Obstructive Lesions of the Trachea

Obstructive lesions of the trachea following intubation occur at four levels, depending on the source of injury. At each level, one or more distinct lesions may produce obstruction. The levels are 1) stomal, 2) the site where the inflatable cuff rested, 3) the segment between the stoma and the level of the cuff, and 4) the locus where a tip of the tube may impinge on the tracheal wall (see Figure 11-1).

Lesions at Stomal Level. Since tracheostomy creates a defect in the wall of the trachea, whether the opening is made by a vertical, horizontal, cruciate, or T incision, by excision of a segment or segments of carti-

lage, or by turning a flap, some scarring is inevitable during healing. Long after healing is complete, inspection, both bronchoscopically and radiologically, will demonstrate dimpling or deformity, an anterior shelflike projection, or softness of the anterior wall at the site of prior tracheostomy. A surprising degree of asymptomatic narrowing may occur. Nearly 50% narrowing of the cross-sectional area of the trachea, or even more, is necessary before a sedentary person experiences dyspnea. Three stomal lesions, seen alone or in combination, may cause obstruction. These are 1) granuloma, 2) a posteriorly depressed flap of tracheal wall above the stoma, and 3) anterolateral stenosis.

Granulation tissue forms at the stoma before and during healing. Granulomas may be noted weeks or months after extubation. As healing progresses, ebullient granulation tissue may form on the inner surface of the trachea at the site of the stoma and become sufficiently bulky to obstruct the airway. Accumulation of this type of papillomatous granulation tissue often occurs in conjunction with deformity at the healing stomal site (see Figure 11-5). If a large granuloma is already present, immediate airway obstruction may follow removal of the tracheostomy tube.

The curve of the tracheostomy tube may produce a depressed tracheal wall flap just above the stoma. The tip of the flap may be thickened or granulomatous, but in most cases, this alone is insufficient to cause serious obstruction when the tube is withdrawn. When the tracheostomy tube has been in place for a long time, the upper flap may remain positioned posteriorly and produce partial or even subtotal obstruction (see Figure 11-1). This tissue may even become calcified prior to removal of a long-standing tracheostomy tube. We do not know whether this flap effect can be avoided by choice of incision for tracheostomy. It seems to occur most commonly in children who have had prolonged tracheostomy, perhaps because of the thinness and pliability of the juvenile trachea.

figure 11-5 A, Anteroposterior tomogram of the larynx showing stenosis and granuloma (large arrow) at the site of cricothyroidostomy. Note the proximity of the vocal cords just above the lesion. B, Lateral view showing narrowing of the airway, deformity, and large granuloma. The "O" marks the stomal site on the skin. Laryngotracheal resection and reconstruction was necessary.

figure 11-5 A, Anteroposterior tomogram of the larynx showing stenosis and granuloma (large arrow) at the site of cricothyroidostomy. Note the proximity of the vocal cords just above the lesion. B, Lateral view showing narrowing of the airway, deformity, and large granuloma. The "O" marks the stomal site on the skin. Laryngotracheal resection and reconstruction was necessary.

The most common lesion of significance at the stomal level is anterolateral stenosis. Following removal of the tracheostomy tube, the patient gradually develops obstructive symptoms. The patient is found bronchoscopically to have an A-shaped stricture with an apex anteriorly, which involves the antero-lateral walls of the trachea (Figures 11-6A,B and Figures 24 and 25 [Color Plate 14]). The membranous wall is usually spared but irritative granulation tissue may be present posteriorly in some cases (Figure 11-6C). The membranous wall may be shortened by deformity of the lateral walls, which are pulled together by the anterior scar. Stomal stenosis results from cicatricial healing of what was or has become a large stomal defect (Figure 11-7). A number of factors appear to play an etiologic role. Occasionally, a surgeon makes a much too generous opening in the tracheal wall, failing to realize that loss of tracheal substance will ultimately be healed by the natural process of contraction of the scar. Tracheostomies probably erode toward the size of their inlying tracheostomy tube due to local pressure necrosis, no matter how the stoma is made. Any opening which is larger than this may only add to the destructive process. All tracheal stomas are inevitably contaminated bacterially. Although invasive sepsis is not frequent, bacterial activity may lead to further local tissue destruction. The most important factor is the weight of unsupported tubing which levers the tracheostomy tube against the margins of the stoma, producing pressure necrosis. Evidence to support this was the decrease in incidence of stomal stenosis in a single respiratory care unit, before and after the introduction of lightweight swivel connectors to tracheostomy tubes.11 Careful suspension of tubes and connectors has essentially eliminated such lesions at Massachusetts General Hospital (MGH).

