2018 Section 6 - Laryngology, Voice Disorders, and Bronchoesophalogy

SHADMEHR ET AL

Ann Thorac Surg 2017;103:246 – 53

SYSTEMIC STEROIDS IN TRACHEAL STENOSIS

Table 5. Bronchoscopic Findings Findings

a shorter segment including only the part with cartilage destruction or established fi brosis would be required to be surgically resected. After laryngotracheal mucosal injury, the wound healing process is started. The sequence of events in wound healing includes three overlapping phases: in fl ammation, proliferation, and maturation [5] . In lar- yngotracheal stenosis, it seems that these stages of physiologic wound healing become pathogenic, leading to considerable tissue remodeling and formation of scar tissue in the airway [6] . Granulation tissue formation is also an important part of the wound healing process, but its overgrowth not only obstructs the airway lumen but also may lead to extensive scarring and fi brosis [7] . When granulation tissue moves, fi broblasts contract and draw the edges together. This concentric wound contracture causes airway stenosis [7] . Regarding these healing processes, any treatment mo- dalities should be used before the beginning or at an early stage to suppress the constricting phase and prevent the development of tracheal stenosis [7, 8] . Corticosteroids, as one of the oldest agents used in this process, suppress the in fl ammation and proliferation phase and consequently prevent fi broblast proliferation, collagen synthesis, and macrophage response [7] . Whether corticosteroid administration can prevent PITS remains to be answered. To the best of our knowledge, there is no consensus in the literature for responding to this question. There are several articles regarding this issue with many inconsistencies in the conclusions. Those are about the time and route (sys- temic versus topical) of administration, the dosage, the study group (animal versus human), the design and type of the study, the sample size, and the fi nal results. Some of the studies support the role of steroids in prevention or management of laryngotracheal stenosis, and some contradict it, although none of them is indisputable. For example, a canine study showed that steroids did not prevent subglottic stenosis, and showed neither a gross nor a histologic difference from controls [9] . In another experimental study on 18 dogs, Doolin and colleagues [10] found that steroids had no signi fi - cant effect on the formation of any type of collagen, and therefore reported that corticosteroids had no effect in preventing subglottic stenosis. A study on rats and another one on rabbits also showed that steroids offered no signi fi cant advantage in preventing tracheal or sub- glottic stenosis [8, 11] . Perepelitsyn and Shapshay [12] by performing 47 procedures in their patients showed no bene fi t for using intraoperative local steroid in- jections as an adjunct to laser for treatment of laryngeal and tracheal stenosis. Conversely, by publishing their case reports, Braidy and associates [13] , Gharde and associates [14] , Abo and colleagues [15] , and Gnanapragasam [16] showed that topical and systemic corticosteroids might be useful in the management of early PITS. Another study by Yokoi and coworkers [17] in 2014 showed that inhaled budesonide is effective for treatment of tracheal granulation tissue in patients with tracheostomies after repair of congenital

Corticosteroid Placebo

p Value

Length of stenosis, mm 28.2 (9.4)

27.7 (7.4)

0.742 0.083

Subglottic involvement

10 (20%)

4 (7.3%)

Many of our patients are not in an ideal situation for airway resection at the time of presentation and undergo several bronchoscopic dilations as a bridge to reach an appropriate time for a de fi nitive airway resection and reconstruction. During this mainly temporary manage- ment, according to the in fl ammatory nature of PITS, we hypothesized that using an antiin fl ammatory agent like prednisolone may be helpful for three reasons. The ra- tionales for these hypotheses are as follows. First, the role of RBD is coring out the granulation tis- sues, aspiration of secretions retained distal to the ste- nosis, and rupture of the circumferential fi brosis to dilate the stenotic segment of the airway. Rupture of fi brotic and scar tissue usually lead to the reformation of fi brotic tis- sue. It seems that corticosteroids could prevent, or at least postpone, the reformation of fi brosis in this step. Second, we know that cartilage destruction and full- grown fi brosis are not reversible events. However, some intubated patients are extubated before the ischemia/ injury and its subsequent in fl ammatory process lead to a well-matured fi brosis or cartilage destruction. In these circumstances, whenever the insult of the cuff or tip of the tube is omitted by extubation, it would be possible that the cascade of the in fl ammatory process becomes stopped, and an antiin fl ammatory agent could be theo- retically helpful in this process. Therefore, some of these patients could be managed by conservative methods and may never need any airway resection. And third, during ischemic events, the extent of tissue edema is always greater than the extent of necrosis, like the coronary artery occlusion that leads to a large extent of myocardial ischemia and edema, but a smaller area of necrosis at the center. In the days after infarction, by decreasing the myocardial demand through bed rest and improving the circulation by appropriate medical man- agement, some of the ischemic/edematous areas return to normal condition and the rest joins to the necrotic region. Therefore, it seems that if we could decrease the amount of the surrounding airway edema before airway resection,

Table 6. Primary and Secondary Outcomes

Corticosteroid (50 Patients)

Placebo (55 Patients)

Outcomes

p Value

Days between

52.3

30.6

0.115

bronchoscopies

Number of patients who fi nally underwent airway resection Length of resected airway, mm

28 (56%)

40 (72.7%)

0.102

38.3

43.6

0.044

293