Postintubation Lesions

The poliomyelitis epidemics of the mid-twentieth century introduced and led to an ever-widening use of mechanical ventilators to treat respiratory failure. The iatrogenic lesions that resulted provided a whole new field of endeavor for the tracheal surgeon. Gradually, a spectrum of lesions was recognized, attributable to ventilatory apparatus: endotracheal and tracheostomy tubes and the cuffs necessary to seal the trachea.84,90,186,212 Principal among these were 1) circumferential stenosis that appeared at the level of the sealing cuff, and 2) anteriorly pointed, arrow-shaped stenosis, which occurred at the stomal level. Additionally, granulomas occurred at the point where a tube tip impinged on the tracheal wall. Areas of malacia were seen less often at the level of the cuff and sometimes in the segment between a tracheal stoma and a cuff stenosis. Tracheoesophageal fistulae occurred principally between the trachea and the esophagus at the cuff level, usually with accompanying circumferential tracheal damage. Rare, but disastrous when they occurred, were tracheal innominate artery fistulae. These lesions proved to be of two types: one where a tra-cheostomy tube rested immediately on the innominate artery near the stoma, and another, where the cuff, or, even less often, the tube tip, eroded through the trachea anteriorly into the innominate artery.

In the 1960s, numerous papers, often single case reports, appeared in Europe and North America, describing surgical resection of postintubation strictures. Included among these together with their colleagues were Forster in 1957, Flavell in 1959, Witz in 1960, Binet and Aboulker in 1961, Van Wien in 1961, Mathey in 1966, Byrn as well as Fraser in 1967, and Jewsbury, Dor, Dolton, Schaudig, Lindholm, and Naef in 19 6 9.40,71,73,75,88,213-221 Series of cases also were reported by the following authors together with their colleagues: Deverall reported 6 patients in 1967, Pearson reported 15 in 1968, Grillo reported 14 whereas Couraud reported 9 in 1969, and Dor reported 9, Levasseur reported 10, and Harley reported 11 in 1971.84,86,89,91-93,212 These last authors, especially Pearson, Grillo, and Harley, with somewhat broader experience, defined the anatomic and pathologic differences between stomal and cuff stenoses and other postintubation injuries, and discussed their pathogenesis. Malacia instead of stenosis was also described, although a rare finding, by Grillo.222 Deverall, Pearson, Grillo, and Couraud and their colleagues stressed the importance of allowing florid inflammation to subside prior to surgical correction.84,86,89,212 Their generally good results showed the superiority of definitive surgical resection and anastomosis over prior alternative methods of treatment, such as repetitive dilation, steroid injection, or cryotherapy. Unfortunately, the lesson is being relearned today, with uncritical use of laser surgery for these lesions,223 and, more lately, with much more disastrous results, the attempted use of stents to treat postintubation stenosis.191

Postintubation lesions became, and remain, the most common indication for tracheal resection and reconstruction. Generally very good results have been obtained in major cumulative series of patients with iatrogenic tracheal and subglottic laryngotracheal stenosis: Bisson and colleagues achieved an 87.5% "cure" in 200 patients in 1992, Couraud and colleagues reported 96% success in 217 patients in 1994, and Grillo and colleagues cited 94% success in 503 patients in 1995.98,224,225

Correction of postintubation stenosis involving the subglottic larynx remains more difficult than lesions confined to the trachea. The evolution of procedures for laryngotracheal resection and reconstruction by partial cricoid resection has been outlined and their application to iatrogenic stenosis noted. Monnier and colleagues applied this approach in infants and children, also with encouraging success.167

Reoperative tracheal resection and reconstruction for unsuccessful repair of postintubation stenosis proved to be surprisingly manageable. In 1997, Donahue and colleagues tallied 92% good or satisfactory results in 75 patients who had failed prior surgical repairs, 59 of whom were referred.226

Tracheoesophageal fistulae (TEF) due to erosion by tracheal cuffs and often of "giant" size were noted early, in 1966 by Le Brigand and Roy and several other French surgeons in the same period, by Flege in 1967, and by Hedden and colleagues in 19 6 9.227-229 Scattered attempts of repair by sometimes multistaged techniques, including Braithwaite's successful use of a cutaneous flap to seal the tracheal side of a large fistula in 1961, did not often meet with success.227,230,231 Grillo and colleagues, in 1976, described a definitive one-stage technique for esophageal closure, tracheal resection (where a circumferential cuff lesion was present), and strap muscle interposition, with good results in 7 patients.232

Postintubation injury, however infrequent, has become the most frequent cause of acquired TEF. It is now effectively managed by the type of procedure noted, and has been further described by Mathisen, Couraud, and Macchiarini and their colleagues.233-235 When the fistula is small and the tracheal lesion is not circumferential, tracheal closure is performed. The techniques developed have been applied effectively to closure of TEF from a variety of causes, including trauma and inflammation.

