Laryngeal Problems Following Intubation

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Laryngologic problems related to tracheal surgery are described in Chapter 35, "Laryngologic Problems Related to Tracheal Surgery." In 1950, Briggs used a plastic endotracheal tube for 42 days to administer prolonged respirator therapy.1 It remains common practice to replace an endotracheal tube used for ventilator treatment in a much shorter period with a tracheostomy tube. A tracheostomy tube is more easily managed by nursing personnel, with less danger of obstruction and more comfort for the patient than an oro- or nasotracheal tube. Endotracheal intubation provides an airway promptly and can avoid tracheostomy when prolonged mechanical ventilation is unnecessary. It is because of this lessened temporal exposure that fewer cuff lesions were seen following endotracheal intubation than after tracheostomy. A cuff that exerts high pressure on the trachea, either because of its innate characteristics or its usage, is as damaging when on an endotracheal tube as when it is on a tracheostomy tube or a cricothyroidostomy tube. Lesions due to cuffs on endotracheal tubes are usually located higher in the trachea because the cuff is seated higher in the trachea than it is with a tracheostomy tube. Tracheal stomal lesions are obviously avoided if tracheostomy is not done. In using prolonged endotracheal intubation, however, the physician exchanges the absence of potential stomal complications for complications at higher levels (nostril, pharynx, and principally larynx).

Although Briggs, in his original case, found only minor ulcerations over the arytenoid and in two small areas of the trachea at autopsy, a spectrum of more severe lesions occurs.2,3

In a series collected from the literature, Lindholm reported approximately 1 death in 120 children as a probable complication rate of prolonged endotracheal intubation.2 Most deaths occurred during the period of intubation as a result of obstruction of the airway and this probably reflects the small caliber of tubes necessarily used in small children. Laryngeal mucosal changes were prospectively observed, without exception, after prolonged endotracheal intubation. These were located on the medial sides of the arytenoid cartilages in the interarytenoid region and against the posterolateral portion of the cricoid. Changes in children were less pronounced. The lesions varied from superficial epithelial damage with only slight inflammation to deep ulceration. Donnelly detailed the histopathology of intubation.4 Within 48 hours, the perichondrium of the vocal processes and cricoid laminae were focally ulcerated, and the severity increased with time. Bergstrom and colleagues had earlier reported similar damage.5 Injury to the mucosa was seen by scanning electron microscopy, as early as 4 hours after endotracheal intubation.6 Lindholm found that 6 of 225 adult patients showed respiratory obstruction after extubation, and in 4 of these patients, the difficulty lay in the larynx.2 Five of 38 children had respiratory obstruction following extubation, and all required tracheostomy. The precise incidence of postintubation lesions of the larynx or trachea has never been satisfactorily determined, nor are such figures very meaningful, given the changing and varied standards of equipment and care both in time and place. The lesions continue to occur today.

Nearly two-thirds of adult patients with erosive lesions healed by primary epithelization within a month. In a third of the patients, a granuloma formed during healing, located largely on the medial side of the arytenoid cartilages. In many cases, the granuloma regressed spontaneously in 1 to 10 months, with a median of 60 days. The symptoms of a granuloma are irritative cough, hoarseness, and transient sensations of suffocation. Granuloma also occurs on the anterior portion of the vocal cord. In his study, Lindholm found two children who formed fibrous scars with circumferential stenosis at the level of the cricoid and a third with a posterior commissural scar bridging the interarytenoid space. Localization of damage is likely related to the curve of the endotracheal tube. When a relatively straight or slightly arched endotracheal tube is reshaped by the patient's airway, considerable force is exerted posteriorly against the medial sides of the arytenoid cartilages and the posterior surface of the cricoid (Figure 11-2).2,7 Another factor may be movement between the larynx and endotracheal tube. More prolonged exposure to pressure by the tube seems to lead to a greater incidence and depth of injury. Lindholm recommended a preshaped tube with a gently curved right angle to try to avoid such pressure.

Subglottic erosions at the cricoid level appear to be caused in large part by tubes that are too large for the particular airway. This is supported by the observation of a probably greater frequency of stenosis at this level in women and smaller males, who tend to have smaller airways. Since the cricoid cartilage is nor a

Bougie Issues Arytenoid Cartilage

a figure 11-2 Pressure on the larynx is exerted by an endotracheal tube, chiefly posteriorly, against medial arytenoid cartilages and posterolateral cricoid. Adapted from Lindholm C-E.2

mally the only complete cartilaginous ring in the upper airway, the absolute limit of the airway's diameter is set by that cartilage. If pressure results only in edema, the condition is reversible. If ulceration occurs following pressure, then a cicatricial stenosis may result during healing. Fortunately, the cricoid cartilage is a rather rugged structure, and it is unusual for it to be eroded very deeply or through its full thickness by an endotracheal tube. This probably accounts for the fact that prolonged stenting of cicatricial lesions in this region may occasionally lead to success, in contrast to the usual failure of stenting for circumferential lesions in the trachea. It may also account for the greater potential for occasional success in laser treatment of obstructive lesions at this level, in contrast with the trachea where laser treatment often fails.

Vocal cord disturbances are common in patients who have undergone prolonged endotracheal intubation. In a small percent, these disturbances may go on for over a month, but frequently regress. Permanent laryngeal paresis does occur in a small number of patients, presumably due to inflammatory involvement of recurrent laryngeal nerves. Such disability is likely to be unilateral.