As noted earlier, an especially complex stomal lesion results if the cricoid cartilage is eroded by upward pressure of the tracheostomy tube. If the anterior cricoid cartilage loses its integrity, anterior sub-glottic laryngeal stenosis occurs in conjunction with upper tracheal stenosis. Even if the first tracheal ring has not been mistakenly divided during tracheostomy, a tube that impinges against it may erode through it and into the cricoid cartilage. This is most likely to occur in older patients with a degree of kyphosis, where hyperextension of the cervical spine fails to draw the larynx far above the sternal notch. Although the tracheostomy tube may be correctly placed at the level of the second tracheal ring, it may have to arch across the cervical tissues to reach the skin surface, exerting pressure against the cricoid (see Figure 11-3B). It is important to recognize the extent of such lesions prior to surgery, since the technique of repair of a purely tracheal stenosis is very different from that for subglottic laryngotracheal stenosis (see Chapter 24, "Tracheal Reconstruction: Anterior Approach and Extended Resection," and Chapter 25, "Larygotracheal Reconstruction"). A comment on terminology is in order. "Subglottic" is often used to describe lesions anywhere from just below the vocal cords to the upper or even midtrachea. Surgical problems and prognosis are quite different at different levels. I prefer to describe a lesion that lies in the larynx between the vocal cords and the lower border of the cricoid cartilage as a subglottic lesion (intralaryngeal). If the upper border of the lesion lies just below the lower border of the cricoid cartilage, it is clearly an upper tracheal lesion, and laryngotracheal spans the subglottic level and upper trachea.

Infrastomal Obstructive Lesions. The principal infrastomal lesion that results from intubation for respiratory support is tracheal stenosis at cuff level or cuff stenosis. It is the most common lesion complicating modern respiratory care and it is clearest in the minds of most physicians (Figure 11-8 and Figures 26 and 27 [Color Plates 14 and 15]).The origin of stenosis at cufflevel was obscure when the lesion was first recognized. It originates from circumferential erosion of the tracheal wall due to the pressure of the cuff and is common to all forms of access to the trachea; endotracheal tubes, tracheostomy tubes, or cricothyroid-ostomy tubes (Figure 11-9). In the extreme, a tracheo-innominate artery fistula can result if erosive pressure is maximum anteriorly, or a tracheoesophageal fistula if the erosion penetrates posteriorly. Conventional high-pressure cuffs formerly in use, whether on endotracheal tubes or tracheostomy tubes, exerted enormous pressures on the tracheal wall. They almost uniformly produced some degree of tracheal injury within 48 hours of placement. The depth and severity of damage is roughly, but not uniformly, related to the duration of exposure to pressure injury. The key etiological factor in the production of stenosis is pressure necrosis caused by the cuff, compressing the tracheal mucosa and, later, the deeper structures of the tracheal wall. The principal evidence supporting these conclusions has been derived from autopsy study of patients who received ventilatory support,12,13 from prospective studies by direct visualization of the tracheae of patients receiving ventilatory assistance,11,14 and from experimental production of identical