Tracheal innominate artery fistula (TIF), described by Lunding in 1964, Silen and Spieker and Stiles in 1965, Couraud and colleagues in 1966, and Foley and colleagues in 1968, as a consequence of tracheostomy and ventilation, was effectively approached surgically by Grillo in 1976, Cooper in 1977, and Couraud and colleagues in 19 84.236-243 The mechanism of fistulization was either erosion of the tracheal wall by a high-pressure cuff, angulation of a tracheostomy tube tip, or most commonly, erosion by the tube in a low-lying tracheostomy where the elbow of the tube essentially rests on the artery. Jones and colleagues reviewed the topic extensively in 1976, including delineation of types of erosion, emergency management, safety and desirability of arterial resection, and success rates.244

The etiology of postintubation stenosis and other injuries was initially unclear. Among the factors thought to be implicated were irritation from materials of which tube and cuff were made, elution of chemicals by gas sterilization, age, debility, steroids, bacterial infection, and direct irritation by the tube's presence. Although some of these likely contributed to the injuries seen, pressure and necrosis from tubes and cuffs, whether endotracheal or by tracheostomy, with subsequent efforts at tissue repair, and, finally, cicatrization, proved to be the fundamental explanation.

Post-tracheostomy stenosis had been pointed out as early as 1886, when Colles found four strictures in 57 patients treated for diphtheria.245 However, only with the growing use of ventilation, during and after the 1952 poliomyelitis epidemic, did postintubation injuries become more frequent.

In 1960, Aboulker and colleagues identified inflammation as a major factor in the spectrum of post-tracheostomy stenosis.186 On the basis of 12 autopsy studies in patients who were ventilated via tracheostomy for differing time periods, Bignon and Chr├ętien in 1962 described inflammation, metaplasia, and stenosis at the tracheostomy site; pseudopolyps, ulceration, and stenosis in the trachea at cuff level; and, sometimes, softening of the tracheal wall.246 They attributed these changes principally to trauma from the cannula above and to ischemic compression by the cuff or erosion by the tip of the tube below. The severity of lesions did not correlate with the length of ventilation.

Yanagisawa and Kirchner as well as Atkins, in 1964, described severe damage to the trachea and stenosis from use of cuffed tracheostomy tubes.247,248 In 1965, after careful autopsy studies of tracheostomized and ventilated subjects, Florange and colleagues reconstructed the evolution of tracheal necrosis from mucosal inflammation to erosion of the mucosa, loss of cartilage, and localized mediastinitis.249 They concluded that this damage could result in stenosis. In 1965, Stiles described severe changes at the stomal, cuff, and tube tip levels in 23 patients in 37 consecutive tracheostomies, all of whom died after ventilation.238 He was inclined to relate the damage to the materials from which the tubes were manufactured. Gibson concluded in 1967 that the "main factors" in producing stenosis were cuff trauma plus infection at the stoma.250 Most tracheae of patients who died while being ventilated via tracheostomy showed necrosis. Murphy and colleagues, in 1966, could only produce stenosis in dogs with cuff tracheostomy when infection was also present.251 In 1968, Foley and colleagues described the tracheal changes due to abutment of tubes and cuffs in patients with fatal burns.240

In 1969, Grillo showed similar changes as a result of ventilation.84 Cooper and Grillo presented a detailed pathologic study of autopsy specimens from patients dying on respirators.252 A spectrum of changes was described similar to that noted by Florange. Lesions appeared within 48 hours and progressed from tracheitis to ulceration of the mucosa, to fragmentation of cartilage, to replacement of the tracheal wall with scar tissue. The location and nature of the lesions also correlated with surgically removed steno-tic lesions. Lindholm presented a detailed study in 1969 of lesions developed in the larynx and also in the trachea from ventilation.221 The severity of histologic changes was vastly greater than those described after tracheostomy alone.253 Andrews and Pearson prospectively examined the trachea of 103 patients receiving ventilator support in 1971.254 Twelve stomal and 6 cuff stenoses developed. Bronchoscopic examination was of little value in predicting which patients would go on to stomal stenosis, but circumferential mucosal ulceration at the cuff level dependably predicted stenosis at that level. Additional statistically significant factors observed in this study were large tracheostomy tubes and high-dose steroids. The same erosive processes were observed to cause tracheoesophageal fistulae and tracheoinnominate artery fistulae.

