This work was partially performed in the Royal College of Surgeons Biomedical Facility, Beaumont Hospital, Beaumont, Dublin, Ireland and the Royal College of Surgeons Ireland Biomedical Facility, Beaumont Hospital, Beaumont, Dublin, Ireland.
Article first published online: 7 SEP 2012
Copyright © 2012 The American Laryngological, Rhinological, and Otological Society, Inc.
Volume 122, Issue 11, pages 2574–2581, November 2012
How to Cite
Kelly, N. A., Murphy, M., Giles, S. and Russell, J. D. (2012), Subglottic injury: A clinically relevant animal model. The Laryngoscope, 122: 2574–2581. doi: 10.1002/lary.23515
The authors have no other funding, financial relationships, or conflicts of interest to disclose.
- Issue published online: 25 OCT 2012
- Article first published online: 7 SEP 2012
- Manuscript Accepted: 22 MAY 2012
- Manuscript Revised: 1 MAY 2012
- Manuscript Received: 14 DEC 2011
- National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland
- Pediatric otolaryngology;
- subglottic stenosis;
- rabbit model;
- endotracheal tube;
To develop a clinically aligned, reproducible model for subglottic injury.
Prospective randomized control pilot study.
Juvenile (3-month-old) New Zealand White rabbits underwent intubation with a 3-cm length of an endotracheal tube that was chosen so that there would be no air leak below 20 cm of water. This tube was one or two sizes above the appropriate tube for the animal. It was held in situ with a suture placed at the trachea and secured over a button in the neck for a period of 1 week. Animals were sacrificed 1 week postextubation, and larynges were harvested. A range of histological techniques and gross morphology were utilized to examine the injury caused at the level of the subglottis. Unintubated animals constituted controlled specimens.
Intubated animals demonstrated considerable histopathology including evidence of ulceration, inflammation, granulation tissue, perichondritis, and chondritis when compared with control animals. Morphometric analysis demonstrated a significant increase in lamina propria thickness (P = .0013), mucosal thickness (P ≤ .0001), and in goblet cell areal density (P = .014). Analysis of mucin types found a significant decrease in acidic (P = .0001) mucin coinciding with a significant increase in mixed mucin types (P = .0013).
Our model provides a reliable and reproducible technique for acute/subacute injury to the subglottis secondary to intubation, which is consistent with previous histological findings of early changes associated with acquired subglottic stenosis (SGS). Future uses of this model could include the examination of current adjunctive therapies and their effects on limiting progression to SGS.