocytic cells in the cyst lining.

Portion of cyst (7 of 7)

Portion of the cyst, lined by oncocytes.

Polyp or Cyst?

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Hoarseness (1 of 4)

During an upper respiratory infection, this older woman developed hoarseness that has not gone away during the past year. Is this the end stage perhaps of a hemorrhagic polyp?

Position of lesion (2 of 4)

In this slightly closer view, with the patient breathing out, the lesion appears too “high” within the laryngeal vestibule, and not truly at the level of the vocal cords.

Close view (3 of 4)

This close view is on the way to determining if there is any attachment to the vocal cords themselves. Not quite yet able to tell…

Anterior saccular cyst (4 of 4)

The tip of the scope has just passed the lesion and the vocal cords are unaffected. As it appears to be arising from the ventricle, it could be classified as an anterior saccular cyst. Likely the saccule or a mucus gland became plugged due to inflammation during the upper respiratory infection a year earlier, and it filled with mucus.

Anterior Saccular Cysts, Swellings, and Mucus: What’s the Main Issue?

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Are cysts the main issue? (1 of 4)

An experienced R & B singer has begun to experience loss of clarity and a “paper rattling” sound especially upper range. Are the bilateral saccular cysts (arrows) the explanation? Let’s look closer.

Closer range (2 of 4)

At closer range and higher pitch of G4 (392 Hz) produced with light falsetto, now we can also see bilateral margin swellings and a tiny capillary “dot.” Is this the explanation? Let's look further.

Pressed chest voice (3 of 4)

Now using pressed chest voice more typical of the patient’s singing style at E4 (330 Hz), the saccular cysts come into greater contact and considerable mucus begins to form.

Vibrating cysts and mucus (4 of 4)

Detailed review at the same pitch reveals that the rattling sound comes from a combination of vibratory participation of the saccular cysts, and a “boiling” sympathetic vibration of the mucus. If hydration, and a brief reflux trial do not help, the cysts will be removed.

Anterior Saccular Cysts as Incidental Finding

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Polyps? (1 of 3)

This man was examined elsewhere for another reason and sent for evaluation of “polyps” in his larynx. Notice the anterior saccular cysts protruding from the anterior ventricle and false cord margin bilaterally (see arrows). He considers his voice to be normal.

Cysts, not polyps (2 of 3)

At closer range, asterisks mark each cyst.

No voice disturbance (3 of 3)

During voice making, notice that neither cyst presses downwards on the vocal cords. That is why voice is normal. Cysts of this sort, diagnosed by intense visual criteria, can be followed once or twice at long intervals, and only occasionally need to be removed due to voice disturbance.


A sarcoma is a malignant tumor that originates in mesenchymal tissue. Mesenchymal tissue comprises muscle, bone, fat, connective tissue, blood vessels, and cartilage. If, instead, a malignancy originates in lining or covering tissues—which includes skin, bronchial tubes, the lining of the mouth, throat, and gastrointestinal tract, and breast and salivary gland ducts—then that tumor is called a carcinoma.

Carcinomas are far more common than sarcomas, and sarcomas involving the larynx are rare, with chondrosarcoma (“chondro-” refers to cartilage origin) heading the list. The clinicians at our laryngology practice have seen hundreds of carcinomas in their career, but probably no more than 20 sarcomas.

Photos of Sarcoma

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Sarcoma (1 of 2)

Sarcoma of larynx. The tumor nearly fills the glottis.

Sarcoma (2 of 2)

Closer view, showing the posterior commissure airway.


Refers to fibrous tissue that remains after healing of an injury. In laryngology, leaving trauma out of the picture, scarring is most often seen in the context of surgery, radiation, or prolonged use of an endotracheal tube. If a wound is created, such as after removing a superficial vocal cord cancer, the tissue that results after complete healing is not as flexible as normal tissue would be; the scarred area typically does not vibrate well, or at all. Sometimes progressive fibrosis occurs after radiotherapy. It is thought that the reduced blood supply and lowered tissue oxygen level caused by radiation damage to microvasculature leads to the gradual replacement of tissue with fibroblasts, because they can tolerate lower tissue oxygen levels.

Breathing Tube Injury—A Rare Complication of Intubation for General Anesthesia

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Inflamed vocal cord (1 of 5)

This patient had severe voice change after intubation for a 2-hour surgical procedure. She says voice was 100% before surgery and she awakened at 15%, a whisper with a bit of voice mixed in. Fortunately, across six weeks she has recovered partially to “70%.” The right cord (left of photo) looks “inflamed.”

Closer view (2 of 5)

At closer range, a little more detail is seen.

Scarring from intubation tube (3 of 5)

Under narrow band light, it appears that there is scarring of that fold likely from a laceration upon insertion of the tube. (She was told intubation was difficult.) A key finding, however: the right vocal process is turned slightly laterally, suggesting weakness of the LCA muscle.

Mucosal Injury (4 of 5)

Under strobe light, closed phase of vibration, it is almost as if there is loss of mucosa upper surface of right cord.

Flaccidity of right vocal cord (5 of 5)

Open phase of vibration shows flaccidity of the right cord, with a much larger lateral excursion / amplitude of open phase on the right (left of photo).

Conclusion: While we try to explain abnormality due to one cause, here, the patient has a mucosal injury and paresis of right TA and LCA muscles, which can also follow intubation. This explains why the initial postop voice was so weak and whispery, and also the rapid partial improvement. This voice will likely continue to improve and be very functional as a speaking voice. Fortunately, this person is not a singer, as clarity especially in upper notes, will likely be remain impaired even after full recovery.

