Complications of General Surgery

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Airway Injury After Tracheotomy and Endotracheal Intubation John M. Streitz, Jr, MD, * and Stanley M. Shapshay, MDt

Iatrogenic airway injury after tracheotomy and endotracheal intubation continues to occur with regularity despite an elucidation over the last several decades of its pathogenesis and methods of prevention. Its incidence has decreased although the actual number of cases remains considerable owing to the increased use of airway intubation in the modern critical care setting. Because injury to the airway is an unusual complication with which most physicians have little experience, the diagnosis and institution of proper treatment are often delayed. Familiarity with the pathogenesis and clinical presentation of this disorder permits all physicians who treat critically ill patients to institute more effective prevention and earlier diagnosis. The technique of surgical resection and reconstruction of subglottic and tracheal stenosis has been refined over the last three decades and can be applied safely and successfully in most circumstances. Glottic injury is a more challenging problem with variable surgical results. ANATOMY

The lower respiratory tract begins at the vocal cords. They join anteriorly at the anterior commissure and are supported posteriorly by the arytenoid cartilages that are located on top of the posterior cricoid plate (Fig. 1). Beneath them is the 1.5 to 2 cm of subglottic larynx that is surrounded by the cricoid cartilage. The trachea begins immediately beneath the cricoid cartilage and is about 11 cm long in the adult, ranging from 10 to 13 cm, with 18 to 22 rings from the lower cricoid cartilage to the carina, about 2 rings per centimeter. Adult tracheal dimensions are about 2.3 cm laterally and 1.8 cm anteroposteriorly. The blood supply to *Staff Surgeon, Department of Thoracic and Cardiovascular Surgery, Lahey Clinic Medical Center, Burlington, Massachusetts; and Clinical Instructor, Harvard Medical School, Boston, Massachusetts tChairman, Department of Otolaryngology-Head and Neck Surgery, Lahey Clinic Medical Center, Burlington, Massachusetts; and Professor of Otolaryngology, Boston University School of Medicine, Boston, Massachusetts

Surgical Clinics of North America-Vo!' 71, No.6, December 1991

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Figure 1. Laryngeal anatomy is shown. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

the trachea arises from branches of the inferior thyroid, subclavian, innominate, and bronchial arteries and is shared with the esophagus and enters laterally, joining a small lateral longitudinal collateral blood supply.19

PATHOPHYSIOLOGY Airway intubation causes injury in the glottis, the subglottis, and the trachea (Fig. 2). Some injuries are isolated; others involve all three areas confluently. The pattern of injury varies with the type of intubation, but similarities between tracheotomy and endotracheal tube injury exist. Both can cause circumferential stenosis or malacia at the cuff site and ulceration and granulation at the tip of the tube. They differ primarily in two ways: the tracheotomy's propensity for stenosis at the level of the tracheostoma and the glottic and high subglottic injury induced by translaryngeal endotracheal tubes. These differences have been the primary indication for converting translaryngeal intubation to tracheotomy: accepting the easily repaired stenosis at the tracheostoma in place of the more difficult to repair, and occasionally irreparable, glottic stenosis. Endotracheal Tube Injury Endotracheal tubes cross the larynx and, forced posteriorly by the tongue, rest on the posterior commissure, arytenoids, and posterior cricoid plate where they can cause ischemic ulceration. This effect is common and can be seen both experimentally and clinically within hours of endotracheal intubation. 8 The pressure exerted by endotracheal tubes on the posterior and medial portions of the glottis have been measured at hundreds of millimeters of mercury. Most injuries of this type heal promptly and completely, but cricoarytenoid joint fixation and severe scarring of the

