Laryngotracheal stenosis: Mechanistic review.

BACKGROUND: The purpose of this review article is to summarize the existing literature surrounding wound healing mechanisms in laryngotracheal stenosis. METHODS: A review of general wound healing pathophysiology, followed by a focused review of iatrogenic laryngotracheal stenosis (iLTS) and idiopathic subglottic stenosis (iSGS) as conditions of aberrant wound healing. RESULTS: iLTS is the scarring of the laryngotracheal complex, coming secondary to injury from prolonged intubation. iSGS is a chronic fibroinflammatory scarring and narrowing of the subglottic airway in the absence of any obvious preceding injury or trauma. They are both thought to result from a prolonged and dysregulated wound healing response that promotes the deposition of pathologic scar in the airway. CONCLUSIONS: Understanding the mechanisms that underlie wound healing will help identify and intervene on the process early in its development and discover future therapies that target individual wound healing mechanisms limiting the incidence of this recalcitrant disease process.

Utility of Routine Spirometry Measures for Surveillance of Idiopathic Subglottic Stenosis.

Importance: Because of the recurrent nature of idiopathic subglottic stenosis, routine follow-up is necessary for monitoring progression of stenosis. However, no easily accessible, standardized objective measure exists to monitor disease progression. Objective: To determine whether peak expiratory flow (PEF) can be used as a reliable and easily accessible biometric indicator of disease progression relative to other validated spirometry measures in patients with idiopathic subglottic stenosis. Design, Setting, and Participants: Prospectively collected data on PEF, expiratory disproportion index (EDI), and total peak flow (TPF) from 42 women with idiopathic subglottic stenosis without comorbid lower airway or parenchymal lung disease who were treated at a single tertiary referral center between 2014 and 2018 were analyzed. The mean follow-up period was 18.2 months (range, 2-40 months). Ten patients initially screened were not included in the analysis owing to comorbid glottic or supraglottic stenosis or nonidiopathic etiology. Main Outcomes and Measures: Measurements of PEF, EDI, and TPF were taken at preoperative visits and at all other visits. Results: Forty-two women (mean age, 51.5 years; 98% white [n = 41]) met the inclusion criteria. The area under the curve for PEF was 0.855 (95% CI, 0.784-0.926). The optimal cutoff value was 4.4 liters per second (264 L/min), with a sensitivity and specificity of 84.4% and 82.0%, respectively. The area under the curve for EDI was 0.853 (95% CI, 0.782-0.925). For TPF, this was 0.836 (95% CI, 0.757-0.916). Conclusions and Relevance: This study provides evidence supporting the use of PEF as a simple, efficient, and accessible way of monitoring progression of idiopathic subglottic stenosis and predicting receipt of surgical intervention. Sensitivity and specificity of PEF were comparable to those of the more complex measures of TPF and EDI.

Lack of Efficacy of Symptoms and Medical History in Distinguishing the Degree of Eosinophilia in Nasal Polyps.

BACKGROUND: Distinguishing eosinophilic nasal polyps (NP) from noneosinophilic NP will impact prognosis and therapeutic responsiveness. OBJECTIVE: To investigate the ability of clinical history and biomarkers to distinguish these conditions. METHODS: A total of 74 consecutive patients undergoing surgery for NP were enrolled. Clinical presentations were evaluated using the 22-item sinonasal outcome test (SNOT-22). Biomarkers included absolute eosinophil count, IgE, and extent of tissue hyperplasia on sinus computed tomography scan. Tissue eosinophilia was quantified in 10 random hpf and data analyzed addressing both peak and average results. RESULTS: No component of the SNOT-22 was predictive of tissue eosinophilia. Similarly, a medical history of allergic rhinitis, asthma, or aspirin-exacerbated respiratory disease was not predictive. An absolute eosinophil count of more than 300 was associated with NP tissue eosinophilia. In contrast, neither IgE nor extent of sinus computed tomography hyperplasia was predictive. CONCLUSIONS: The ability to individualize therapies for NP is dependent on identifying clinical features or biomarkers of eosinophilia. However, with the exception of circulating eosinophilia, we could not identify a clinical feature or biomarker that robustly predicted the presence of tissue eosinophilia. Even more problematic, even the seeming "criterion standard" determination of tissue pathology was of limited value, as our cohort displayed a continuous spectrum of tissue eosinophil expression, making arbitrary any definitive cutoff distinguishing these conditions.