Secondary Gain

Advantage gained from holding on longer than necessary to an illness—be it organic or nonorganic. At our practice, the phenomenon of secondary gain is most commonly seen in nonorganic voice and breathing (tracheal or laryngeal) disorders. An example might be that a person consciously or subconsciously maintains “laryngitis” after the initial organic infection has resolved, for the secondary gain of being excused from school or work. In this case the loss of voice is “worth it” as compared with the “gain” achieved. The secondary gain may have to do with attention, avoiding a responsibility, punishing or controlling another person, or possibly other issues.


Sedation is a state of reduced excitement or anxiety induced by the administration of sedative agents such as lorazepam (Ativan) and diazepam (Valium). At our practice, we occasionally administer lorazepam, given orally a couple of hours before a procedure, to allay anxiety.

Segmental Vibration

In the normal larynx, segmental vibration occurs when both chest and falsetto (head) registers are produced by vibration of the anterior 2/3 of the vocal cords. The posterior 1/3 is “inhabited” by the arytenoid cartilage and does not vibrate.

In certain pathological circumstances such as displayed in the photo sequences below, only a small part of the vocal cords vibrates.

This segmental vibratory phenomenon is typically seen in vocal cords that are damaged—such as by vocal nodules, polyps, cyst, scarring, etc. In such persons, upper voice is typically particularly impaired, until, as the person continues to try to ascend the scale, suddenly a crystal-clear “tin whistle” kind of voice emerges and may continue upwards to very high pitches.

Some in the past have talked about flagelot, flute, bell, or whistle register.  We suspect that this was in the days before videostroboscopy and at least in some cases may have been segmental vibration.

The best way to determine if what sounds like a “tin whistle” upper voice extension is due to segmental vibration is by videostroboscopic examination during that kind of phonation. The other way is for the individual to produce their “tin whistle” kind of voice very softly and then try to crescendo. If full length vibration, smooth crescendo will be possible. If segmental, there will be a sudden “squawk” as the vocal cords try to go (unsuccessfully) from segmental to full-length vibration.


Segmental Vibration Compared to Full-length

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Translucent polypoid swellings (1 of 4)

A younger man with chronic hoarseness due to large translucent polypoid swellings, not seen well at closed phase of full-length vibration at E3 (165 Hz).

Open phase, E3 (2 of 4)

Open phase of vibration at the same pitch showing that the full length of both cords swings laterally. Now the large polyp left vocal cord (right of photo) is easily seen.

Closed phase, E4 (3 of 4)

At E4 (330 Hz), vibration is damped (not allowed) except for the short anterior segment indicated by arrows.

Open phase, E4 (4 of 4)

At the same pitch, but open phase of vibration of that same short segment.

Whistle Register or Tin-whistle Segmental Vibration?

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Closed phase (1 of 4)

Closed phase of vibration at C4 (~ 262Hz) in a woman who is chronically hoarse and is a "vocal overdoer". Note the early contact at the bilateral swellings (right greater than left), and the MTD posturing (separation of vocal process "grey" zone posteriorly).

Open phase (2 of 4)

Open phase of vibration, shows that the entire length of the vocal cord margin participates in vibration at this pitch.

Segmental vibration (3 of 4)

Segmental vibration at F5 involves only the short anterior segment (brackets). The vocal cord swellings do not vibrate, nor does the posterior vocal cord. This is the closed phase of vibration.

Whistle register (4 of 4)

Open phase of that tiny anterior segment. This imparts a truly tiny "tin whistle" quality that cannot be maximized to a volume above beyond pianississimo. In some cases, singers who have not seen their vocal cords at this kind of high magnification under strobe light believe this to be a normal "whistle register".

Search not Only for Nodules, but Also for Segmental Vibration and Look at the Posterior Commissure for MTD

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Open phase (1 of 4)

In a young pop-style singer, the open phase of vibration under strobe light at C#5 (554 Hz). This magnified view is best to see the large fusiform nodules.

Closed phase (2 of 4)

Closed phase of vibration at the same pitch shows touch closure—that is, that the nodules barely come into contact.

Segmental vibration (3 of 4)

Even when patients are grossly impaired in the upper voice as is the case here, the clinician always requests an attempt to produce voice above G5 (784 Hz), in order to detect segmental vibration. Here, the pitch suddenly breaks to a tiny, crystal-clear D6 (1175 Hz) Only the anterior segment (arrows) vibrates.

Posterior commissure (4 of 4)

A more panoramic view that intentionally includes the posterior commissure to show that the vocal processes, covered by the more ‘grey’ mucosa (arrows), do not come into contact. This failure to close posteriorly is a primary visual finding of muscular tension dysphonia posturing abnormality.

Sulcus and Segmental Vibration

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Glottic sulci (1 of 4)

Closed phase of vibration, strobe light, at G3 (196 Hz) in a young high school teacher/ coach who is also extremely extroverted. Faint dotted lines guide the eye to see the lateral lip of her glottic sulci.

Open phase (2 of 4)

Open phase of vibration at the same pitch, showing full-length oscillation.

Closed phase (3 of 4)

Closed phase of vibration at E-flat 5 (622 Hz). Arrows indicate closure of the short oscillating segment.

Segmental vibration (4 of 4)

Open phase of vibration also at E-flat 5, Only the tiny segment opens significantly. As expected the patient’s voice has the typical segmental “tin whistle” quality.

Open Cyst and Sulcus; Normal and Segmental Vibration

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Margin swelling (1 of 6)

Breathing position of the vocal cords of a very hoarse actor. Note the margin swelling of both sides. The white material on the left vocal cord (right of photo) is keratin debris emerging from an open cyst. Find the sulcus of the right vocal cord (left of photo) which is more easily seen in the next photo.