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Figure 2. Airway injury from (A) endotracheal tube and (B) tracheotomy tube is shown. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

posterior commissure can occur. These lesions are relatively difficult to treat, and the results of surgical therapy either through endoscopic or open approaches are often poor. Less common injuries include scarring of the anterior commissure and vocal cord paresis from direct trauma to the cord or from pressure injury by the cuff to the recurrent laryngeal nerves as they enter the subglottic larynx. Tracheal injuries are almost always the result of pressure necrosis from the tube cuff. Older endotracheal tubes had high-pressure low-volume cuffs that forced the trachea to conform to their rigid shape and resulted in ischemic injury. When used properly, the high-volume low-pressure cuffs that are currently available conform to the shape of the trachea and cause no damage from pressure. They may easily be overinflated, however, to become high-pressure cuffs that can lead to circumferential ischemic necrosis. This injury heals by contraction and results in a fibrous stenosis that may involve the submucosa only, preserving normal tracheal cartilage anatomy, or may be transmural with complete fibrous replacement of the tracheal wall (Fig. 3). Occasionally, transmural injury of this sort leads to loss of cartilaginous support and tracheomalacia with resultant collapse of the airway. Less commonly, stenosis occurs in the subglottic area from injury to the cricoid cartilage with granulation and scarring. Injury may also occur at the tip of the tube from impingement on the tracheal wall, which is most commonly an anterior tracheal ulceration that heals by granulation. Tracheotomy Tube Injury The most common airway injury caused by tracheotomy is stenosis at the site of the stoma because of granulation, scarring, and contraction. This

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Figure 3. Tracheal stenosis with submucosal thickening and transmural fibrosis. A, Gross specimen.

(Illustration continued on opposite page)

Injury occurs frequently but usually to a minor degree without clinical significance. 17 Granulations around the stoma occur commonly and may be extensive enough to prevent decannulation because of obstructive symptoms. Extensive granulation tissue around the stoma usually mirrors extensive intratracheal granulation caused by foreign-body reaction to the tracheotomy tube. In general, less tissue reaction occurs to stainless steel or silver than to Silastic. Patients who have diabetes or who are immunocompromised tend to have formation of copious granulation tissue and require meticulous tracheotomy care and frequent (4 to 6 weeks) tube changes. Healing of the tracheostoma after decannulation can produce a triangular retraction of the anterior tracheal walls severe enough to be obstructive (Fig. 4). In addition, posterior displacement of the anterior tracheal wall on the superior aspect of the stoma by the tracheotomy tube may cause narrowing of the airway. Low subglottic injury can occur when the tracheotomy is made in the first tracheal ring or through the cricothyroid membrane that permits cricoid erosion, infection from pressure necrosis, and subsequent stenosis. Injuries from the cuff and tip of the tube are similar to injuries caused by endotracheal tubes.

PREVENTION Glottic Injury The appearance of glottic edema and mucosal ulceration is common and occurs within hours of endotracheal tube intubation. Most of these

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Figure 3 (Continued). B, Photomicrograph shows submucosal inflammation and fibrosis with anatomy of the cartilage preserved.

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Figure 4. Stomal stenosis results from scarring and contraction of the tracheal walls. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

injuries resolve promptly after extubation; however, some Injuries unpredictably progress to laryngeal granulations or scarring and stenosis of the posterior commissure. Although most patients undergoing more than several days of endotracheal tube intubation have some degree of acute laryngeal dysfunction, usually mild edema, most problems will resolve completely within several weeks. The effect the duration of intubation has on the incidence of glottic injury is not clearly defined. Whited22 prospectively studied 200 patients and reported the incidence of stenosis of the posterior commissure to be 0 in patients intubated from 2 to 5 days, 4% in patients intubated from 5 to 10 days, and 12% when patients had continuous intubation from 11 to 24 days. This strong correlation between the duration of intubation and the likelihood of severe laryngeal damage is not well established, however. 14 Colice et al4 prospectively observed 82 patients and found a typical pattern of posterior glottic edema and ulceration in 94% of patients after prolonged intubation but found no correlation between the severity of observed injury and the development of chronic hoarseness. They also observed no instances of stenosis of the posterior commissure, which suggests that translaryngeal intubation may be safe for long periods and that the decision to perform tracheotomy should be based on reasons other than prevention of laryngeal stenosis, such as reduction of dead space, ease of weaning and pulmonary toilet, comfort and mobility of the patient, oral hygiene, and psychologic factors. Evidence 2 exists that larger tubes worsen the pressure injury to the posterior larynx, and the choice of a tube suited to the patient's glottic size may reduce such injury. A linear relationship of tracheal lumen size to the patient's height appears to exist. In our experience, a commonly made mistake is the use of an overly large endotracheal tube in obese individuals, particularly women, assuming that the tracheal size corresponds to the patient's weight.