Tracheal Necrosis

figure 11-6 A, Surgical specimen of stomal stenosis showing the typical triangular lumen with apex anterior. A granuloma is also present where the stoma lay. The membranous wall is smooth. B, Longitudinal view of the same specimen demonstrating that the tracheal walls are pulled together by the cicatricial closure of the stomal defect. C, Another specimen showing stomal stenosis with active inflammatory granulation tissue everywhere, including the membranous wall of the trachea. An endotracheal tube had been wedged into the stenosis on several occasions. Also, see Figures 24 and 25 (Color Plate 14).

figure 11-6 A, Surgical specimen of stomal stenosis showing the typical triangular lumen with apex anterior. A granuloma is also present where the stoma lay. The membranous wall is smooth. B, Longitudinal view of the same specimen demonstrating that the tracheal walls are pulled together by the cicatricial closure of the stomal defect. C, Another specimen showing stomal stenosis with active inflammatory granulation tissue everywhere, including the membranous wall of the trachea. An endotracheal tube had been wedged into the stenosis on several occasions. Also, see Figures 24 and 25 (Color Plate 14).

figure 11-7 Evolution of stomal stenosis. Cross-sectional diagrams of the trachea at the stomal site. A, The tracheostomy tube may be leveraged against the stomal margins, causing their erosion. B, The resulting large stoma exhibits granulations and inflammation at its margins. C, Contraction of scar tissue forming across the defect pulls the tracheal stomal margins to the midline. D, The result is an A-shaped lumen. The posterior wall is also often shortened. Scar tissue is present, in most anteriorly only.

lesions.15 Correlation of these observations with surgically removed specimens further supports this the-sis.16 Final confirmation is that removal of excessive cuff pressure has eliminated the lesions in a very large number of patients at risk over a long period of time, at MGH.

Cooper and Grillo examined the tracheae of 30 patients who died while receiving ventilatory assistance through cuffed tracheostomy tubes as well as 4 additional patients who had received such assistance through cuffed endotracheal tubes only for short periods of time.12 Both metal and plastic tracheostomy tubes and plastic and rubber cuffs had been used. At that time, all cuffs were of designs that produced high intracuff pressures. A consistent pattern of tracheal damage was observed, with the major damage located at the site of the cuff. The period of mechanical ventilation and the degrees of damage generally correlated. Superficial tracheitis and fibrin deposits appeared within 48 hours of placement of the tube. Small, shallow ulcerations were then seen, overlying the cartilaginous rings. With time, the size of the ulcers increased and cartilages were exposed. The inflammatory process spread laterally and deeply, followed by fragmentation of cartilage (Figure 11-10). The tracheal wall in many cases bulged where the balloon was located. These lesions usually began approximately 1.5 cm below the inferior margin of the tracheostomy stoma and extended downward for a length of about 2.5 cm, that is, the location of the cuff. Usually, between two to four cartilages were completely bared in time. Eventually, segments of cartilage sloughed and, in advanced cases, the balloon site was completely devoid of cartilages. Severe damage was observed between 10 days to 2 weeks after placement of the cuff. Additional ulcerations were occasionally seen, corresponding to the tip of a tracheostomy tube below the cuff injury. Changes that occurred at cuff sites from endo-tracheal tubes compared closely to those seen from cuffs on tracheostomy tubes with similar duration of intubation. These lesions were located more proximally in the trachea, since the cuff of an endotracheal tube is sited more proximally than that from a tracheostomy tube (see Figure 11-9).

Microscopic examination elaborated the progressive changes that were found grossly (Figure 11-11). Acute inflammation and fibrin appeared early. Microscopic ulceration followed, overlying the cartilaginous rings where the mucosa had been compressed between the balloon and the underlying cartilage (see Figure 11-11A). As the ulcers deepened, the surfaces of the cartilages were bared, and inflammatory degeneration ensued. Inflammatory cells infiltrated beneath the cartilages (see Figure 11-11B). Fragmentation of

Lesion Trachea

figure 11-8 A, Cuff level stenosis. The lesion is circumferential. The lumen is less than 5 mm in diameter, the level at which the patient became dyspneic on bed rest while recovering from multiple orthopedic injuries and after a remote period of ventilation. B, The same lesion just prior to resection (arrows). A Penrose drain lies beneath the stenotic segment. C, Photomicrograph of the lesion. Dense fibrosis and partial cartilaginous destruction are evident (hematoxylin and eosin; x25 original magnification).