Narrow band light (2 of 6)

Further magnified and under narrow band light. The right sulcus is within the dotted outline. Compare now with photo 1.

Open phase, strobe light (3 of 6)

Under strobe light, open phase of vibration at A3 (220 Hz). The full length of the cords participate in vibration.

Closed phase, same pitch (4 of 6)

At the same pitch, the closed phase again includes the full length of the cords.

Segmental vibration (5 of 6)

At the much higher pitch of C5 (523 Hz) a “tin whistle” quality is heard and only the anterior segment (at arrows) is opening for vibration. The posterior opening is static and not oscillating, as seen in the next photo.

Closed phase (6 of 6)

The closed phase of vibration involves only the tiny anterior segment of the vocal cords, at the arrows. The posterior segment is not vibrating and is unchanged.

Tiny Vibrating Segment Gives Tiny Tin Whistle Voice

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Prephonatory instant (1 of 6)

This young woman has been hoarse for many years. This preparatory posture shows marked separation of the cords posteriorly, suggesting MTD as well.

Phonation (2 of 6)

Now producing voice, with vibratory blur of the entire length of the cords on both sides.

Gaps due to nodules (3 of 6)

Under strobe light at a lower pitch of A4 (440 Hz), closed phase of vibration. Large gaps anterior and posterior to the polypoid nodule(s) explain breathy quality and short phonation time.

Open phase (4 of 6)

Open phase of vibration also at A4 (440 Hz) shows that the full length of the vocal cords are vibrating. Compare with the following two photos.

"Tin whistle" sound (5 of 6)

Now at A5 (880 Hz), the patient can only make an extremely tiny (tin whistle) quality. The only segment vibrating is within the circle (here, closed phase). The posterior segment does not vibrate.

"Tin whistle" at open vibration (6 of 6)

Still at A5 (880 Hz), the open phase of vibration, again of *only* the tiny anterior segment.

Sensory Neuropathic Cough

A chronic cough disorder that is thought to have a neurogenic cause. Sensory neuropathic cough (SNC)1 is also sometimes referred to as a cough caused by “laryngeal sensory neuropathy,” or is sometimes grouped within the more general category of “refractory chronic cough.”

Symptoms of sensory neuropathic cough:

A person with SNC may cough dozens to hundreds of times per day, often also waking up at night to cough. A few of these daily coughing attacks may become violent and last 30 seconds to several minutes. The person’s eyes may tear up and the nose may run; the person may gag or throw up; the person may leak urine, or worse; a few of our patients have even broken one or more ribs during a violent coughing attack.

A key characteristic of SNC is that a coughing attack is typically, though not always, preceded by an abrupt sensation in the throat; this sensation may be described as a “tickle,” a “sudden dry patch,” “like inhaling a powdered doughnut,” “dripping mucus,” or something else.

Possible explanation for sensory neuropathic cough:

SNC is thought to be a relative to neuralgia, like post-herpetic neuralgia (persistent pain long after an outbreak of shingles has resolved), or even diabetic neuropathy (“I feel bees stinging my feet”), except that the sensations felt by SNC patients are not painful. With SNC, it may be that the nerve endings in a person’s throat have become damaged, so that they “misfire” and cause this cough-provoking tickling or similar sensations.

Treatment for sensory neuropathic cough:

Many individuals with SNC have found relief through use of a neuralgia medication, such as amitriptyline,2, desipramine3, gabapentin4, pregabalin, oxcarbazepine, and others.

These kinds of medications may help to reduce or abolish a person’s coughing by diminishing the nerve-ending “misfires” caused by SNC. In our experience, patients sometimes need to work through more than one of these neuralgia medication options, at varying dosage levels, before they arrive at a satisfactory degree of relief. Another treatment option that can be tried is capsaicin. For more about treatment, see our second video below.


Interview with a SNC patient:

Second interview with a different SNC patient:

SNC and throat clearing of 36 Years’ duration:

Fourth interview with a different SNC patient:

SNC cough phenomenology: different than that of pneumonia, asthma, or acid reflux!

Note: Some aspects of these patient’s experiences are atypical; not every patient has the same experience with SNC.


Bruise caused by cough: Series of 2 photos

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Closer view of bruise (2 of 2)

A person with violent sensory neuropathic coughing may injure the vocal cords, as illustrated by this bruise, right vocal cord (left of photo).

Bruise caused by violent coughing (1 of 2)

Closer view of bruise, with small collection of white mucus in the middle.

Bruising from sensory neuropathic cough

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Bruising from SNC (1 of 1)

This individual occasionally coughs to the point of hoarseness. Particularly noteworthy is the subglottic bruise (arrow, dotted line) caused by profound Valsalva-retching kind of coughing. The rest of the right cord (left of photo) is also bruised.

Vocal cord bruising from coughing

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Bruise from coughing (1 of 3)

This man had an episode of aggressive coughing a week earlier. Note the bruising over the vocal processes, which receive the major collisional force during coughing.

Pre-phonatory instant (2 of 3)

The vocal processes are approaching the point of touching (contact would occur gently with onset of talking and more aggressively with coughing).

Phonation (3 of 3)

Vocal cords are now in full contact. Note the unrelated moderately-severe vocal cord bowing.


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sensory neuropathic cough

SNC patient (1 of 6)

A very worried patient with sensory neuropathic cough has scheduled a return appointment. On arrival she states that she cannot rest due to a trace of hemoptysis a week earlier. What begins as a simple upper aerodigestive tract examination represented by this view of her normal nasopharynx is easily expanded…
base of tongue, hypopharynx, and laryngeal vestibule

Panoramic view (2 of 6)

Detailed inspection of base of tongue, hypopharynx, and laryngeal vestibule, represented by this panoramic view, also show no abnormality. And the examination can continue…
upper trachea

Lidocaine (3 of 6)

Simple instillation of lidocaine into the trachea allows this view into the upper trachea.

