Inhibition of subglottic stenosis with mitomycin-C in the canine model.

The objective of this randomized, prospective study was to study the efficacy of topical mitomycin-C in the inhibition of subglottic stenosis in a canine model. Subglottic stenosis was elicited with the carbon dioxide laser in 10 mongrel dogs. Radial incision and serial dilation of the subglottic airway were then carried out. The animals were randomized to receive a topical solution of 1% mitomycin-C to the dilated area for a 5-minute duration or no further treatment. Weekly direct microlaryngoscopy and photodocumentation were performed during the 6-week study. Airway distress developed in 4 of the 5 control dogs, requiring early sacrifice, while all treatment group animals survived the duration of the study (p < or = .006). Morphometric analysis of the subglottic photographs confirmed a greater than 100% increase in the percentage of relative airway at sacrifice in the treatment group (p < or = .049). A statistically significant (p < or = .015) decrease in collagen formation in the subglottic scar of dogs treated with topical mitomycin-C was documented. Mitomycin-C favorably altered the clinical progression of subglottic stenosis, improved quantified airway patency, and reduced the amount of subglottic collagen formation in the canine model.

Histomorphometric and laryngeal videostroboscopic analysis of the effects of corticosteroids on microflap healing in the dog larynx.

The histologic and functional effects of unilateral, layered corticosteroids on lateral microflap healing in 15 dogs were analyzed. Histologic sections of steroid-treated vocal folds (VFs) were studied with computer morphometry to examine differences in the tissue healing response. Paired analysis revealed increases in the inflammatory infiltrate around the microflap in the steroid-treated VFs at 2, 4, and 6 weeks (6.3%, 30.6%, and 34.9%, all with p < .02). The neovascular response in the steroid-treated VFs was less at 2 weeks (-20.9%, p < .005) but greater at 4 and 6 weeks (16.3% and 4.3%, p < .005). To better characterize the effect of steroids on the healing process, a normal, time-dependent distribution was applied to the histologic data and demonstrated a delay in the steroid-treated VF tissue response of 12 days for the inflammatory infiltrate and 21 days for the neovascular response. Qualitative and quantitative analysis of in vivo laryngeal videostroboscopy (LVS) samples taken preoperatively and at sacrifice could not identify significant differences in appearance, amplitude, mucosal wave, or suppleness between the 2 VFs. Therefore, although corticosteroids cause a delay in wound healing, LVS does not discern differences in microflap characteristics between healing steroid-treated and control VFs at 2, 4, or 6 weeks. If steroids are used, the surgeon should account for a probable delay in wound healing, but should not expect an overall difference in functional outcome.