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Although nasotracheal intubation and paralysis reduce the shearing effect of tube motion on the larynx, they have not been shown to reduce severe laryngeal injury. Stomal Stenosis Careful radiologic examination will show some degree of tracheal narrowing at the level of a healed tracheostoma in virtually every patient after tracheotomy, although only 3% to 12%1,21 of patients will have clinically significant stenoses requiring treatment. Stomal stenoses result from loss of the anterior tracheal wall from surgical technique, pressure injury, or infection. Prevention depends on reducing the extent of the defect and limiting damage to the adjacent airway. A careful operation vertically incising the second and third tracheal rings without excessive removal of tracheal cartilage and avoiding the insertion of an overly large tube minimizes the tracheal defect. Incision of the first tracheal ring or cricoid cartilage can induce cricoid infection, necrosis, and subsequent stenosis. Pressure necrosis at the site of the stoma can be reduced by the use of swivel connectors and ventilator tubing supports that will prevent undue traction on the tracheotomy tube. Careful wound care can help prevent local infection that may lead to further destruction of the exposed tracheal cartilage. Tracheal Cuff Injury The circumferential tracheal injury frequently seen in the 1960s was clearly shown5 to be caused by the use of tubes having high-pressure lowvolume cuffs. A change in tube design in the 1970s to a low-pressure highvolume cuff dramatically reduced the incidence of these injuries. Injuries continue to occur, however, because the low-pressure cuff can easily be overinflated, exceeding the tracheal mucosal capillary perfusion pressure of 20 to 30 mm Hg. Careful and frequent monitoring of cuff pressures to keep them below 20 mm Hg should eliminate injuries caused by the cuff. Permitting a small amount of leakage of air around the cuff is occasionally required, especially in ventilator-dependent patients with high peak inspiratory pressures. The measurement of cuff pressure requires the use of a four-way stopcock that permits inflation of the cuff with a syringe with simultaneous measurement of the inflation pressure. Attaching a manometer to an already inflated cuff underestimates inflation pressures because of compression of the air within the manometer tubing when the cuff is opened to the manometer.15 The tracheal mucosa is sensitive to erosion,13 and motion of the tip of the tube against the tracheal wall can be reduced by proper positioning and securing of the tube. Nasotracheal intubation provides a more secure, less mobile tube that may reduce this sort of injury.

CLINICAL PRESENTATION The clinical manifestations of laryngeal injury range from a mild change in the quality of the voice to severe stridor, hoarseness, and dyspnea,

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depending on the degree of injury. Hoarseness early after extubation is common but usually resolves rapidly. Patients with severe glottic injury, instead of improving gradually over weeks, show persistence or worsening of their symptoms as granulations and scar tissue form. Patients with subglottic and tracheal stenosis may present from hours to years after extubation with obstructive symptoms. Exertional dyspnea is the usual presenting symptom and usually does not appear until the diameter of the airway is less than 10 mm. Dyspnea and stridor at rest appear only when the airway is narrowed to 5 mm or less. Patients are often treated for asthma, including corticosteroid therapy, for various lengths of time, with no improvement in symptoms. They invariably exhibit a progressive decrease in exercise tolerance as the stenosis worsens and may also complain of trouble clearing secretions, of discomfort in the chest and throat, and of chronic coughing.

