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Subglottic injury: a clinically relevant animal model.

Nicola A Kelly¹, Madeline Murphy, Seamus Giles

¹School of Medicine and Medical Science, University College Dublin, Dublin, Ireland. nicola.kelly@ucdconnect.ie

The Laryngoscope

|September 11, 2012

Summary

A new rabbit model reliably reproduces subglottic injury from intubation, showing inflammation and tissue changes. This model aids research into preventing acquired subglottic stenosis.

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Area of Science:

Otorhinolaryngology
Pathology
Animal Models

Background:

Endotracheal intubation can lead to subglottic stenosis (SGS).
Developing a reproducible animal model is crucial for studying SGS pathogenesis and testing interventions.
Existing models may not fully capture the acute/subacute injury spectrum.

Purpose of the Study:

To establish a clinically relevant and reproducible animal model for subglottic injury.
To investigate the histological and morphometric changes following intubation in a juvenile rabbit model.
To provide a foundation for future studies on preventing or treating acquired subglottic stenosis.

Main Methods:

Prospective randomized control pilot study using juvenile New Zealand White rabbits.
Intubation with oversized endotracheal tubes for 1 week, followed by sacrifice and larynges harvest.

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Histological techniques and gross morphology analysis to assess subglottic injury, with unintubated animals as controls.

Main Results:

Intubated rabbits showed significant histopathology: ulceration, inflammation, granulation tissue, perichondritis, and chondritis.
Increased lamina propria thickness (P = .0013), mucosal thickness (P ≤ .0001), and goblet cell density (P = .014).
Significant decrease in acidic mucin (P = .0001) and increase in mixed mucin types (P = .0013).

Conclusions:

The developed rabbit model reliably replicates acute/subacute subglottic injury from intubation.
Findings align with early histological changes observed in acquired subglottic stenosis.
This model can be used to evaluate therapies aimed at limiting SGS progression.