Tracheal Stenosis
Julina Ongkasuwan, M.D.
February 9, 2006

My topic this morning is tracheal stenosis. An outline for my presentation today: We are going to start with a case presentation, followed by an introduction to tracheal stenosis, identify some keys to diagnosis, and then talk about some treatment modalities, both endoscopic and surgical.

Our case begins with S.A. She is a 33-year-old female with a history of acanthosis nigricans and also history of airway obstruction requiring intubation at age 21. She presented to the Methodist Hospital in July 2005, with shortness of breath and difficulty breathing. She was diagnosed with an upper airway obstruction and taken to the operating room where she underwent endoscopy. At that point, she was noted to have an area of tracheal stenosis in the cervical trachea, just distal to the cricoid. A silicone stent was placed at that time by interventional pulmonology. She did well postoperatively and was subsequently discharged home. She represented, in September 2005, with URI‑type symptoms and shortness of breath and difficulty breathing yet again. She was taken back to the operating room for a repeat endoscopy and was noted to have some granulation tissue just distal to her stent and evidence of stent infection. The stent was removed and mitomycin-C was placed at the area of stenosis as well as on the granulation tissue. She again did well postoperatively and went home.

A month later, she again presented to the Methodist ER, again with shortness of breath. A soft tissue neck film, which was done at this time, showed an obvious area of stenosis visible in her neck. An airway CT was also performed, which revealed an area of stenosis beneath the cricoid. 3D reconstruction showed the area of stenosis, and then the airway was patent distal to the area of obstruction down to the level of the carina. She was taken to the OR and underwent endoscopy for the third time. In these intraoperative images, you can see her vocal cords and her immediate subglottis appear to be clear and then a tight area of stenosis just distal to the cricoid. Distal to this stenosis, the airway was open again all the way down to the carina. She underwent dilation again at this third trip to the operating room. As you can see here in this 3D rendering of her airway, measurements taken during endoscopy showed that the area of stenosis began approximately 3 cm below the vocal cords. This was approximately 2.8 cm in length and was located approximately 6 cm above the carina.

After this third trip to the operating room, she was presented with two different options. The first was permanent tracheostomy placement in order to protect her airway, and the second was a tracheal resection. The patient felt very strongly that she did not want to live with a permanent tracheostomy. Thus, she was set up for a tracheal resection. In November 2005, she underwent tracheal resection with primary anastomosis in conjunction with the cardiothoracic surgery service. She did very well postoperatively with no further episodes of difficulty breathing and with a good swallow.

Basic anatomy of the trachea: As you know, the trachea is located in the midline. You have the glottis and the subglottis and then the cervical trachea, which we are defining as below the inferior border of the cricoid to approximately the sternal notch, and then the thoracic trachea located from the sternal notch down to the carina. The trachea is approximately 12 cm long in a male, 10 cm long in a female, and consists of about 15-20 tracheal rings. Of note, when you place the neck in extension, approximately 50% of the trachea can be visualized above the sternal notch.

By far, the most common cause of tracheal stenosis is trauma, specifically internal trauma. This refers usually to the placement of an endotracheal tube or a tracheostomy. External trauma can also cause tracheal stenosis. There are other potential causes of tracheal stenosis; this includes chronic inflammatory diseases such as sarcoid and amyloidosis. Various neoplastic conditions can cause stenosis whether it be benign, such as respiratory papillomatosis or malignant disease, various collagen vascular diseases such as Wegener’s can also cause stenosis, and then there is idiopathic stenosis. In this particular case, S.A. may have been a patient with idiopathic stenosis, in which, as this name implies, the pathophysiology is not fully understood. There is a strong female preponderance in the patients who present with idiopathic stenosis, and there is thought to be estrogen or perhaps reflux playing a role; but it remains unclear. In this talk, we are going to concentrate primary cause of this disease.

So a very, very brief history of intubation: The idea of intubating people has actually been around since ancient times, but the first modern reports were in the late 1800s. Then the idea of tracheostomy, again, has been around for many centuries; however, our modern idea of tracheostomy was pioneered by ChevalierJackson in early 1900s.

There was a large increase in the incidence of tracheal stenosis during the polio epidemic of the 1950s where you had transition from the negative pressure ventilation system in the form of an iron lung to positive pressure ventilation, which required the placement of either an ET tube or a tracheostomy. The primary problem with the ET tube is the cuff. The cuff is usually located beyond the vocal cords in the cervical trachea. When the cuff on the ET tube is blown up such that the pressure in the balloon is greater than 30 mmHg, this pressure then exceeds the capillary perfusion pressure of the trachea. So then, you develop mucosal ischemia, chondritis, granulation tissue and, finally, scar and contraction of scar and fibrosis tissue, which leads to the stenosis.