figure 11-8 A, Cuff level stenosis. The lesion is circumferential. The lumen is less than 5 mm in diameter, the level at which the patient became dyspneic on bed rest while recovering from multiple orthopedic injuries and after a remote period of ventilation. B, The same lesion just prior to resection (arrows). A Penrose drain lies beneath the stenotic segment. C, Photomicrograph of the lesion. Dense fibrosis and partial cartilaginous destruction are evident (hematoxylin and eosin; x25 original magnification).

cartilage occurred next (see Figure 11-11C) and, finally, only an ulcerated bed remained where the cartilage had sloughed (see Figure 11-11D). In some cases, the tracheal wall was totally replaced with granulation tissue as repair competed with erosion (see Figure 11-11E). At the margins where the epithelium remained, squamous metaplasia was evident. Although the membranous wall sometimes escaped changes as severe as those in the noncompliant cartilaginous portion of the tracheal wall, severe erosive inflammatory changes were produced nonetheless. The circumferential lesion reflected circumferential pressure injury. In several cases, the membranous wall was reduced to paper thinness, and there were inflammatory changes in the adjacent esophageal wall. Complete fistulization occurred in other specimens. Florange and colleagues reported similar pathologic findings.13

Tracheostomy Clone Internal
trization of granulation tissue. The resulting scar is circumferential. A, Cuff lesion from an endotracheal tube. B, Cuff lesion from tracheostomy tubes. The lesion is usually lower than that from an endotracheal tube.

These changes were compared with a group of surgically resected specimens of cuff stenosis, where a circumferential ring of dense fibrous tissue resulted at 1 to 3.5 cm below the tracheostomy site. In these resected specimens, the residual effective airway often measured 2 to 5 mm in diameter. Externally, the area of stenosis was usually demonstrable, frequently hourglass in shape, but without external indication of the extreme narrowness of the minimal internal airway (see Figures 11-8A,B). In longstanding cases, metaplastic squamous epithelium was present. In most, the scar tissue of the stenotic ring remained unepithelialized. In some, residual pieces of tracheal cartilage were present in a greater or lesser degree (Figure 11-12). In fully advanced cases, not even vestigial remnants of tracheal architecture were identifiable. Patients with cuff stenoses following endotracheal intubation often had marked cicatricial stenosis, but relatively intact outer cartilages, presumably because the length of exposure to pressure had been too brief to necrose the cartilages completely. A striking finding was that all patients with the then-conventional cuffs in place had notable changes. These findings were confirmed in a prospective study by Andrews and Pearson, who examined the tracheal wall endoscopically through the stoma at the time of removal of the tracheostomy tube.11 We made similar endoscopic observations in a study of the comparative effects of standard cuffs and an experimental low-pressure cuff.14

Many etiologic possibilities for these lesions had earlier been suggested, including the influence of sepsis, the fact that many patients had periods of hypotension during their illness which could impair circulation in the compressed mucosa, damage by toxic materials in the tubes, and cuffs and from gas steril-ization.17 Shelly and colleagues questioned the effect of systemic hypotension, on the basis of animal experiments.18 Experimental reproduction of the lesions helped to clarify these questions.15 Murphy and colleagues attempted to reproduce the lesions in dogs, but were able to do so only with the combination of cuff and tracheostomy.19 We placed short segments of Portex endotracheal tubes with cuffs perorally into the tracheae of dogs, and fixed them with percutaneous wires.15 Tracheostomy was avoided to minimize infection. The tubes were clean but not gas sterilized. The cuff was inflated just sufficiently to provide a seal at 25 cm of water ventilatory pressure, and this pressure was then maintained throughout the experiment. Destructive lesions were uniformly produced within 1 week (Figures 11-13A,B). Removal of the tube was

Trachea Scar Revision Icd Code

figure 11-10 Postmortem tracheal specimens of patients ventilated with high-pressure cuffs then in use. A, Trachea opened posteriorly. Portex tube and cuff are evident. Ventilation wasfor 19 days. The patient was age 55 years. B, Ulceration and loss of cartilage at the cuff site. C, Trachea of a 69-year-old woman, ventilated for 16 days. Metal tracheostomy tube with latex cuff are evident. D, Mucosa is destroyed at the cuff site and cartilages are bared and fragmented.