Carina (4 of 6)

And this view, with the carina in clear view.
right mainstem bronchus

Right mainstem bronchus (5 of 6)

Deep inside right mainstem bronchus and…
Left mainstem bronchus

Left mainstem bronchus (6 of 6)

...into left mainstem bronchus also reveal no lesions and no “trail of blood.” Simple watchful waiting for more hemoptysis is acceptable to the patient. CXR is optional in the near-term.


Sensory Neuropathic Cough, Part I: Coughing That Won’t Go Away
Sensory neuropathic cough is a chronic cough condition that does not respond to the usual treatments. Many individuals who have been coughing for years find relief from treatment with “neuralgia” medications.
Sensory Neuropathic Cough, Part II: Medications
In this video, Dr. Bastian introduces potential medications to treat sensory neuropathic cough.
Still Coughing After COVID? | Sensory Neuropathic Cough (SNC)
In this video, Dr. Robert W. Bastian explains three explanations for coughing in the context of Covid-19 infection, with emphasis on the potential for sensory neuropathic cough (Phase 3).

  1. Bastian RW, Vaidya AM, Delsupehe KG. Sensory neuropathic cough: a common and treatable cause of chronic cough. Otolaryngol Head and Neck Surg. 2006; 135(1): 17-21. 

  2. Jeyakumar A, Brickman TM, Haben M. Effectiveness of amitriptyline versus cough suppressants in the treatment of chronic cough resulting from postviral vagal neuropathy. Laryngoscope. 2006; 116: 2108-2112. 

  3. Bastian ZJ, Bastian RW. The use of neuralgia medications to treat sensory neuropathic cough: our experience in a retrospective cohort of thirty-two patients. PeerJ. 2015; 3:e816. 

  4. Ryan NM, Birring SS, Gibson PG. Gabapentin for refractory chronic cough: a randomized, double-blind, placebo-controlled trial. Lancet. 2012; 380(9853): 1583-9. 


Attached completely at the base and without an intervening stalk; the opposite of pedunculated.

Shattered vibration

Shattered vibration is a chaotic kind of vibration in which there may be several independent segments vibrating erratically to create a characteristic sound quality. May be seen, for example, in an individual who has vocal cords that are not symmetrical with respect to vocal cord mass, flaccidity, and tension, and that are not “of one piece” within themselves, so that a fold may have two different vibratory patterns within itself.


The cycle-to-cycle variability of the period amplitude of vocal cord vibration. Shimmer is used as one of the measures for the micro-instability of vocal cord vibrations. Given that shimmer may vary dramatically with changes of voice production within the same voice, and also that a given shimmer measurement is non-specific to any particular voice disorder, this measure is considered superfluous to the integrative diagnostic model. Shimmer is therefore not used routinely at our practice.


A highly inert silicone rubber that has wide use for medical applications. The term silastic comes from the combination of the words silicone and plastic.

Laryngologists commonly place silastic implants into flaccid, paralyzed vocal cords in order to plump and firm them up so that they can serve as better partners to the non-paralyzed cord. See also: medialization laryngoplasty.


Extrusion of Vocal Cord Implant

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Extrusion of vocal cord implant (1 of 3)

Patient with a paralyzed left vocal cord (right of image), who several years ago had successful medialization of that cord with a silastic wedge. More recently, several months ago, she noticed pain and swelling during some intense aerobic activity and then a persistently roughened voice quality. This view shows that the left cord is inflamed.

Extrusion of vocal cord implant (2 of 3)

Strobe lighting. Note the convex shape of the left cord’s anterior end (the lower end, in this photo). This convexity is not caused by over-medialization, but instead by the inflammatory reaction.

Extrusion of vocal cord implant (3 of 3)

Closer view shows that the problem is exposure of the silastic implant. The actual silastic is bare at the arrow. Whitish exudate covers the remaining exposed implant. This is a rare event after medialization with a silastic implant.

Silent aspiration

Aspiration that does not provoke an expected, normal response of coughing or throat clearing. Silent aspiration suggests a very high risk of aspiration pneumonia.

Singing voice qualified

Singing voice qualified, when used to refer to a speech pathologist or physician, means that the clinician has personal knowledge of the expected phenomenology and capabilities of the voice, including those only encountered in the singing voice. Typically, this kind of qualification comes from personal voice training and singing experience on the part of the clinician.

Single Modality Treatment

Single modality treatment refers to a situation in which only one treatment modality is chosen from among several options available for that disease process. This is in contrast to combined modality treatment or even multi-modality treatment.


An uninterrupted sound that begins very low in a person’s vocal range and ascends to a very high pitch, sometimes the highest possible pitch that person can produce. A single siren could also go from low to high and back to low one or more times without interruption. A clinician might ask a patient to perform a siren during the vocal capability battery in order to assess pitch range capability or even vocal skill.


