Laryngeal Contact Ulcer (Granuloma)

Laryngeal contact ulcers and contact granulomas develop on the medial surface of the arytenoid cartilage (vocal process), where the cartilaginous portions of the vocal folds collide forcefully during phonation or where an endotracheal tube has caused mucosal trauma. Three main etiologies are recognized: laryngopharyngeal reflux (LPR), vocal abuse and hyperfunctional voice use, and post-intubation injury. The lesions begin as superficial ulcers and progress to fibroepithelial granulomas with a characteristic pedunculated appearance.

Patients describe persistent hoarseness, throat clearing, globus sensation, mild odynophagia, and frequent voice fatigue. Posterior laryngitis with arytenoid edema and erythema accompanies LPR-associated lesions. Stroboscopic findings include reduced mucosal wave on the affected side, asymmetric vibration, and the granuloma occluding glottic closure during phonation.

Treatment is largely conservative. First-line therapy targets the underlying cause: high-dose proton pump inhibitor with dietary and lifestyle reflux measures, voice therapy to reduce hard glottal attack and effort, and treatment of post-intubation lesions with steroid inhalers. Botulinum toxin injection into the lateral cricoarytenoid muscle reduces collision force and accelerates healing for refractory cases. Microsurgical excision is reserved for airway compromise, biopsy concern for malignancy, or persistent lesions despite 6-12 months of medical therapy; recurrence after surgery is common without addressing the underlying cause.