Prevention of postintubation injury quickly became a priority once the origin of these lesions was evident. In 1957, Adriani and Phillips found that most of the intracuff pressure necessary to inflate the then conventional cuffs (90 to 220 mm Hg) was expended on distending the cuff, and the pressure on the tracheal wall was low (10 to 15 mm Hg) in order to develop ventilatory pressures of 10 to 20 mm Hg.255 Cooper and Grillo later pointed out that excessive pressures were necessary to seal the irregularly-shaped trachea by distending the relatively rigid small volume cuffs that were then in use.256 Knowlson and Bassett also noted that small increments over the minimal occlusive volume necessary for the seal of conventional cuffs at 20 cm H2O caused a rapid rise in the pressure exerted on the tracheal mucosa.257 In 1943, Grimm and Knight had proposed that the ideal cuff "should have sufficient volume when inflated, without stretching, to fill the diameter of the trachea."258 Lomholt offered a cuff of thin and elastic Teflon in 1967, lying in folds so that intracuff pressure would be identical with pressure on the mucosa.259 Carroll and colleagues, in 1969, recommended a cuff with large residual volume, a large sealing area, a centered tube, and the development of only small increases in tracheal wall pressure with overinflation.260

Cooper and Grillo reproduced severe stenosing cuff lesions in dogs in 1969, which were entirely parallel with lesions seen in man (Figure 8).256 They used standard balloon cuffs and inflation necessary for ventilation at 20 to 25 cm H2O. Intraluminal pressures were 180 to 250 mm Hg. Experimental large-volume, thin-walled latex cuffs produced seals at 20 to 40 mm Hg intraluminal pressure, and no mucosal damage followed. Since this conclusively proved that tracheal lesions were due to cuff pressure, a large-volume, compliant cuff was designed for clinical use by Grillo and colleagues.261 Forty-five patients were randomly selected for ventilation with a then standard Rusch cuff or the experimental large-volume, compliant latex cuff, and the resulting tracheal injuries were evaluated and compared. Any degree of injury severe enough to evolve into stenosis was produced by the standard (high pressure) cuff. The average intracuff pressure in the new cuff was 33 mm Hg compared with 270 mm Hg in the standard cuff. In extensive clinical use, no tracheal lesions resulted from use of this large-volume, compliant cuff.

figure 8 Joel D. Cooper, MD, in about 1970, when, as surgical resident at Massachusetts General Hospital, he worked with Dr. Grillo on the etiology and prevention of postintubation cuff tracheal stenosis. Dr. Cooper went on to perform successful lung transplantation at Toronto General Hospital and developed lung volume reduction surgery for emphysema when Chief of Thoracic Surgery at Barnes-Jewish Hospital and Professor of Surgery at Washington University in St. Louis.

figure 8 Joel D. Cooper, MD, in about 1970, when, as surgical resident at Massachusetts General Hospital, he worked with Dr. Grillo on the etiology and prevention of postintubation cuff tracheal stenosis. Dr. Cooper went on to perform successful lung transplantation at Toronto General Hospital and developed lung volume reduction surgery for emphysema when Chief of Thoracic Surgery at Barnes-Jewish Hospital and Professor of Surgery at Washington University in St. Louis.

For economic reasons, manufacturers later abandoned latex in favor of plastic cuffs, which lack extensibility. When overinflated just a bit, the present day large-volume cuffs invariably produce steep rises in intracuff pressure, with the potential for tracheal injury severe enough to result in stenosis.257 Careful attention to cuff inflation and pressures, however, have avoided any incidents of cuff stenosis since 1970 at MGH. A variety of other seals, including prestretched cuffs, flanges, and alternating cuffs, were also proposed as solutions, but they lacked the simplicity and effectiveness of properly used large-volume cuffs.

After adopting the lightweight swivel trachea connectors used at MGH, Andrews and Pearson observed a drop in the incidence of stomal stenosis from 17.5% to 6.9%.254 The addition, since then, of a suspension of connecting tubing to avoid leverage of the tube against the tracheal stoma, has essentially eliminated stomal stenosis at the MGH.

Elimination of TEF has followed proper use of large-volume cuffs for ventilation, along with avoidance of inlying rigid nasogastric tubes. TIF has all but disappeared with attention to accurate placement of tracheostomy tubes at the level of the second and third tracheal rings and not below, and also, by appropriate use of large-volume, low-pressure cuffs.

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