SLAD-R (Selective laryngeal adductor denervation-reinnervation). This procedure was introduced by Dr. Gerald Berke of UCLA in the late 1990’s. It is a surgical option for adductory spasmodic dysphonia. The concept is to sever the anterior branch of the recurrent laryngeal nerve. This denervates the spasming laryngeal adductors (particularly thyroarytenoid and lateral cricoarytenoid muscles). The squeezed, strained quality and/ or “catching, cutting out, stopping” of the voice are replaced initially with an extremely breathy and weak voice. This initially weak voice is analogous to what one might sound like after a Botox injection that is far too high a dose. To return strength to the voice, a branch of the ansa cervicalis nerve that normally supplies some relatively “unimportant” neck muscles is anastomosed (connected) to the severed nerve. It takes 3 months to a year for tone to begin to return to the adductory muscles. Since the “unimportant” neck muscles were not affected by the dystonia, the hope is that the new nerve supply to the laryngeal muscles may not be affected by dystonia.


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Six years post SLAD-R (1 of 4)

Six years after SLAD-R performed elsewhere. Note that re-innervation appears greater for left (right of photo) than right (left of photo) thyroarytenoid (TA) muscle. Signs of continuing atrophy of the TA muscle within the right cord (left of photo) include capacious ventricle ('V'); absence of “conus” ('C') bulk below the free margin (see contrast between /--/ on both sides); slight concavity or bowing of the free margin; and narrower band of the vocal cord itself that we sometimes refer to as the “spaghetti-linguini” larynx.

TA + LCA muscles (2 of 4)

While TA is more recovered on the left (right of photo) as seen in photo 1, here we see that the lateral cricoarytenoid (LCA) muscle has recovered more on the right (left of photo). At the prephonatory instant, the failure of the left (right of photo) vocal process to turn to the midline indicates continuing weakness of the LCA muscle.

Greater amplitude of right cord (3 of 4)

Under strobe illumination, open phase of vibration shows greater amplitude of right cord (left of photo), consistent with the atrophy of the permanently somewhat weak TA muscle seen in photo 1.

Patient has returned to Botox (4 of 4)

Closed phase of vibration. A few years after SLAD-R, this man’s spasms recurred sufficiently that he has resumed Botox injections.


One Man’s Experience Over Time with SLAD-R
SLAD-R is a surgical alternative to ongoing “botox” injections for treatment of adductory spasmodic dysphonia. The surgery involves intentionally cutting the nerves that close the vocal cords for voice and reconnecting a different nearby nerve supply (reinnervating the nerves). This surgery requires the patient’s willingness to endure an extremely breathy voice for many months after the procedure, while awaiting reinnervation.

Smoker’s Polyps

Diffuse swelling of the vocal cords, due to build-up of edema fluid within the mucosa. Smoker’s polyps are also referred to as Reinke’s edema or polypoid degeneration.

Audio with photos:

Voice sample of a patient with smoker’s polyps, BEFORE surgery (see this patient’s photos just below):

Same patient, two months AFTER surgery (the occasional syllable dropouts are due to the recentness of surgery):

Smoker’s Polyps, before and after Surgery

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Smoker's polyps, BEFORE surgery (1 of 4)

Even during quiet breathing, the convexity of the vocal cord margins (dotted lines show where normal margins would be) reveal the presence of smoker's polyps.

Smoker's polyps, BEFORE surgery (2 of 4)

During inspiratory phonation: the polyps are drawn inward and are easier to see.

Smoker's polyps, AFTER surgery (3 of 4)

Two months after surgery, during quiet breathing. The vocal cord margins are now straight.

Smoker's polyps, AFTER surgery (4 of 4)

During inspiratory phonation: the margins are drawn into a mildly convex contour, but far less than preoperatively. The patient's voice is also much improved, albeit the occasional syllable dropouts due to recentness of surgery (listen to this patient's voice samples in the audio section of the encyclopedia entry).


Smoker’s Polyps / Reinke’s Edema

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Smoker’s polyp / Reinke’s edema (1 of 2)

Quiet breathing, under standard light. The edematous mucosa is not yet evident.

Smoker’s polyp / Reinke’s edema (2 of 2)

Elicited inspiratory phonation in-draws and thereby reveals the edematous mucosa, greater on the right (left of image) than the left. The dashed lines indicate the normal location and contour of the vocal cords' free margins.

Smoker’s Polyps with Leukoplakia

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Long-term smoker (1 of 4)

A long-term smoker whose (female) voice has become deep and rough. Note the rounded (convex) vocal cord margins, "fat" vocal cords, and hazy leukoplakia. Interarytenoid pachyderma can be from acid reflux or chronic smoking.

Forced inspiration (2 of 4)

Forced inspiration sucks the excess polypoid tissue inward and reduces the space available for air to pass, explaining the harsh inspiratory noise one hears at the same time.

Closer view (3 of 4)

Closer visualization.

Rapid inspiration (4 of 4)

Rapid inspiration. The demarcation of the leukoplakia is seen well here.

Smoker’s Polyps / Reinke’s Edema

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Smoker’s polyps / Reinke’s edema (1 of 3)

This patient is a long-term smoker, and also is talkative. Her voice has been gradually deepening for years. Here, with the vocal cords in abducted breathing position, one can only see somewhat underwhelming, broad-based, low-profile swelling, along with some hazy leukoplakia in the mid-cord.

Smoker’s polyps / Reinke’s edema (2 of 3)

Phonation. Again, there is only very low-profile, broad-based convexity of the margins, and again, the hazy leukoplakia in the mid-cords.

Smoker’s polyps / Reinke’s edema (3 of 3)

Elicited inspiratory phonation. Now, one can see that, contrary to the appearance in the prior two views, this patient in fact has moderate-sized “smoker's-type” polyps, aka Reinke’s edema. The increased mass explains the virilization of the sound of this woman’s voice.

Smoker’s Polyps in Various “Poses”

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Smoker’s polyps in various “poses” (1 of 4)

Vocal cord abduction for breathing, during expiratory phase. Left polyp (right of photo) appears to be the only finding. This is in a middle aged smoker with several years of gradually deepening / masculinized and now rough voice. The black dot and white "X" are reference points, facilitating comparisons with the other photos.

