Abstract
Acquired laryngeal stenosis is the most serious long-term complication of endotracheal intubation in children. Employing the whole-organ serial section technique, the sequence of histopathologic changes leading to stenosis was studied. Ulceration occurs when an endotracheal tube causes mechanical abrasion and/or induces pressure necrosis on the laryngeal mucosa. Secondary healing of ulceration produces granulation tissue and subsequent fibrous scar tissue. Most exuberant granulation tissue resolves without sequelae, but some becomes firm, almost avascular fibrous scar tissue. The accumulation of submucosal fibrous tissue may decrease the size of the glottic or subglottic lumen. Contraction of scar tissue causes a distortion of glottic and subglottic laryngeal complex, leaving a reduced and irregularly shaped glottic and subglottic lumen. Submucosal mucous gland hyperptasia directly reduces the inner diameter of the airway. Finally, compromise of the laryngeal lumen may occur when the duct of a mucous gland is obstructed by scarring resulting from intubation: mucus accumulates in the dilated duct, producing a ductal cyst.