Trach Erosion

figure 11-11 Photomicrographs from postmortem specimens of tracheae injured by ventilation using high-pressure cuffs. Tracheal lumen is above in A, B, and C. The lumen is at the right in D and E. A, Erosion of mucosa over cartilages due to cuff compression. Submucosal inflammation. B, Cartilages now bared by progress of mucosal and submucosal necrosis. Lamina propria has been thickened by inflammation. C, Necrosis of cartilage follows with increased inflammatory intensity in surrounding tissues. D, Total destruction of cartilages occurs. Inflammation extends deeply into tracheal wall. E, The tracheal wall is now essentially replaced with inflammatory tissue and beginning reparative response of granulation tissue (hematoxylin and eosin; x25 original magnification).

Granulation Tissue Tracheostomy

figure 11-12 Photomicrograph of transverse section of a fully developed cuff stenosis. A fragment of degenerated cartilage is essentially the only immediately recognizable remnant of the tracheal architecture. Otherwise, a ring of scar tissue has replaced the trachea, and its contraction leaves only a very reduced lumen. Mucosa is lacking (hematoxylin and eosin; x11 original magnification).

figure 11-12 Photomicrograph of transverse section of a fully developed cuff stenosis. A fragment of degenerated cartilage is essentially the only immediately recognizable remnant of the tracheal architecture. Otherwise, a ring of scar tissue has replaced the trachea, and its contraction leaves only a very reduced lumen. Mucosa is lacking (hematoxylin and eosin; x11 original magnification).

followed by cicatricial stenosis and airway obstruction (Figure 11-13C). Although the experimental and clinical evidence do not rule out possible additive contributions by other factors mentioned as well as others unknown, the principal common denominator appears to be necrosing pressure on tissue. We saw no cuff stenoses in over 5 years and in many hundreds of patients, following the design and introduction of a latex low-pressure cuff, although no other factors changed during this period. Since then, despite the necessary but careful use of plastic low-pressure cuffs, since latex cuffs are not available, no cuff stenoses have been produced at MGH in thousands of ventilated patients.

Varying degrees of tracheitis occur in the segment between the level of the stoma and the level of the cuff. The segment is usually short, but it lies in close proximity to two areas of damaging influences. In many cases, secretions puddle above the cuff, despite intermittent deflation. Heavy bacterial colonization is routine around tracheostomies. Varying degrees of gross and microscopic inflammation are seen in this segment of trachea. The cartilages may be thinned and inflamed while the mucosa, although inflamed, is intact. At operation, the tracheal wall at this point may be markedly inflamed and its architecture partly destroyed. This becomes evident once part of the trachea is detached from surrounding supporting tissues.

Tracheal malacia occurs in this segment and is demonstrable fluoroscopically or bronchoscopically. Such changes can be of great importance in planning surgical excision of cuff stenoses, since the segment of trachea requiring removal may be almost double the length apparent in preoperative static images of a cuff stenosis. In a few patients, the area of cuff damage itself may be primarily malacic rather than firmly stenotic, producing valve-like obstruction on deep breathing or coughing (Figures 11-14A,B). Routine tracheal x-rays may show only slight or no deformity at cuff level. Functional obstruction becomes evident only when deliberately sought for fluoroscopically or during an awake flexible bronchoscopy. In these patients, cartilaginous rings are absent, and the fibrous wall is covered with squamous metaplastic epithelium (Figure 11-14C). The evolution of mala-cia rather than fibrous stenosis at cuff level has not been explained.