Polyp begins to fall off (2 of 4)

At the beginning of elicited rapid inspiration, showing the polyp beginning to be displaced from upper surface to the margin. That is, previously-unseen polypoid tissue (at " X") is now indrawing from upper surface of the right cord (left of photo) as well, and margin has become convex rather than straight as it was in photo 1.

Polyps displace (3 of 4)

The left-sided polyp (right of photo) is now displaced below the margin of that cord. The right polyp (left of photo) is now fully displaced/ indrawn to the margin of the right cord (left of photo).

Edematous tissue causes a rough voice (4 of 4)

During voice-making, most of the edematous tissue relocates back to the upper surface of the cords where it vibrates chaotically to add not only masculine but also rough voice quality.

Smoker’s Polyps and Thulium Laser

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Pre-laser surgery, respiration (1 of 12)

During respiration, showing the large right vocal cord (left of photo) smoker’s-type polyp. The voice is accordingly deep, rough, and effortful to produce.

Pre-laser surgery, onset of phonation (2 of 12)

Onset of phonation, with vibratory blurring, and showing the mismatch of the cords.

Pre-laser surgery (3 of 12)

Just before starting laser treatment, in-drawing of large right vocal cord polyp (left of photo).

During laser surgery (4 of 12)

Mostly contact mode Thulium laser treatment. The glass fiber is piercing the polyp to deliver laser energy to the gelatinous content of the polyp.

Post surgery, 28 days later (5 of 12)

28 days later, the upper 2/3 of this gelatinous polyp has sloughed away, but the portion on the free margin “escaped,” and remains visible.

Second laser surgery (6 of 12)

A second Thulium laser treatment of the residual polyp.

Post surgery, 21 days later (7 of 12)

Twenty-one days after second laser treatment , the polyp is no longer seen. Voice is dramatically improved from the time of original evaluation. Mild right vocal cord (left of photo) inflammatory changes remain, as expected.

Post surgery, in-drawing of vocal cords (8 of 12)

At same examination, after asking the patient to produce inspiratory phonation, notice the indrawing of both vocal cord margins, consistent with mild residual Reinke’s edema.

Post surgery, one year later (9 of 12)

One year later. Voice remains excellent.

Post surgery, residual Reinke's edema (10 of 12)

With inspiratory phonation, the patient is able to in-draw to a convex vocal cord margin bilaterally, again indicating residual Reinke’s edema.

Post surgery, closed phase of vibration (11 of 12)

Strobe light: mostly closed phase of vibration.

Post surgery, open phase of vibration (12 of 12)

Strobe light: open phase of vibration, showing good oscillatory flexibility of both cords.

Reinke’s (smoking-related) edema and how to see it: Series of 4 photos

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Convexed vocal cords (1 of 4)

Abducted, breathing position. Note that the margin of both vocal cords is slightly convex. See dotted line for normal, perfectly straight margin.

Inspiratory phonation (2 of 4)

Inspiratory phonation in-draws the mild Reinke’s edema (smoker’s type polyp formation).

Open phase, faint translucency (3 of 4)

Strobe illumination, at E4 (approximately 330 Hz), mostly open phase.

Closed phase, faint translucency (4 of 4)

Note again in closed phase.

Smoker’s Polyps with Two Explanations for Bruising

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Bruising of left vocal cord (1 of 4)

With a 40-year smoking history, this woman has a masculine voice quality. She is often called “sir” on the phone by people who don’t know her. Note her large smoker’s polyps. The left vocal cord (right of photo) has suffered a recent bruise. As a quiet person, the explanation for her bruise may not be due to vocal overuse, but may be due in part to her use of aspirin.

A year later (2 of 4)

A year later, she returns for re-examination. The bruising has resolved. However, the convex margins and translucence remain. Note the large ectatic capillaries, that may have (along with aspirin) increased vulnerability to the bruising that happened a year earlier (see photo 1).

Inspiratory phonation (3 of 4)

The elicitation of inspiratory phonation makes the left-sided polyp (right of photo) even more obvious.

Translucent polyp, different view (4 of 4)

A different inspiratory view sucks the left polyp (right of photo) underneath the right (left of photo), and now the right-sided more translucent polyp (left of photo) is more obvious.

Smoker’s Polyp Reduction Improves Voice Even Though the Larynx Result May not be “Pretty”

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Smokers Polyp (1 of 5)

Six years after vocal polyp removal elsewhere. As a result of continued smoking, the voice is deep and rough, and an obvious recurrent/residual "smoker's" polyp is seen on the right vocal cord(arrow, left of photo). The patient "hates" her rough and masculine voice quality.

Reine's edema (2 of 5)

Inspiratory phonation is elicited to "pull" the redundant tissue medially, revealing a lot of Reine's edema of the left vocal cord, too. The dotted lines show the ellipse of mucosa that will be removed during surgery. Mucose will be preserved at the margins and the gelatinous lateral within the polyps will be suctioned away if liquid, and dissected away if fibrotic.

A week after surgery (3 of 5)

The dotted lines show the extent of mucosal excision—an area that will take a few weeks to re-mucosalize. Since this was a polyp "reduction," though hoarse this early post, she has a " functional" voice. There should be no alarm if patients are aphonic for a week or even a few weeks while inflammation resolves.

Residual Reinke's edema (4 of 5)

At two months post, the patient is very pleased and says the improvement to voice is "large." Here, it appears there may be some residual Reinke's edema especially of the left vocal cord (right of photo) judging by the slightly convex margin.

