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Background  Tracheostomy and endotracheal intubation can result in subglottic tracheal stenosis, and predisposition to keloid scar formation can increase stenosis risk after tracheal injury. This study aims to compare the incidence and severity of subglottic tracheal stenosis in keloid and non‐keloid patients following iatrogenic tracheal injury, in particular tracheostomy.    Methods  From 2012 to 2017, 218 573 patients were intubated for surgery; 2276 patients received tracheostomy in People’s Hospital of Zhengzhou University, China. Among these patients, 133 patients, who developed tracheal stenosis after intubation and/or tracheostomy, were divided into keloid or non‐keloid groups; their Myer and Cotton grading of tracheal stenosis, time‐to‐onset of airway stenosis, and treatment outcome were assessed and compared.    Results  The percentages of high grade (Myer and Cotton grading III/IV) tracheal stenosis were higher among keloid patients than non‐keloid patients (intubation: 83.3% vs 25.7%; tracheostomy: 77.7% vs 33.3%). Time‐to‐onset of airway stenosis following intubation (tracheostomy) was 27 ± 5 (38 ± 13) and 41 ± 7 (82 ± 14) days for keloid and non‐keloid patients, respectively ( P  < 0.01). The incidence of tracheal stenosis is higher in keloid than non‐keloid subjects (19.4% vs 1.82%,  P  < 0.001). Keloid patients also required more frequent treatment ( P  < 0.01) of longer duration, yet cure rate was significantly lower ( P  < 0.01).    Conclusions  Our study suggests that tracheostomized patients with keloid phenotype are more susceptibility to develop iatrogenic tracheal stenosis of greater severity and with poorer treatment outcome. Greater cautions may be required when performing tracheostomy in keloid subjects. More substantive analysis is warranted to establish keloid phenotype as a risk factor for tracheal stenosis.

acta anaesthesiologica scandinavica

Iatrogenic subglottic tracheal stenosis after tracheostomy and endotracheal intubation: A cohort observational study of more severity in keloid phenotype