DIAGNOSIS

The diagnosis of laryngeal injury or dysfunction is often easily made on clinical grounds. Indirect or fiberoptic direct nasolaryngoscopy is a simple technique to confirm clinical suspicions and clearly define pathologic findings. Video laryngoscopy with stroboscopy using flexible nasolaryngoscopes or rigid rod lens telescopes (60- or gO-degree angled lenses) is an excellent diagnostic tool for uncovering the most subtle laryngeal pathologic processes, such as vocal cord paresis. Tracheal and subglottic stenoses are more subject to diagnostic delay. Because of their relative infrequency, these stenoses are often mistaken for a primary pulmonary pathologic process when first seen. Previously intubated patients who present with the new onset of exertional dyspnea should be suspected of having stenosis of the airway. A plain film of the chest will often show an irregularity in the tracheal air column that is diagnostic of stenosis. Pulmonary function tests can show a typical flattened flow volume loop characteristic of upper airway obstruction, but this finding is diagnostic only when the airway is 8 mm or less in diameter. The most useful noninvasive test for evaluating the larynx and trachea is plain linear tomography that shows excellent detail of the airway in coronal and sagittal views (Fig. 5). Contrast tracheography is unnecessary. Computed tomography is less useful because the axial views make it difficult to visualize the contour and extent of the airway injury. Magnetic resonance imaging is useful but, for the added expense, adds little diagnostic information over plain tomography. Bronchoscopy should be performed in all patients to evaluate the nature of the stenosis and to assess the length of involved airway and the degree of laryngeal involvement. Flexible bronchoscopy is a useful diagnostic procedure but carries some hazard. Insertion of a flexible fiberoptic telescope across a narrow stenosis can completely occlude the airway. Rigid bronchoscopy is the best diagnostic technique because it permits thorough assessment of the airway while providing an adequate channel for ventilation. Careful measurements of the stenotic area can be made, and

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Figure 5. Linear tomography demonstrates midtracheal stenosis.

dilation of the stenosis with the bronchoscope can be performed. General anesthesia is usually employed, maintaining spontaneous ventilation so that a tenuous airway is not abruptly lost with paralysis and so that areas of tracheomalacia may be identified.

TREATMENT OF GLOTTIC STENOSIS Glottic granulations and epithelialized granulomas usually occur on the vocal processes of the arytenoid cartilages. They are easily removed with biopsy forceps or the carbon dioxide (C0 2) laser. Pedunculated granulomas present little difficulty, but sessile lesions may require careful resection avoiding the perichondrium. Antibiotics and systemic corticosteroids are helpful in treating this inflammatory process after the granuloma is carefully removed. Medical treatment is continued, often for weeks, until healing takes place. The simplest and most reversible form of glottic injury is the formation

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of adhesions or webs. An anterior commissure web can be treated endoscopically using the CO 2 laser with a micromanipulator attachment to a standard operating microscope. Exposure is obtained with an operating laryngoscope placed on a suspension system attached to the operating table. Thick fibrotic webs may require reinforced Silastic stents fixed in place endoscopically with translaryngeal sutures to prevent restenosis after treatment with the CO 2 laser. Stenosis of the posterior commissure is a difficult problem to treat, and results are variable. Vertical incision of the interarytenoid web of scar tissue releases the stenosis, extending into the muscle when necessary. To prevent recurrence of the scarring, the denuded area is covered with a pedicled mucosal flap. Some surgeons 6 use a superiorly based flap taken from the posterior cricoid performed through a thyrotomy approach. We prefer to use a medially based flap of arytenoid mucosa, spot welded in place using the CO 2 laser through a microlaryngeal approach. A conforming intralaryngeal stent is not usually used unless paralysis of the vocal cords is present. Division of the stenosis and stenting without the use of a mucosal flap usually result in recurrence. TREATMENT OF LARYNGEAL PARALYSIS