Residual submucosal edema (5 of 5)

With inspiratory phonation, the residual submucosal edema is made obvious, especially on the left. This was (as intended) a polyp "reduction" approach, rather than polyp "removal" as the latter is too hard on voice, and it is not possible to "put back" if too much tissue is taken. Here, there is no stiffness, and if desired, more can be removed. Of course, since the patient is so pleased with her voice, no further treatment is needed.


Smoker’s Polyps (aka Polypoid Degeneration or Reinke’s Edema)
This video illustrates how smoker’s polyps can be seen more easily when the patient makes voice while breathing in (called inspiratory phonation). During inspiratory phonation, the polyps are drawn inward and become easier to identify.

Spasmodic Dysphonia: Definition and Treatments

A non-life-threatening neurological disorder in which the muscles of the larynx involuntarily spasm and interfere with the voice. Spasmodic dysphonia (SD) is a focal dystonia, in this case involving the larynx—i.e., laryngeal dystonia. Laryngeal dystonia typically affects the voice, but can occasionally also affect breathing (respiratory dystonia). The term spasmodic dysphonia refers specifically to voice-affecting laryngeal dystonia.

Adductor vs. abductor:

There are two main variants of spasmodic dysphonia (SD). In the first variant, adductor SD (AD-SD), the vocal cords are pressed together excessively, intermittently cutting off words or giving the voice a constant strangled quality; this variant comprises 90% of the cases of SD. In the second variant, abductor SD (AB-SD), the vocal cords are abruptly and momentarily pulled apart while talking, causing the voice to drop out completely or down to a whispery, breathy sound. There are some cases in which a person has both of these variants: this is called mixed AB-AD SD.

Classic vs. tonic:

Another distinction that can be made is between classic variant and tonic variant cases of SD. In classic variant SD, the spasms cause phonatory arrests—that is, while the person is speaking, intermittent words or syllables are choked off (with AD-SD) or drop out (with AB-SD). In tonic variant SD, the spasms are more continuously sustained, so that the voice continuously sounds either strained (with AD-SD) or breathy (with AB-SD), but without any actual phonatory arrests. Because the presence of phonatory arrests is the symptom most often associated with SD, tonic variant SD goes undiagnosed or misdiagnosed far more frequently than does classic variant SD.

Treatment for spasmodic dysphonia:

There is no definitive “cure” for SD, but for most patients, periodic injections of Botox™ into the muscles of the larynx help a great deal, if there is optimal dosage and placement. These injections relax the malfunctioning muscles of the larynx, thereby minimizing the spasms and their impact on the voice. The effect of an injection typically lasts a few months, and then another injection is needed. For those having difficulty getting good results with Botox™ therapy, see our video below “Spasmodic Dysphonia: When Botox Disappoints.”

The leading surgical treatment currently offered for SD, Selective Laryngeal Adductor Denervation-Reinnervation, can be an option for individuals with the AD-SD variant. However, no treatment for SD works satisfactorily for all. The history of each of the several surgical treatments for SD always includes some failures.

Speech therapy is another treatment sometimes suggested for SD. While there are strong and even passionate individual proponents of speech therapy, the consensus view is that speech therapy is not expected to substantially improve the voice’s capabilities or reduce spasms other than perhaps in the therapy room1. A brief course of speech therapy can be very helpful for patient education and perhaps a search for sensory tricks. Much confusion surrounds this subject, because individuals who have a nonorganic voice disorder can be mistakenly diagnosed with SD, and nonorganic voice disorders are routinely “cured” with speech therapy alone.


Adductory Spasmodic Dysphonia

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AD-SD (1 of 2)

Sustained, clear phonation, standard light. Note vibratory blur of the vocal cord margins. The false vocal cords (lines) are in normal relation to the true vocal cords.

AD-SD (2 of 2)

Involuntary adductory spasm. Note that the false vocal cords suddenly over-close (arrows) as a result of the adductory spasm, and voice momentarily stops (along with vibratory blur).

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AB-SD (1 of 4)

Prephonatory instant, with arytenoid cartilages involuntarily positioned apart. Mostly tonic position giving voice relatively constant breathiness.

AB-SD (2 of 4)

Phonatory blur, standard light. Again note the separation of the arytenoid cartilages posteriorly (upper end of the photo), and broad vibratory blur, both consistent with breathy voice.

AB-SD (3 of 4)

Occasionally, patient is able to bring posterior cords together for an instant of normal-sounding voice.

AB-SD (4 of 4)

An instant later, the vocal cords involuntarily separate due to an abductory spasm, dropping the voice again to a whispery quality.

Abductor Spasms, Worsened by Cognitive Loading

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Abductor spasmodic dysphonia patient (1 of 4)

Vocal cords in normal breathing position, in a person with abductor spasmodic dysphonia (SD). The next three photos show how the vocal cord spasms seen with SD can get worse when the person performs more cognitively loaded or involved tasks (that is, the person has to think more). This pattern is related to the widespread understanding that SD's symptoms can be task-specific.

Limited abductor spasms (2 of 4)

When making voice with guttural vocal fry or sustained creaky falsetto, this person is able to keep the vocal cords together, at least part of the time.

Increased abductor spasms (3 of 4)

When the person tries to sustain a sung tone (slightly more cognitively loaded), the vocal cords involuntarily separate, producing a very breathy voice.

Even greater abductor spasms (4 of 4)

When the person speaks (even more cognitively loaded), the vocal cords separate even further, and the voice's breathiness is pronounced.

Adductory Spasm

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Adductory spasm (1 of 2)

Continuous phonation, standard light. Note the position of the false cords in relation to each other, and also the distance between the anterior face of the arytenoids and the petiole of the epiglottis.

