Graded Carbon Dioxide Laser–Induced Subglottic Injury in the Rabbit Model

Chafin, J. Brett; Sandulache, Vlad C.; Dunklebarger, Joshua L.; Otteson, Todd D.; Hoffmann, Paul A.; Hebda, Patricia A.; Dohar, Joseph E.

doi:10.1001/archotol.133.4.358

Cited by 22 publications

(52 citation statements)

References 50 publications

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“…While these injuries provide predictable hisotologic changes, the ability to achieve a predictable overall degree of stenosis has not been clearly demonstrated. 8,11 Although still unable to obtain highly consistent degrees of stenosis, we still demonstrate an extremely rapid and reliable method to induce tracheal injury and resultant stenosis.…”

Section: Resultsmentioning

confidence: 87%

“…11 We chose to model our open group after a method described by Nakagishi et al 12 In their model, they produced an injury through a tracheotomy with a 5.5 mm nylon brush with a total of 10 brush strokes. The differences between their method and ours include: the use of Japanese White rabbits; the use of antibiotics; and the measurement of stenosis, in which sections of each trachea were photographed and analyzed at multiple days after injury (days 9-28).…”

Section: Resultsmentioning

confidence: 99%

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Tracheal Stenosis Induction: A Comparison of Open Versus Endoscopic Methods in a Rabbit Model

Wycherly¹,

Hesham²,

Malekzadeh³

et al. 2009

The Laryngoscope

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EDUCATIONAL OBJECTIVE At the conclusion of this presentation, the participants should be able to appreciate the value of an endoscopic method of inducing tracheal stenosis in a rabbit model. OBJECTIVE METHODSFifteen adult male New Zealand White rabbits underwent induction of tracheal stenosis. Six animals received mucosal injury directly through a tracheotomy and 10 strokes of a nylon brush. Nine animals received tracheal injury endoscopically: a rigid bronchoscope was placed a measured distance below the inferior edge of the cricoid cartilage and a nylon brush was passed 4 times in each of the 4 quadrants. Endoscopies were performed 3 weeks after injury. Stenosis was measured as a percentage of luminal narrowing by a consensus of 3 individuals viewing the procedure on a television monitor. RESULTSOnly 1 animal in the tracheotomy group had noticeable stenosis (40%). In the endoscopic group, all animals had some degree of stenosis, ranging from 10-80% (mean 40%). The mortality rate was 20% (3/15). In the tracheotomy group, 1 mortality occurred secondary to antibiotic-induced gastroenteritis. In the endoscopic group, 2 mortalities occurred in the immediate postoperative period secondary to laryngeal edema. These 2 animals were the first to undergo the procedure, which lasted approximately 30 minutes. After refining our technique, succeeding procedures lasted an average of 5 minutes and there were no mortalities. The average duration of the tracheotomy procedure was 45 minutes. CONCLUSIONSUsing an endoscopic method can greatly improve the induction of tracheal stenosis by reducing operative time and eliminating an open wound and the need for antibiotics. It also achieves stenosis more consistently than an open technique.

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Section: Resultsmentioning

confidence: 87%

Section: Resultsmentioning

confidence: 99%

Tracheal Stenosis Induction: A Comparison of Open Versus Endoscopic Methods in a Rabbit Model

Wycherly¹,

Hesham²,

Malekzadeh³

et al. 2009

The Laryngoscope

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“…Specifically, we have confirmed that SGS development is accompanied by a robust inflammatory component. (6, 13, 14) Second, we have shown that the histologic and morphologic characteristics of SGS closely parallel those of hypertrophic scars and keloids (with the exception of extension outside the boundaries of initial injury in case of keloids). (7) Third, we have demonstrated an aberrant SGS fibroblast phenotype in human pathologic specimens with respect to both basal activities and in response to putative anti-fibroplastic agents including PGE2 (Sandulache and Singh, manuscript in preparation).…”

Section: Introductionmentioning

confidence: 78%

“…Briefly, the subglottis was entered using an anterior cricothyroidotomy and the posterior quadrant was injured using a laser or chemical cautery. A CO2 laser was used to deliver 1 second continuous exposure, with a beam diameter of 2 mm, power settings of 12W delivered in 4 pulses spaced in a arc across the posterior subglottic region in each airway, as previously described (6,7). Chemical injury was made using a AgNO3 cautery stick applied to the posterior subglottis using a single rolling pass, for a total of 1 second, as described in detail in our previous publication (3).…”

Section: Methodsmentioning

confidence: 99%

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Subglottic Stenosis Examined as a Fibrotic Response to Airway Injury Characterized by Altered Mucosal Fibroblast Activity

Singh¹,

Sandulache²,

Otteson³

et al. 2010

Arch Otolaryngol Head Neck Surg

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Objective To investigate the association between mucosal fibroblast activity and subglottic stenosis (SGS) development. Design Animals were assigned to either cricothyroidotomy and CO2 laser injury, or cricothyroidotomy and silver nitrate (AgNO3) injury groups. Airways were excised for histologic analysis and the establishment of primary fibroblast cultures. Surgical excision of established SGS followed by recovery was used to analyze SGS recurrence in this animal model. Subjects New Zealand white rabbits. Interventions The subglottis was approached via cricothyroidotomy and subjected to either CO2 laser or AgNO3 injury prior to closure. The SGS lesions were excised between 8 and 10 weeks and used to establish explants for fibroblast culture. The animals underwent recovery for an additional 14 days to follow recurrence of SGS. After 14 days all the animals were euthanized and subglottic tissue was harvested for histological evaluation. Rates of migration and contraction of SGS and normal airway fibroblasts were assayed using established in vitro methods under basal conditions and with prostaglandin (PG) E2 treatment. Results 1) Mucosal injury resulted in acute fibroplasia and chronic SGS. 2) Surgical excision of mature SGS at 8 weeks resulted in rapid recurrence of stenosis. 3) SGS derived fibroblasts were relatively refractory to the effects of PGE2 on migration and contraction. Conclusion SGS represents a fibrotic airway repair process, involving fibroblasts that produce recurrent, excessive scar formation. We suggest that SGS development and recurrence may be partially dictated by altered fibroblast responsiveness to anti-fibroplastic signals during mucosal repair.

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