Postmortem studies have shown the precise location of postintubation ulceration or necrosis of the larynx in 33 patients to be as follows: 3 had ulcers in the interarytenoid area, 26 had ulceration or necrosis on the medial side of the arytenoid cartilages, and 33 ulcerative lesions were seen on the inner posterolateral part of the cricoid.2,5 Eight of 26 patients also had tracheal lesions. In other reported series, the incidence of subglottic stenosis of the larynx following prolonged endotracheal intubation in children has run from 0 to 8%, with one series reporting as high as 20%.

In clinical practice, one may see the following at the glottic level: arytenoid fixation, interarytenoid posterior commissural scar preventing separation of the cartilages, anterior commissural stenosis, and vocal cord thickening, ulceration, or granulomas. Unilateral vocal cord paralysis that is present as a consequence of endotracheal intubation, tracheostomy, or prior surgical procedures may affect the adequacy of the glottic aperture or contribute to aspiration on deglutition. The rare presence of a bilateral cord paralysis, most often post-traumatic or postsurgical, may cause airway inadequacy or aspiration. Subglottic intralaryngeal narrowing due to cicatricial stenosis may begin immediately below the glottis or at any level below that. It is often maximal at the cricoid level for the reasons explained. Often, this subglottic laryngeal stenosis is confluent with a stenosis that extends into the upper trachea. In 50 patients treated surgically for postintubation subglottic stenosis with such a major component in the larynx, 31 resulted from endotracheal intubation alone, 16 from high or eroded tracheostomy, and 3 from cricothyroidostomy (Figure 11-3).8

The obvious statement must be made that wherever a foreign body impinges forcefully on the airway, whether a stoma is present or not, erosion may occur and be followed by cicatricial stenosis. Cuff lesions are common to all types of tubes and independent of them, except with regard to the level of cuff impingement. Stenotic injuries unique to endotracheal and cricothyroidostomy tubes are necessarily within the larynx. The stomal lesion from a tracheostomy lies within the trachea, except when a stoma is placed too high or, more often, in an older kyphotic patient, where erosion of the anterior cricoid occurs. "Subglottic stenosis," that is, laryngotracheal stenosis beginning below the cords and usually extending into the upper trachea, is circumferential following injury from endotracheal tubes (see Figure 11-3A and Figure 28 [Color Plate 15]). Those stenoses that are caused by cricothyroidostomy tubes or eroding tracheostomy tubes may be largely anterior or also circumferential (see Figures 11-3B,C). In all cases, we are dealing with laryngotracheal "bed sores," since pressure necrosis is the primary damaging factor (Figures 11-4A-E).

Brantigan and Grow proposed eliminating tracheal stomal stenosis by transferring the stoma to the cricothyroid membrane.9 Although they were fortunate that their series had no stomal complications (or cuff stenosis), clearly, this approach merely transfers the location from the trachea to the larynx (Figures 11-5A,B).3,8 Subsequent studies by these and other authors showed that cricothyroidostomy contributes to a significant and often irreversible subglottic stenosis, with an overall airway coimplication incidence of up to 52%.10 Kuriloff and colleagues pointed out that the short length of the cricothyroid membrane (5 to 12 mm)

Tracheal Stint

figure 11-4 Subglottic postintubation stenoses. A, Roentgenogram of the larynx and upper trachea. A slight 25-year-old man was ventilated with an endotracheal tube for head injury. Upper arrow indicates the vocal cord level. Lower arrow is at the cricoid level, also the point of maximum stenosis. The entire subglottic space is markedly narrowed. B, Laryngoscopic view just below the glottis in the same patient. The stenosis is severe, irregular, but circumferential. The glint of a tracheostomy tube is seen distally. Tracheostomy was necessary prior to laryngotracheal resection and reconstruction. C, Laryngotracheal stenosis following ventilation via "high tracheostomy," probably cricothyroidostomy, after repair of ruptured chordae tendineae in a 71-year-old man. Lateral cervical roentgenogram. Arrows indicate severe constriction of the lower larynx and trachea. D, Airway restoration following laryngotracheal reconstruction. Normal lumen is restored (arrow). See also Figure 28 (Color Plate 15).

figure 11-4 (continued) E, Surgical specimens from a young woman who was ventilated after multiple injuries for a long period via an endotracheal (ET) tube, continued via a tracheostomy tube. Subglottic stenosis from ET tube injury is shown at left and result of the combined ET cuff and tracheal stomal injury is on the right.

figure 11-4 (continued) E, Surgical specimens from a young woman who was ventilated after multiple injuries for a long period via an endotracheal (ET) tube, continued via a tracheostomy tube. Subglottic stenosis from ET tube injury is shown at left and result of the combined ET cuff and tracheal stomal injury is on the right.

is less than the outer diameter of most commonly used tracheostomy tubes (10 to 12 mm).10 Although most purely tracheal stomal stenoses can be corrected surgically on a first attempt with almost certain success, many laryngeal lesions are not correctable or only partially correctable from the outset. I, therefore, deplore use of elective cricothyroidostomy for ventilation. It should also be noted that concern about contaminating sternotomy incisions after cardiac surgery, by an immediately adjacent tracheostomy tube, may be obviated by using an endotracheal tube for ventilation for a few days. If tracheostomy is needed subsequently, tissue planes will have already sealed.

Preexisting neurologic deficits unrelated to the postintubation injury, particularly in patients who have suffered central nervous system trauma, may affect protective laryngeal reflexes and result in aspiration on deglutition. Such a deficit may preclude airway repair since tracheostomy may then be necessary to protect the airway and to clear secretions. Such functional deficits must be identified prior to a tracheal reconstruction.

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