A disorder in which the laryngeal saccule is inflated and becomes abnormally enlarged. A common symptom of a laryngocele is hoarseness.
How it develops:
The laryngeal saccule, or laryngeal appendix, is a very small blind sac—a dead-end corridor, so to speak—which is located just above the vocal cords, one on each side, and is lined with glands that supply lubrication to the cords. When a person makes voice, it is possible for a little bit of the air being pushed up out of the trachea to slip into this saccule. If over time enough air enters the saccule with enough force, the saccule may begin to be inflated and stretched out, leading to a laryngocele.
In some cases, the air that slips into and inflates the laryngocele will slip back out again as soon as the person stops making voice, so that the laryngocele abruptly inflates and deflates with each start and stop of speech or voice-making. (The photos and video below are an example of this.) In other cases, the air cannot exit the laryngocele as easily, but it may be reabsorbed slowly during quiet times or during sleep—only to be inflated again at the next instance of more active speaking.
Laryngocele vs. saccular cyst:
A much more common disorder of the laryngeal saccule (compared with a laryngocele) is a saccular cyst, which can occur if the entrance to the laryngeal saccule becomes blocked. In this scenario, air is absorbed, but secretions build up and gradually expand the saccule.
Symptoms and treatment:
A common symptom is hoarseness, because while the saccule is inflated, it may press press down on the vocal cords, not allowing them to vibrate freely, or it may block the laryngeal vestibule just above the cords and partially muffle the sound produced by the cords. Standard treatment is surgical removal, through one of two approaches: a small incision on the neck that leads into the larynx from the outside, or a laryngoscope that is inserted through the mouth and down into the larynx so that the laryngocele can be removed using a laser.
Laryngocele: Series of 5 photos
Laryngocele (1 of 5)
Before phonation begins: the laryngocele is not visible.
Laryngocele (2 of 5)
Phonation begins: the saccule suddenly begins to inflate.
Laryngocele (3 of 5)
The saccule is at peak inflation. Note how this obstructs the laryngeal airway.
Laryngocele (4 of 5)
Phonation ending: the saccule is deflating. Note the motion blur; inflation and deflation each happens in a fraction of a second.
Laryngocele (5 of 5)
Phonation ended: the laryngocele is again fully deflated and hidden from view.
Bilateral laryngocele, before and after removal: Series of 8 photos
Bilateral laryngocele (1 of 8)
Vocal cords approaching point of best closure possible (due to left cord paresis). Faint dotted lines outline the approximate boundary of each laryngeal saccule, which not yet inflated.
Bilateral laryngocele (2 of 8)
As air just begins coming upward between the cords, one can see subtle inflation (dotted lines), particularly of the right saccule (left of image).
Bilateral laryngocele (3 of 8)
As phonation continues, inflation of the (now diagnosable) laryngocele becomes obvious, and the left laryngocele (right of image) is now more obviously inflated than before, again indicated by the dotted lines.
Bilateral laryngocele (4 of 8)
Near the end of a sustained period of voicing, maximum inflation of the laryngoceles is seen (dotted lines). On the right side (left of image), the stretching mucosa is so thinned as to appear translucent.
Bilateral laryngocele, after removal (5 of 8)
Same patient, breathing position, 12 weeks after complete removal of the bilateral laryngoceles via false cord incisions (lines of incision shown by dotted lines). This patient also has long-standing paralysis of the right vocal cord (left of image) and limited mobility of the left cord, so the cords don’t open fully for breathing.
Bilateral laryngocele, after removal (6 of 8)
Phonatory position. Note the lack of inflation of the now-absent laryngoceles, and compare that with photos 3 and 4 of this series.
Bilateral laryngocele, after removal (7 of 8)
Closer view of the posterior ends of the true vocal cords during maximal abduction for breathing. Space between the vocal cords is an estimated 50% of normal, because of the paralyzed right cord and the limited mobility of the left cord.
Bilateral laryngocele, after removal (8 of 8)
Same close-up view, but during phonation. The left vocal cord (right of image) has shifted slightly toward the midline, but the cords do not actually close and, thus, the patient cannot produce glottic (true vocal cord) voice. An implant could help to close this gap, but the patient will first try developing a “false cord voice.”
Laryngocele, seen in a CT image: Series of 1 photo
Laryngocele, seen in a CT image (1 of 1)
The patient’s left-sided saccule is dilated and filled by air, forming a laryngocele (the largest black spot in the image). The right-sided saccule is not seen because it is of normal size. The two smaller black spots show air in the pyriform sinuses (a normal finding).
Laryngocele: A Cause of Hoarseness
A laryngocele is a disorder of the saccule, or laryngeal appendix, in which air abnormally expands it. Watch this video to see how a laryngocele behaves in real-time, and why that can affect the voice.
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: Series of 4 photos
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: Series of 2 photos
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: Series of 3 photos
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: Series of 2 photos
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: Series of 3 photos
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: Series of 4 photos
Subglottic / Tracheal stenosis (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.
Subglottic / Tracheal stenosis (4 of 4)
Close view, showing the inflammatory nature of the stenosis.
Hypopharyngeal stenosis: Series of 2 photos
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: Series of 2 photos
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: Series of 5 photos
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: Series of 5 photos
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: Series of 8 photos
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.
Tracheal stenosis (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.
Tracheal deformity and stenosis, before and after repair: Series of 6 photos
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: Series of 4 photos
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: Series of 4 photos
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: Series of 4 photos
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: Series of 6 photos
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: Series of 6 photos
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: Series of 4 photos
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: Series of 8 photos
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: Series of 5 photos
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: Series of 4 photos
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: Series of 6 photos
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: Series of 7 photos
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: Series of 8 photos
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: Series of 4 photos
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: Series of 4 photos
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: Series of 4 photos
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.
