Multimodal imaging guidance for laser ablation in tracheal stenosis

Authors

  • Septimiu D. Murgu MD,

    Corresponding author
    1. Pulmonary and Critical Care Medicine , Department of Medicine, University of California School of Medicine, Irvine, California, U.S.A.
    • UCI Medical Center, 101 the City Drive South, City Tower, Suite 400, ZOT code 4095, Orange, CA 92868-3217
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  • Henri G. Colt MD,

    1. Pulmonary and Critical Care Medicine , Department of Medicine, University of California School of Medicine, Irvine, California, U.S.A.
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  • David Mukai PhD,

    1. Beckman Laser Institute , University of California, Irvine, Irvine, California, U.S.A.
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  • Matt Brenner MD

    1. Pulmonary and Critical Care Medicine , Department of Medicine, University of California School of Medicine, Irvine, California, U.S.A.
    2. Beckman Laser Institute , University of California, Irvine, Irvine, California, U.S.A.
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  • The authors have no financial disclosures and no conflicts of interest related to the content of this article.

Abstract

Objective/Hypothesis:

Laser-induced damage of tracheal wall microstructures might contribute to recurrence after bronchoscopic treatment of tracheal strictures. The purpose of this study was to demonstrate how multimodal imaging using white light bronchoscopy (WLB), endobronchial ultrasound (EBUS), and optical coherence tomography (OCT) might identify in vivo airway wall changes before and resulting from Nd:YAG laser ablation and dilation of tracheal stenosis.

Study Design:

Case study.

Methods:

Commercially available WLB, high frequency EBUS using a 20-MHz radial probe and time-domain, frontal imaging OCT systems were used to characterize the extent, morphology, and airway wall microstructures at the area of hypertrophic fibrotic tissue formation before, during and after treatment of postintubation tracheal stenosis.

Results:

WLB revealed the location of a complex, extensive, severe stricture. EBUS showed a homogeneous layer overlying a hyperechogenic layer corresponding to disrupted cartilage. OCT showed a homogeneous light backscattering layer and absence of layered microstructures, confirming absence in close proximity of normal airway wall. After laser ablation, OCT of charred tissue showed high backscattering and shadowing artifacts. OCT of noncharred tissue showed a thinner, homogeneous, light backscattering layer. EBUS showed thinner but persistent hypertrophic tissue suggesting incomplete treatment. WLB revealed improved airway patency postprocedure and recurrence 3 weeks later.

Conclusions:

EBUS identified cartilage disruption and residual hypertrophic tissue, the evidence of which might contribute to recurrence. OCT revealed homogeneous light backscaterring representing persistent noncharred hypertrophic tissues but it did not visualize cartilage disruption. Future studies are warranted to confirm whether these technologies can help guide bronchoscopic treatments.

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