Development of a Clinically Relevant Rabbit Model of Acute Laryngeal Injury

Acute laryngeal injury (ALgI) is created as a result of endotracheal tube pressure ulcer formation leading to fibrosis and inflammation. This condition often leads to airway obstruction and voice and swallowing dysfunction. This study demonstrates a reliable animal model of ALgI to reproduce the acute wound process seen clinically, to explore the pathophysiology of this disease process, and to serve as a reproducible injury suitable for the evaluation of therapeutic interventions.

An ALgI model was developed in New Zealand White rabbits using precise mucosal stripping of the posterior larynx, followed by intubation with an oversized 4.0 endotracheal tube for 1 h to mimic intubation-associated trauma and pressure ischemia. Laryngoscopy and laryngeal harvest were performed 2 weeks post-injury for histologic and immunofluorescent evaluation.

Injured rabbits demonstrated an eightfold increase in posterior glottic thickness (1.57 vs. 0.19 mm in controls; p = 0.0004) and an 11-fold increase in collagen content (1.93 vs. 0.17 mm²; p = 0.005). Collagen subtype analysis revealed a shift toward active collagen within the injured larynx compared to the uninjured, with increased Type III Collagen (69.0% vs. 26.1%; p < 0.0001) and reduced Type I Collagen (27.2% vs. 73.9%; p < 0.0001) in the posterior glottis, consistent with the proliferative phase of wound healing. Collagen fiber alignment analysis demonstrated increased coherency in injured tissues (0.36 vs. 0.21; p = 0.023), indicating early organized collagen formation consistent with scar formation within the posterior glottis.

The model offers a robust platform for studying the acute pathogenesis of laryngeal injury and for testing the treatment options in the management of ALgI.

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