Lesions may overlap and it may be difficult to ascertain the precise etiology, especially if a stenosis appears late. In obese or aged individuals, for example, the cuff may reside immediately within the stoma, with confluence of stomal and cuff injuries. Multiple tracheostomies also serve to confuse the issue, since records of prior treatment are often imprecise. Stenosis resulting from prior endotracheal intubation may be lost sight of after a series of therapeutic tracheostomies and laser treatments.

Occasionally, trachiectasis occurs. In a few patients with persistent respiratory failure from chronic lung disease, who are managed for lengthy periods of time with conventional equipment, the requirement for volume of air to seal the cuff gradually increases. Generally, high ventilatory pressures are needed. The trachea in one patient required a balloon volume of approximately 200 cc for a seal.

Granuloma formation at a site of ulceration by the tip of a tracheostomy tube can also cause obstruction, although rarely. With the older type of high-pressure cuffs that expanded eccentrically, the tip of the tracheostomy tube could easily be angulated against the tracheal wall. A tracheostomy tube with a 90° angle accentuates this possibility. This also happened in children where no cuff was used at all, where slight angulation of a tracheostomy tube levered the tip against the tracheal wall (Figure 11-15). After the tube is removed, an ulcer may heal, with profuse connective tissue formation, producing an inflammatory granuloma. The incidence of such lesions in children has diminished remarkably with the development and use of improved pediatric tracheostomy tubes (see Chapter 10, "Tracheostomy: Uses, Varieties, Complications").

Granulation tissue may form around the lower end of a tracheostomy tube while a patient is still on a ventilator. This occurs most often in patients who have long been on mechanical assistance, who have

Tracheostomy Clone Internal

figure 11-13 Experimental production of cuff stenosis in dogs. A, Segment of the endotracheal tube with high-pressure (standard) cuff after 7 days of exposure to the seal at standard ventilatory pressure. B, Mucosal destruction has occurred, cartilages are bare, and the trachea is distended. C, In another specimen, 13 days of exposure has produced copious granulation tissue, replacing the normal tracheal structure.

figure 11-13 Experimental production of cuff stenosis in dogs. A, Segment of the endotracheal tube with high-pressure (standard) cuff after 7 days of exposure to the seal at standard ventilatory pressure. B, Mucosal destruction has occurred, cartilages are bare, and the trachea is distended. C, In another specimen, 13 days of exposure has produced copious granulation tissue, replacing the normal tracheal structure.

Spot Trachea

figure 11-14 Diagnostic images from a 38-year-old woman with attacks of dyspnea and changes of voice worsening over a year, following emergency tracheostomy and ventilation for obstructive laryngitis. A, "Spot film" from fluoroscopy demonstrating an apparently normal upper tracheal diameter (arrows). The adducted vocal cords and subglottic larynx are clearly defined above. Symptoms were thought to be of psychiatric origin because of similar static x-rays of the trachea elsewhere. B, Fluoroscopic picture of the segmental malacic tracheal collapse (arrows) on cough. Resection of the damaged trachea fully relieved her complaints. C, Surgical specimen from a 70-year-old woman who was twice ventilated for long periods for respiratory failure. Circumferential cuff lesion was principally malacic, with some fibrosis.

diffuse tracheitis, and who may have significant injury at cuff level. Bronchoscopic removal of granulations provides only transient relief. A longer tube or one with a different angle may be inserted, but the danger remains that the process will extend distally, ultimately to the carina, unless the patient can be weaned. Granulations in a supracarinal location present a special hazard, since a tube may slip back only a few millimeters and obstruction from the granulations may slowly form below the tip of the tube while the physician has an illusion of safety.

How To Reduce Acne Scarring

How To Reduce Acne Scarring

Acne is a name that is famous in its own right, but for all of the wrong reasons. Most teenagers know, and dread, the very word, as it so prevalently wrecks havoc on their faces throughout their adolescent years.

Get My Free Ebook


Post a comment