In the 1970s, new cuffs were developed, which were high-volume low-pressure cuffs. These were able to decrease the incidence of tracheal stenosis almost 10-fold. However, any low-pressure cuff can be easily converted to a high pressure cuff by over-inflating the balloon. A study in the early 1980s looked at these high-volume low-pressure cuffs in their patients and reported that even with these cuffs 11% of patients on endoscopy had evidence of tracheal stenosis though they may not have been actually symptomatic. In a more recent paper by Goblin et al, they examined residents and attendings and the common way that we often feel the pressure by testing the external balloon, and found that it was a very, very poor predictor of what your actual cuff pressure is. So, a good rule of thumb is often to inflate your cuff on your endotracheal tube to the point you are just not getting an air leak around the cuff on positive pressure ventilation. But truly the best way is to get a quantitative measure of what your cuff pressure is.

This is a diagram from a book written by Dr. Grillo of Harvard, who has recently published the entire book on the management of diseases of the trachea and the bronchi. It shows some of the different lesions that can be attributed to the ET tube and tracheostomy. There are glottic and subglottic lesions, which we are not going to address in this talk, as that is a different spectrum of disease. But here you can see at the location of the stoma from a tracheostomy, you can have both granulation tissue formation, you can have deflection of the edges of the stoma into the airway, you can have subsequent stomal stenosis. You can see here, you can have injury due to the cuff, which we discussed earlier. In some patients, if they have been intubated for quite a while, they can get cuff stenosis and then, subsequently, tracheal stenosis They can have both cuff and stomal stenosis, often with a malacic segment between. In addition, at the distal end of the tracheostomy or ET tube, you can have irritation of the tracheal wall distally. The severity of the stenosis is defined by the degree. Mild is considered less than 70%, moderate at 70-90%, and severe at greater than 90%.

A couple of keys to diagnosis is the patients usually present days to weeks after they have been extubated. They often present with an inspiratory stridor and/or an expiratory wheeze. It is at this presentation that almost half of these patients are often misdiagnosed with asthma on initial presentation. It is important to note that this "asthma" will be unresponsive to bronchodilators and can be provoked with neck extension and forced inspiration. Most patients do not develop symptoms at rest until they have reached approximately 70% stenosis.

Dr. Grillo has written an important rule of thumb to think about: any patient who develops symptoms of airway obstruction who has been intubated in the recent past must be considered to have an organic lesion until proven otherwise and should not just be given the diagnosis of asthma or adult-onset asthma.

Flow volume loops can be useful in evaluating these patients. Here on the far left you can see the flow volume of a normal patient. Here is one example of asthma where you can see some flattening of the expiratory curve. Over here you can see what a flow volume can look like in the presence of a fixed upper airway obstruction such as tracheal stenosis; you have flattening of both the inspiratory and the expiratory phase.

Imaging can be very useful in trying to evaluate these patients. As you saw earlier, plain x-ray can also show you your area of stenosis; but a CT is really extremely useful diagnostic tool when evaluating these patients. It is important to get an airway CT, as opposed to just like a neck CT or a chest CT, that evaluates the entire airway and it also can be evaluated with thinner cuts. If you have thicker cuts on your CT scan, you can underestimate or you can entirely miss the area of stenosis. With these newer CT modalities, including multi-slice and helical CT, the data can be reconstructed into virtual bronchoscopy or 3D images. This is an example of some of the newer modalities, the fancy things that you can have to help visualize the airways, the computer programs that can interpret this CT data. This is, of course, no substitute for a diagnostic endoscopy where you can actually see the lesion with your eyes, but it can help you in your preoperative workup.

On the management of these lesions, surgery, of course, is the definitive management for tracheal stenosis. However, if the patient presents in extremis, and you do not have time for preoperative planning and you need to go straight to the operating room, there are endoscopic tools that can be used to help these patients. In addition, if the patient is not a surgical candidate or they have other things going on, and you wish to delay surgery for whatever reason, again there are various endoscopic tools that can be used.

Brichet et al, in 1999, published a paper, which I think has a very useful algorithm in thinking about these patients. They looked at 32 patients with post intubation tracheal stenosis, and they were taken to the operating room for diagnostic bronchoscopy. Those patients who looked like they had what they called a "web-like stenosis," that is a stenosis that was less than 1 cm in length, were circumferential, and did not involve the underlying cartilage, were treated with some limited lasering and then dilation of the area of the stenosis. They found, in their study, that they were able to cure about 60% of these web-like stenoses patients in either one to three serial treatments of dilation. If these patients recurred after a third treatment with laser and dilation, the patients were evaluated and, if they were deemed to be operable, they were referred for tracheal resection. If they were deemed inoperable, they entered this other arm of this algorithm.