Unilateral vocal cord paralysis usually does not require treatment. Airway distress or aspiration is not often a problem; however, dysphonia can be troublesome. Endoscopic injection of Teflon under local anesthesia or laryngoplasty performed through an external approach interposing a Silastic implant will serve to displace the paralyzed vocal cord medially for better phonation. Bilateral vocal cord paralysis, on the other hand, usually produces severe stridor. Treatment consists of permanent tracheostomy or arytenoidectomy. Arytenoidectomy, however, is usually associated with worsening of the voice or with aspiration-induced pneumonia. When necessary, we prefer endoscopic arytenoidectomy using the CO 2 laser, providing the patient with a satisfactory posterior glottic airway without worsening of the voice. Postoperative aspiration of liquids is usually transitory. TREATMENT OF TRACHEAL STENOSIS

Medical Treatment

No effective medical therapy exists for tracheal stenosis. Corticosteroids have no proved benefit in reducing the amount of inflammation and subsequent stricturing. They may, in fact, be implicated in the origin of some tracheal stenoses by permitting bacterial overgrowth and infection. Corticosteroids may, in addition, delay epithelial migration and healing of areas denuded of mucosa. Patients who have been taking corticosteroids for the treatment of presumed asthma should have them withdrawn gradually before surgical resection because of the known adverse effect corticosteroids have on tracheal healing.

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Bronchoscopic Dilation The mainstay of initial therapy for subglottic and tracheal stenosis is rigid bronchoscopy and dilation. Initial dilation of a tight subglottic or tracheal stricture may be accomplished with Jackson dilators passed through the laryngoscope or bronchoscope using graded increases in sizes. Thereafter, progressive insertion with a corkscrew motion of gradually larger bronchoscopes will dilate the stricture further. Overdilation should be avoided to prevent splitting of the rigid fibrous stricture. Dilation is only a palliative measure. Gradual recurrence of symptoms is expected in all but a few patients. By use of this technique, virtually any stenosis of the airway can be enlarged to permit adequate ventilation and time for thorough evaluation of the patient. In patients with uncomplicated stenoses, dilation may be performed in the operating room just before resection. Emergency tracheotomy should rarely, if ever, be necessary. Patients who require tracheotomy because of glottic stenosis or whose tracheal resection and reconstruction must be delayed for medical reasons should have the stoma placed in the stenotic trachea and not in the normal distal trachea to leave undamaged as much airway as possible for use in subsequent reconstruction. Endotracheal Stent A tracheal T tube may be used as an alternative to resection in patients with a functional glottis who are not surgical candidates for medical reasons or whose stenosis is too long to permit safe resection. The T tube is an intratracheal Silastic stent that holds open a stenotic or malacic airway and is secured in position by a limb brought out through an anterior tracheotomy.16 The stent maintains an airway while permitting the normal use of the glottis, which enables normal phonation, coughing, and clearing of secretions. The T tube should not be used when plugging of the external limb is not possible because of an inadequate glottic airway. An open external limb will lead to tracheal secretions plugging the tube and causing airway obstruction. Daily instillation of a saline solution is necessary to keep secretions from inspissating within the tube, and changing the stent every 6 months is required. Laser Excision Some short weblike stenoses and areas of granulation are easily treated with the CO 2 laser.20 By making radial incisions in the area of stenosis followed by dilation with the rigid bronchoscope, the airway can be enlarged with minimal trauma and good and often long-lasting results (Fig. 6). When stenosis recurs, the duration of symptomatic palliation seems to be appreciably longer than with dilation alone in our experience. It is important not to excise the entire stenotic area because the resulting circumferential area denuded of epithelium will restenose within 6 weeks to 2 months. Longer, more complex stenoses are best treated surgically. INDICATIONS FOR OPERATION Ferguson et al9 in 1950 and Cantrell et aP in 1961 proved experimentally that extensive tracheal resection and reconstruction with primary

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Figure 6. CO 2 laser excision of tracheal stenosis. A and B, Proposed lines oflaser incision in the weblike stenosis are outlined by Xs. C and D, Radial laser incision of stenosis is carried out in quadrants.

