Objectives/Hypothesis: We sought to characterize rates of progression to posterior glottic stenosis (PGS) from autoimmune or idiopathic subglottic stenosis.Study Design: This was a retrospective review. Methods: Patients from a tertiary-care laryngology practice over a 10-year period with autoimmune or idiopathic subglottic stenosis (SGS) were included. Patients with a history of prolonged intubation or other causes of iatrogenic stenosis were excluded. PGS was confirmed on videostrobolaryngoscopy recordings by a fellowship-trained laryngologist. PGS type (1-4) was also recorded. Demographic information was recorded, and if applicable, autoimmune disease type was specified. Time until PGS was recorded along with the number of interventions. Chi-squared analysis was used to compare PGS in autoimmune and idiopathic SGS.Results: A total of 77 patients were identified with autoimmune (32 patients) or idiopathic (45 patients) subglottic stenosis. Autoimmune pathologies included systemic lupus erythematosus, granulomatosis with polyangiitis (GPA), rheumatoid arthritis, relapsing polychondritis, and sarcoidosis, with GPA the most common (14/32). Patients with autoimmune SGS had a higher rate of PGS (10 of 32) compared to idiopathic subglottic stenosis (1 of 45) for an odds ratio of 20 (95% CI: 2.4-166.4, P = .006). Patients with idiopathic SGS were more likely to be female (all 45 compared to 29/32 autoimmune, P = .07) and older (mean 53 (range 29-75) compared to 46 (20-82), P = .02).Conclusions: In this large patient cohort, autoimmune SGS patients were found to have a higher likelihood of developing PGS compared to their idiopathic counterparts, suggesting that counseling for this progression may be warranted.

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Objective The goal of this study was to characterize the symptoms and outcomes of patients with a symptomatic cervical inlet patch (CIP). Study Design Retrospective case series. Setting Tertiary care laryngology clinic in Charlottesville, Virginia. Methods A retrospective chart review of the patient's demographics, comorbidities, prior workup, interventions, and response to treatment was performed. All patients received flexible nasolaryngoscopy and barium swallow study. The analysis was descriptive. Results Eight patients (6 female) were followed for the management of symptoms related to CIP. The mean age at presentation to our clinic was 64.9 (standard deviation = 15.7). Five out of 8 patients presented with a chief complaint of dysphagia, and the remaining 3 with chronic coughs. Five out of 8 patients demonstrated findings of laryngopharyngeal reflux (LPR) including vocal fold edema, mucosal erythema, or postcricoid edema. Swallow study demonstrated hiatal hernia in 3 of 8 patients, and cricopharyngeal (CP) dysfunction (CP hypertrophy, CP bar, and Zenker's diverticulum) in 3 of 8 patients. One patient presented with a history of Barrett's esophagus. Treatment included increased acid suppression therapy and management of coexisting esophageal pathologies. Ablative procedures were performed in 5 out of 8 cases, with 2 patients requiring repeat procedures. All patients experience subjective symptom improvement. Conclusion CIP tends to present in complex patients with multifactorial dysphagia, with the most common symptoms being dysphagia and cough. Clinical features of CIP overlap with other more common pathologies encountered by otolaryngologists including LPR and CP dysfunction, and future prospective studies in larger populations should seek to clarify these associations.

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