Posterior Glottic Stenosis: A Canine Model

Abstract

Posterior glottic stenosis is a disabling disease in which the vocal folds are fixed near the midline. This allows adequate vocal fold adduction for voicing, but does not permit useful abduction for ventilation. The most common cause is prolonged endotracheal intubation for mechanical ventilation, and the incidence is estimated at 4% for intubations between 5 and 10 days. Currently, our understanding and treatment modalities are based on retrospective reviews of small, nonrandomized clinical experiences. The purpose of this project was to develop an animal model that would improve our understanding of histologic changes and allow future prospective randomized trials for therapeutic intervention. Twelve dogs, 15 to 25 kg, were randomly divided into three groups. Animals in group I had a superficial injury produced in the tissue over the right cricoarytenoid joint; animals in group 2 had a deep soft tissue injury produced; and animals in group 3 underwent joint opening. The animals were allowed to recover for 2 months. Morphometric analysis of the harvested larynges demonstrated clinically significant limitation in motion in the animals with deep soft tissue injury and in animals with joint disruption. Histologic analysis revealed various degrees of injury, from loss of subepithelial soft tissue to cartilaginous resorption and fusion of the arytenoid to the cricoid. These findings were directly related to the depth of the initial injury. It is possible to produce posterior glottic stenosis in the canine species. This will serve as a reliable animal model for future study.

Predictors of Posterior Glottic Stenosis

“…The endotracheal tube (ETT) places pressure at the posterior commissure as it bends in a caudal direction in the around the tongue base to allow the distal end to sit coaxial within the proximal trachea, positioning helped by the balloon cuff (4). In PGS, this pressure results in mucosal ulceration, prolonged inflammation, granulation tissue, and fibrosis that ultimately contracts the arytenoids and often extends into the cricoarytenoid joint (Figure 1) (4, 6, 8–9). Bogdasarian proposed a classification system with an interarytenoid scar band with posterior sinus tract (Class I), limited motion of arytenoids (Class II), fixation of one cricoarytenoid joint (Class III), and ultimately fixation of both cricoarytenoid joints (Class IV) however, this classification system has not been assessed to be predictive of therapy or outcomes (2).…”

Bacterial Laryngotracheitis and Associated Upper Airway Obstruction

“…[2][3][4]13 Outcomes of LTS with associated inflammatory changes and granulation tissue are known to improve with local surgical therapy. [2][3][4]13 Outcomes of LTS with associated inflammatory changes and granulation tissue are known to improve with local surgical therapy.…”

Pathological changes of larynx in inhalational thermal injury causing laryngeal stenosis based on a canine model

“…In fact, in order to study the interventions to laryngeal stenosis, a series of animal models have been previously established. In 1998, Msrk S. et al [8] reported a New Zealand rabbit model, which developed posterior glottic stenosis by injury of CO 2 laser ablating laryngeal tissues in different depths. In addition, in the study conducted by Cláudia Schweiger [9], with the use of the New Zealand rabbit model, it was observed that the subglottic stenosis was caused by intubation, nylon brush and Bugbee cautery, in which most animals survived at two weeks after injury for further observation of laryngotracheal stenosis.…”