(Illustration continued on opposite page)

anastomosis were possible. In the 1960s and 1970s, Grillo lO , 11 and Pearson et al17, 18 developed and perfected the technique of subglottic and tracheal resection for stenoses caused by intubation injury, Surgery for these lesions today, as a result, is routine, safe, and effective and is the preferred treatment for most patients with benign airway stenosis, Any patient with symptomatic subglottic or tracheal stenosis who is a good medical risk should be considered a candidate for resection and reconstruction. Operation may be contraindicated for reasons other than severe coexisting medical illness, Patients on ventilators or who are likely

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Figure 6 (Continued). E and F, Final airway after dilation with rigid bronchoscope leaves bridges of mucosa that facilitate re-epithelialization. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

to require assisted ventilation in the future should not be operated on because their airway will be subject again to the risk of intubation injury. Patients who do not have a functioning glottis should have their operations staged with repair of the glottic injury first so that at the time of tracheal resection, the tracheotomy tube can be removed. Injuries that require resection of more than 50% to 60% of the trachea are usually unreconstructable with primary anastomosis because of unacceptably high tension on the suture line. Severe subglottic injury that extends to the vocal cords makes reconstruction extremely difficult because no subglottic space is present to which the trachea can be sewn, although a successful repair of this type has been reported. 7 Open resection of the stenosis with laryngoplasty should be performed before tracheal resection whenever possible.

SURGICAL TECHNIQUE The resection and reconstructive technique for tracheal and subglottic stenosis has been described in detaip2 and will be olltlined briefly (Figs. 7 through 13). The patient is positioned supine with an inflatable thyroid bag beneath the shoulders, and the neck is fully extended. Cervical exposure through a collar incision provides adequate exposure in most instances. Exposure of stenoses that are within several centimeters of the carina is facilitated by splitting the manubrium. The entire trachea from cricoid to carina is mobilized along its anterior surface sharply in the cervical region

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Figure 7. The airway is intubated beyond the stenosis, and exposure is obtained through a cervical incision. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

and with blunt finger dissection in the thoracic portion. This important step relieves anastomotic tension and can be carried out easily and safely because all of the tracheal blood supply enters laterally. Because no margin is required, dissection may proceed directly along the tracheal wall, and the

Figure 8. A, Complete anterior mobilization of the trachea is performed. B, Dissection around the stenosis is carried out along the tracheal wall to avoid injury to the recurrent laryngeal nerves. The endotracheal tube is withdrawn before division of the stenosis (arrow). (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

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Figure 9. A, The stenotic area is divided, and distal trachea is intubated. B, All damaged trachea is resected. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

recurrent laryngeal nerves (Fig. 8) need not be exposed, which protects them from damage. Circumferential dissection of the trachea should be limited to the area to be excised and 1 cm of proximal and distal trachea, which is enough to permit placement of anastomotic sutures. More extensive circumferential dissection risks devascularizing the tracheal anastomosis. When the trachea is encircled, the stenosis is transected and the distal trachea is intubated from the surgical field. Resection of the stenosis proximally and distally is performed in stages to avoid resecting excessive length; however, all of the abnormal trachea must be resected to minimize the risk of recurrence. Lateral traction sutures of 2-0 Vicryl are inserted, and interrupted anastomotic sutures of 4-0 Vicryl are placed 3 mm apart and 3 mm back from the tracheal edge. The use of absorbable sutures has

Figure 10. A, Lateral traction sutures and anastomotic sutures are inserted. B, The endotracheal tube is advanced into the distal trachea when all sutures are in place. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