Adductory spasm (2 of 2)

A moment later, an adductory spasm occurs. The spasm may momentarily stop the voice (phonatory arrest). Note the inward squeezing of the entire supraglottis (false cords, arytenoids, and petiole).

Laryngology 401: PCA-only Paresis, but the Actual Voice Problem Is Spasmodic Dysphonia

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Sense of instability (1 of 3)

This person had a major voice change after thyroidectomy for a large goiter. Within 2 months, voice recovered fully--except for a sense of instability. The PCA-only paresis is not the explanation because voice-making muscles (TA + LCA) are intact. And in fact vocal capability testing shows that both yell and projected voice are normal. The visual finding here of vocal cord bowing and capacious ventricle do not count as a breathing position finding with PCA-only paresis due to the unopposed action of LCA muscle, combined with an uncontracted TA muscle, both of which cause pseudo-bowing.

Vibratory amplitude (2 of 3)

During phonation under strobe light, with TA tensing, "bowing" disappears. Furthermore the vibratory "blur" at the margin of the left fold (right of photo) is equal to the right (left of photo), telling us that vibratory amplitude is approximately the same on both sides.

Spasm (3 of 3)

An audible/ visible spasm occurs when the right vocal cord jerks laterally for 4 frames (~ 1/8th of a second). The problem isn't PCA weakness on the left (right of photo), but instead an abductory spasm on the right (left of photo), fully mobile cord!

Remarkable Task-Specificity of Spasmodic Dysphonia

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Young singer (1 of 4)

This young soprano has had to put singing to the side due to a peculiar instability at a very specific part of her singing range: approximately G4 to B4. Speaking voice is completely normal. Above and below G4 to B4 the voice works well. Here, during somewhat distant view during breathing, no mucosal abnormality is seen.

Phonation (2 of 4)

During phonation at high pitch designed to reveal margin swelling, there is a slight gap of “physiologic bowing” but arytenoids seem to approximate well.

Closed phase (3 of 4)

Closed phase of vibration at G4 (392 Hz). Nothing significant is seen in this admittedly somewhat distant view.

Sudden spasm (4 of 4)

Ten frames, a fraction of a second-later, a sudden spasm is seen (arrows) and heard. This adductory spasm happens consistently and repeatedly with numerous elicitations, but only in the narrow pitch range already noted in caption 1.

Assessment of Vocal Phenomenology Protects from Visual Red Herrings

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Swelling? (1 of 2)

The vocal cords of a physical education teacher with mild, intermittent ‘hoarseness’ and cracking of voice. Given her occupation, the mind goes to “voice abuse” and the margin swelling seen here might play into the diagnosis of “vocal overdoer with mucosal injury.” However, the vocal capability battery (voice testing) protects from a misdiagnosis.

Spasmodic dysphonia (2 of 2)

During the vocal capability testing (part 2 of the Integrative Diagnostic Model), one hears no significant mucosal swelling phenomenology (during application of vocal cord swelling checks), but instead a quivery, jittery instability. The actual diagnosis? Spasmodic dysphonia.

Spasmodic Dysphonia: A Peculiar Voice Disorder
Dr. Robert Bastian reviews the various types and subtypes of spasmodic dysphonia (SD). Numerous voice examples are included, along with video of the vocal folds. SD is a rare neurological disorder caused by laryngeal dystonia, and it interferes with the smooth functioning of the voice. Tiny spasms of the vocal folds may cause the voice to catch or cut out, strain or squeeze away, and sometimes to drop momentarily to a whisper.
Spasmodic Dysphonia: When Botox Disappoints
In this video, Dr. Bastian discusses common problems with Botox treatment for spasmodic dysphonia (SD) and offers clear, practical advice to increase the effectiveness of these treatments.
2014 NSDA 25th Anniversary Symposium
In this video, Dr. Bastian leads a panel discussion on Spasmodic Dysphonia.

  1. Ludlow CL. Treatment for spasmodic dysphonia: limitations of current approaches. Curr Opin Otolaryngol Head Neck Surg. 2009; 17(3): 160–165. 

Speech Pathologist

An individual who has a graduate degree (master’s or doctorate) in speech-language pathology. After successful completion of the CFY (clinical fellowship year), a speech pathologist may work behaviorally with a wide variety of conditions that affect breathing, voice, and swallowing.

Some speech pathologists are generalists, potentially working within the same day with: a child whose speech is not clear; a person who is trying to recover clear speech after a stroke; a singer with vocal nodules; and an elderly person who is aspirating when she swallows. A speech pathologist’s activities may be divided between evaluation (including by use of the videofluoroscopic swallowing study or videostroboscopy to assess the voice) and therapy or treatment – teaching and coaching the patient in ways that improve their voice, breathing, and swallowing.

At our practice, our speech pathologist is singing voice qualified, working nearly exclusively with voice and breathing disorders. Adjunct speech pathologists from Good Samaritan Hospital are typically involved with our patients who have swallowing disorders.




Spirometry measures the breathing capacity of the lungs using an instrument that measures expired lung volumes and flow-volume curves.

Squeezedown (of the voice)

A vocal phenomenology term coined to refer to adductory spasms that do not “complete” all the way to a phonatory arrest. Virtually exclusively a manifestation of spasmodic dysphonia.


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.
fenestrated tracheotomy tube within the high trachea

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.
circular scar in esophagus

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

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.
distal chip flexible scope

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

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 after curative radiation for a vocal cord cancer

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.
mucosa indraws and vibrates

Involuntary inspiratory voice (2 of 8)

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

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.
vibrating mucosa in open phase