Let us go back and look at the patients who had rigid bronchoscopy. If they were determined to have a complex stenosis, which was basically defined as anything that was not a web-like stenosis, a silicone stent was placed through the area of stenosis. The patients were then evaluated six months later. If they were determined to be an operative candidate, the stent was then removed. If they subsequently recurred and had evidence of stenosis, they were then referred for resection. If they did not recur, they were then considered cured and just followed symptomatically. Finally, if the patient was deemed inoperable after six months for whatever confounding medical reasons or the length of their stenosis, the stent was left in place and the patient was purely followed symptomatically.

Dilation: This is typically done using serial dilation using various sizes of Jackson bronchoscopes. The various studies have showed that mechanical dilation used alone can have a recurrence rate of stenosis of greater than 90%. Thus, various adjunctive procedures have been developed in order to try to decrease the rate of restenosis.

Mitomycin-C is an example of one of these adjunctive agents. It is a chemical derived from the Streptomyces caespitosus bacterium, which was discovered in the 1950s. It is an alkylating agent which cross-links DNA, and it inhibits fibroblast production. It was actually originally used in the ophthalmologic literature for using glaucoma, and a lot of our dosing actually comes from that literature. Most of the original research on mitomycin-C was used in animal and retrospective studies. However, a recent double blind placebo controlled study that was done out of Cincinnati, by Dr. Cotton and his associates, on 24 pediatric patients actually showed no statistical difference in the rates of recurrence of tracheal stenosis between mitomycin-C and the placebo. This data is relatively new and mitomycin-C is still very widely used.

Laser is another adjunctive modality for treatment of tracheal stenosis. Commonly either the CO 2 or the Nd:YAG lasers have been used with many various different techniques, as proposed by Dedo and Ossoff, including radial cuts made with dilation. This is a scenario with some amount of controversy. Dr. Grillo, in his book, is not in favor of the laser because he feels that it can cause coagulation, necrosis, and damage to normal trachea on either side of the lesion leading to extension of the area of stenosis and making further subsequent surgical management more difficult. So, this does remain an area of some controversy.

Stents can also be used as an adjunctive procedure during endoscopy. The word stent is derived from a dentist named Charles B. Stent, in the 19 th century, who developed various dental molds and prostheses. He was also developing things to help support skin grafts and, eventually, his name became synonymous with any material that was used to support tissues from collapse. Montgomery, in the 1960s, developed his famous T-tube. It is a silicone prosthesis in a T-shape that is placed via a tracheostomy to help stent open the airway. Dumon and Bauer, in the 1970s, modified Montgomery's T-tube by cutting off the end and making it a long cylinder and placing it via an endoscope. In the 1990s, with the growing popularity of various intracardiac, vascular, and cardiac stenting, people started taking those actual metal stents and placing them in the airway to stent open the airway. This is an image of some of the many, many different types of stents, which have been available on the market.

We are going to talk about some of the two primary types of stents; again the silicone stent, this is the picture of the Montgomery T-tube, and then the Dumon stent is another very commonly used stent. You can see that the Dumon stent has these little stubs on the side, which help it dig into the trachea when it is expanded so as to decrease the amount of migration of the stent. It comes in various shapes and sizes and, as you can see here, this one is bifurcated to be used at the carina. Because of the thickness of the plastic, they do have a relatively smaller internal diameter, but they are removable. This is a key thing about silicone stents, that they can be removed in one piece. Different studies have shown varying rates of migration up to 17.5%, some amount of obstruction with mucus secretions, and some development of granulation tissue within the stents.

Metallic stents: some of the commercially available types include the Wallstent and the Ultraflex. They do have a lower rate of migration because this metal basically becomes incorporated into the tracheal wall and, because they are not so thick, they have a larger internal diameter. These are relatively permanent because of their tendency to really get incorporated into the tracheal wall; and they are associated with many, many complications. In fact, the FDA, in July this past year, released a notification to physicians about the use of metallic stents in the patients with these in place. Part of the big problem is that they really limit your ability to do further surgical resection on these patients. They can develop problems with granulation tissue, they can increase the length of your stenosis by really irritating the tracheal wall, they have problems of mucus plugging and infection and stent fracture, as the metal rusts.

This is an image, of one of these stents, being removed. You can see that they do not come out nicely in one piece, but rather piecemeal and broken, and they cause a lot of damage to the trachea and make it difficult to do further management of these patients. So, they are not really recommended at this time, especially for benign disease.

Surgery, as I said before, is the definitive management for these lesions. The classic surgical procedure for this is tracheal resection with an end-to-end anastomosis. It is important, of course, to get a good idea of how long the stricture is and how many areas are involved, as well as any potentially complicating factors, such as a T-E fistula or vocal cord paralysis.