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Figure 11. A, With the neck in flexion, the lateral traction sutures are tied. B, The anastomotic sutures are tied. C, The neck is secured in flexion with a suture to the chin. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

Figure 12. Flexion of the neck reduces anastomotic tension by permitting descent of the larynx. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

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Figure 13. Laryngotracheal resection for subglottic and tracheal stenosis. A, Lines of incision are shown. B, The anterior cricoid cartilage is excised obliquely, and thickened submucosa over posterior cricoid plate is removed. C, The cricoid cartilage is covered with a posterior membranous tracheal Hap. D, The final anastomosis is shown. (Reprinted with permission of the Lahey Clinic, Burlington, MA.)

eliminated the problem of granulomas at the suture line. After all of the sutures are placed, the thyroid bag is deflated, the neck is flexed, and the lateral traction sutures and then the anastomotic sutures are tied. The assessment of anastomotic tension is a matter of experience; experimental evidence3 suggests that it should be less than 1700 gm, but 1000 gm or less is often the goal. Flexion of the neck is the simplest and most effective means of reducing tension (Fig. 12). When tension seems excessive despite cervical flexion, laryngeal release, usually of the suprahyoid type, is employed and will provide an additional 1.5 cm of length. Division of the right inferior pulmonary ligament and right hilar release are rarely needed. The wound is closed leaving a paratracheal drain, which is removed on the first or second postoperative day. The neck is secured in flexion with a heavy suture from the chin to the anterior chest that is removed on the seventh to tenth postoperative day. The patient is discharged if tomography shows a satisfactorily healed anastomosis (Fig. 14).

SUBGLOTTIC STENOSIS Upper tracheal stenoses may extend into the lower subglottic larynx, requiring partial cricoid excision (see Fig. 13). As long as some subglottic

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Figure 14. Surgical outcome. A, Preoperative tomogram shows tracheal stenosis. B, Tomogram on the 7th postoperative day shows well-healed anastomosis.

space remains, a laryngotracheal anastomosis may be performed successfully. The resection begins as an oblique resection of the entire anterior cricoid cartilage and ends laterally at its inferior border to prevent injury to the recurrent laryngeal nerves. The thickened mucosa and submucosa overlying the posterior cricoid plate are excised down to the cartilage and about half the distance to the vocal cords. The distal tracheal end is beveled posteriorly, leaving a flap of membranous trachea that is sutured to the denuded posterior cricoid plate in two layers. After tying of the posterior anastomotic sutures, the endotracheal tube is advanced into the trachea, and the remainder of the sutures are placed and tied. Distal tracheotomy is not commonly used but may be considered when severe postoperative glottic edema is anticipated. SUMMARY

Iatrogenic airway injury after tracheotomy and endotracheal intubation continues to be a serious clinical problem. Endotracheal tubes cause

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pressure injury to the glottis and may result in severe commissural scarring that is difficult to treat. Tracheotomy tubes may result in severe stomal stenosis in the trachea or subglottic region, which is more amenable to surgical treatment. Both methods of airway intubation may result in pressure necrosis from the tube cuff that can be prevented by careful monitoring of inflation pressures. The technique oflaryngotracheal resection and reconstruction has been well developed and may be applied successfully to most patients with subglottic and tracheal stenosis. The surgical treatment of glottic stenosis remains a challenge.