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.
Cryptococcus neoformans laryngitis is a rare fungal infection of the larynx. The infection usually occurs as a primary pulmonary infection but can spread to other regions of the body. Common characteristics of cryptococcus neoformans include longstanding hoarseness, sore throat, or edema of the vocal cords. Cryptococcus neoformans laryngitis is treated with oral anti-fungal medications such as fluconazole.
Photos of cryptococcus neoformans:
Cryptococcus infection of the larynx: Series of 4 photos
Panoramic view (1 of 4)
Panoramic view of laryngeal vestibule in a man with very longstanding hoarseness and sore throat. Note intense redness and bumpy mucosal surface. Biopsy revealed Cryptococcus neoformans.
Closer view (3 of 4)
Closer view of the vocal cords shows similar intense inflammation and rough surface.
One year later (3 of 4)
After a one-year course of fluconazole, an oral anti-fungal medication. Symptoms are gone. The larynx is no longer inflamed, and the mucosal surface is smooth. White area of scarring (dotted surround), and scar band (parallel dotted lines).
One year later, close-up (4 of 4)
Close-up of the vocal cords shows similar resolution of redness and cobblestoned surface.
Chronic hoarseness, papilloma (1 of 5)
60-something man with chronic hoarseness due to these lesions, seen under standard light. Biopsy shows "papilloma" and HPV testing reveals subtypes 84 & 11.
Stippled vascularity, leukoplakia (2 of 5)
At closer range under narrow band light, the stippled "HPV effect" vascularity is seen more clearly. The lesion marked by 'X' in this photo and photo 1 shows a subtle degree of leukoplakia.
Post treatment, voice is very good (3 of 5)
After several micro laryngoscopes, first using cidofovir as an adjuvant, and then avastin, the larynx looks quite clear. Voice is also very good.
Closed phase (4 of 5)
Under strobe light, closed phase of vibration.
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.
SLAD-R: Series of 4 photos
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.
Pharyngeal paralysis, seen with pharynx contraction: Series of 2 photos
Pharyngeal paralysis (1 of 2)
View of the laryngopharynx. This patient has pharyngeal paralysis on one side, which is already slightly evident because the posterior pharyngeal wall's midline (dotted line) is deviating here slightly to one side, even at rest.
Pharyngeal paralysis, more obvious with pharynx contraction (2 of 2)
The pharynx is contracted, and the posterior pharyngeal wall (midline again at dotted line) now deviates dramatically toward the non-paralyzed side of the pharynx. This pharynx contraction was elicited via extremely high-pitched voicing.
Pharyngeal paralysis: Series of 1 photo
Pharyngeal paralysis (1 of 1)
Panorama of the laryngopharynx. Note the capacious left pyriform sinus (right of photo), one strong indicator of paralysis of the pharynx on that side.
Pharyngeal paralysis: Series of 1 photo
Pharyngeal paralysis (1 of 1)
Blue-stained water swallowed by the patient has preferentially pooled in the left pyriform sinus (right of image), due to weakness of the left inferior pharyngeal constrictors.
Also known as laryngotracheitis or laryngotracheobronchitis, croup ((Meyer, Anna. “197. Pediatric Infectious Disease” Cummings Otolaryngology Head and Neck Surgery. Ed. Paul Flint. 6th ed. Vol. 3. Philadelphia, PA: Elsevier, 2015. 3045-3054.)) is a primarily pediatric viral disease affecting the larynx and trachea. Though it may resemble a simple cold at first, the infection causes a loud barking cough and stridor (unusual, high-pitched breathing noises indicating partial airway obstruction). The majority of croup cases are caused by parainfluenza viruses (types 1, 2, and 3) but a variety of other viruses can lead to croup symptoms.
The central problem for patients with croup is the swelling of the subglottic region of the larynx, which is the narrowest part of the airway in children. Croup varies in its severity and can last anywhere from three days to two weeks. Most patients do not require hospitalization, as home treatment or prescribed antibiotics or steroids are typically sufficient.
Croup, aka laryngotracheitis: Series of 4 photos
Croup, aka laryngotracheitis (1 of 4)
Though croup is most often seen in children, this woman developed a barking cough and mild, non-anxiety provoking stridor in the context of an upper respiratory infection. In this panoramic view note in particular the prominence and redness of the conus part of the vocal cords (indicated by white lines).
Croup, aka laryngotracheitis (2 of 4)
Closer view. Dotted lines signify normal airway diameter.
Croup, aka laryngotracheitis (3 of 4)
Even closer view showing redness and narrowing of the posterior subglottic airway.
Croup, aka laryngotracheitis (4 of 4)
View within the posterior subglottic narrowing.
Chondroma of thyroid cartilage: Series of 4 photos
Chondroma of thyroid cartilage (1 of 4)
CT scan of the larynx, showing the thyroid cartilage (outlined by gray dotted lines) and an abnormality deforming the thyroid cartilage on one side (between the white arrows). Note how the thyroid cartilage bulges on that side, as compared with the opposite side, and the black speck which indicates varying densities in the cartilage.
Chondroma of thyroid cartilage (2 of 4)
Same patient, endoscopic view of the larynx, again showing the abnormality (at arrows). Here the abnormality looks similar to a saccular cyst, but the scan (and subsequent biopsy) shows that it is cartilaginous and a chondroma, not chondrosarcoma.
Chondroma of thyroid cartilage (3 of 4)
Closer view of the chondroma, showing an almost bi-lobed appearance.
Chondroma of thyroid cartilage (4 of 4)
Under strobe lighting, which shows that the left vocal cord (right of photo) is apparently at a lower level than the opposite cord.