The surgical technique: something to keep in mind when you are doing one of these procedures is that the blood supply to the trachea arises laterally. It is an arborization of a lot of these smaller feeding vessels from the inferior thyroid artery to the innominate and, again, comes in laterally; so it is important to maintain the dissection of the midline and to try not to disrupt this blood supply. Dr. Grillo in his text does not routinely dissect out the recurrent laryngeal nerves in this procedure. It varies between surgeons, as some do and some do not. His reasoning for not is that he does not want to disrupt this lateral blood supply.

In this procedure, a low collar incision is made in the neck and, depending on where the lesion is, sometimes this is combined with a median sternotomy incision. The dissection is made down to the left area of the trachea, again staying in the midline until you identify the area of stricture, and that is the only area where a circumferential dissection is performed. The stenotic area is removed in one piece, and then the oral ET tube is backed out. A clean ET tube is passed across the field, and the distal segment is intubated directly. Interrupted Vicryl sutures are placed posteriorly, and then they come around laterally. Then, before your last couple of sutures are placed, you remove that distal ET tube and then advance the oral ET tube again across the anastomotic segment and then tie down your knots. Various papers have reported success rates from anywhere from 71-97%, success being defined as no further tracheal stenosis, no further airway symptoms, with the 2% mortality. Grillo reports that in his experience he has about an approximately 5% failure rate.

The key to preventing restenosis in the trachea is to develop a tension-free anastomotic line. Some of the variables that can go into this includes the elasticity of the tissues and the age of the patient, of course, because as you age the elasticity decreases; whether the patient has had any previous surgery, and the extent of mobilization of the trachea.

Various techniques to decrease tension include maintaining dissection along the trachea and pretracheal plane, using cervical flexion, that is flexing the patient’s head either 15-25 degrees and then, at the end, placing of a chin suture, the suture that goes from a chin to the chest, to maintain the patient’s head in flexion. In addition, various laryngeal release maneuvers have been made; these are primarily useful in cervical stenoses. These include a thyrohyoid release, that was described by Dedo and suprahyoid release by Montgomery. This is an image of the suprahyoid release. You can see you basically divide of the muscles superior to the hyoid and letting it drop. The thyrohyoid release, especially, has been associated with some short-term problems with dysphagia, which reportedly improve with time. In addition, for more thoracic tracheal lesions that are further down, various hilar release maneuvers have been developed, which involve releasing of the pulmonary ligaments to help mobilize that distal segment.

Complications of the surgery include granulation tissue formation at the anastomotic line. Studies have found that if you use an absorbable suture material, as opposed to the nonabsorbable, that drastically decreases the rate of granulation tissue, cervical mediastinal sepsis, dehiscence of suture—again that has to do with tension on the anastomotic line, rupture of the innominate, aspiration, and recurrent laryngeal nerve palsy.

In summary, if you see a patient who presents with airway obstruction, difficulty breathing, adult-onset asthma, and they have a history of recent intubation, you have to think about tracheal stenosis on your differential. As part of your workup, an airway CT can be extremely useful in delineating these lesions; but, of course, endoscopy for both diagnostic purposes as well as management can be very useful in addition to stent placement. However, you have to keep in mind that surgery is really the only definitive management for these lesions if the patient is a surgical candidate.

Case Presentation:

S.A. is a 33-year-old female with a history of extensive acanthosis nigrans. In July of 2005, she presented to the Methodist emergency room with complaints of difficulty breathing and shortness of breath. She reported a similar incident at age 21, which required intubation; though no other interventions were described. Work up was consistent with upper airway obstruction for which she underwent an endoscopy. This revealed an area of stenosis in the cervical trachea, just below the cricoid cartilage. A silastic stent was placed. She did well post-operatively with resolution of her symptoms and was discharged home.

In September of 2005, she developed upper respiratory tract infection symptoms and shortness of breath. Repeat endoscopy revealed granulation tissue distal to the stent and evidence of stent infection. The stent was removed intra-operatively by the Interventional Pulmonology service. Mitomycin C was placed over the area of stenosis.

Again in October of 2005, she began experiencing shortness of breath and dyspnea with exertion. Upon endoscopy she was noted to have a severe >90% stenosis of the cervical trachea. Dilation was performed with excision of granulation tissue using laser.

After the third endoscopy, she was given the options of permanent tracheostomy versus primary resection of the stenosed segment. She felt very strongly against permanent tracheostomy, opting, instead, for surgical resection.

In conjunction with the Cardiothoracic Surgery service, the Otolaryngology service performed a tracheal resection with primary re-anastomosis in November of 2005. She has done well since then, with no further episodes of shortness of breath and a good swallow.

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