REFERENCES 1. Andrews MJ, Pearson FG: Incidence and pathogenesis of tracheal injury following cuffed tube tracheostomy with assisted ventilation: Analysis of a two-year prospective study. Ann Surg 173:249-263, 1971 2. Bishop MJ: Mechanisms of laryngotracheal injury following prolonged tracheal intubation. Chest 96:185-186, 1989 3. Cantrell JR, Folse JR: The repair of circumferential defects of the trachea by direct anastomosis: Experimental evaluation. J Thorac Cardiovasc Surg 42:589-598, 1961 4. Colice GL, Stukel TA, Dain B: Laryngeal complications of prolonged intubation. Chest 96:877-884, 1989 5. Cooper JD, Grillo HC: The evolution of tracheal injury due to ventilatory assistance through cuffed tubes: A pathologic study. Ann Surg 169:334-348. 1969 6. Cotton R, Silver P, Nuwayhid NS: Chronic laryngeal and tracheal stenosis. In Paparella MM, Shumrick DA (eds): Otolaryngology, vol 3. Philadelphia, WB Saunders, 1980, pp 2931-2950 7. Couraud L, Hafez A: Acquired and non-neoplastic subglottic stenoses. In Grillo HC, Eschapasse H (eds): International Trends in General Thoracic Surgery, vol 2: Major Challenges. Philadelphia, WB Saunders, 1987, pp 39-58 8. Donnelly WH: Histopathology of endotracheal intubation: An autopsy study of 99 cases. Arch Pathol Lab Med (Chicago) 88:511-520, 1969 9. Ferguson DJ, Wild Wangensteen OH: Experimental resection of the trachea. Surgery 28:597-619, 1950 10. Grillo HC: The management of tracheal stenosis following assisted respiration. J Thorac Cardiovasc Surg 57:52-71, 1969 ll. Grillo HC: Primary reconstruction of airway after resection of subglottic laryngeal and upper tracheal stenosis. Ann Thorac Surg 33:3-18, 1981 12. Grillo HC: Congenital lesions, neoplasms and injuries of the trachea. In Sabiston DC Jr, Spencer FC (eds): Surgery of the Chest. Philadelphia, WB Saunders, 1983, pp 244279 13. Hilding AC: Laryngotracheal damage during intratracheal anesthesia: Demonstration by staining the unfixed specimen with methylene blue. Ann Otol Rhinol Laryngol 80:565581, 1971 14. Kastanos N, Estopa Mira R, Marin Perez A, et al: Laryngotracheal injury due to endotracheal intubation: Incidence, evolution, and predisposing factors. A prospective long-term study. Crit Care Med 11:362-367, 1983 15. Lewis FR Jr, Schlobohm RM, Thomas AN: Prevention of complications from prolonged tracheal intubation. Am J Surg 135:452-457, 1978 16. Montgomery WW: Silicone tracheal T-tube. Ann Otol Rhinol Laryngol 83:71-75, 1974 17. Pearson FG: A prospective study of tracheal injury complicating tracheostomy with a cuffed tube. Ann Otol Rhinol Laryngol 77:867-882, 1968 18. Pearson FG, Cooper JD, Nelems JM, et al: Primary tracheal anastomosis after resection of the cricoid cartilage with preservation of recurrent laryngeal nerves. J Thorac Cardiovasc Surg 70:806-816, 1975 19. Salassa JR, Pearson BW, Payne WS: Gross and microscopical blood supply of the trachea. Ann Thorac Surg 24:100-107, 1977

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20. Shapshay SM, Beamis JF Jr, Hybels RL, et al: Endoscopic treatment of subglottic and tracheal stenosis by radial laser incision and dilation. Ann Otol Rhinol Laryngol 96:661664, 1987 21. Westgate HD, Roux KL Jr: Tracheal stenosis following tracheostomy: Incidence of predisposing factors. Anesthes Analg 49:393-401, 1970 22. Whited RE: A prospective study of laryngotracheal sequelae in long-term intubation. Laryngoscope 94:367-377, 1984

Address reprint requests to John M. Streitz, Jr, MD Department of Thoracic and Cardiovascular Surgery Lahey Clinic Medical Center 41 Mall Road Burlington, MA 01805

Airway injury after tracheotomy and endotracheal intubation.

Iatrogenic airway injury after tracheotomy and endotracheal intubation continues to be a serious clinical problem. Endotracheal tubes cause pressure i...
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