Quantification of airway thickness changes in smoke-inhalation injury using in-vivo 3-D endoscopic frequency-domain optical coherence tomography

Sang-Won Lee,Andrew E Heidary,Zhongping Chen,Joseph Jing,Matthew Brenner,Gangjun Liu,Jiechen Yin,Sari Mahon,David Yoon,Tirunelveli Ramalingam,David Mukai

doi:10.1364/boe.2.000243

Abstract

Smoke inhalation injury is frequently accompanied by cyanide poisoning that may result in substantial morbidity and mortality, and methods are needed to quantitatively determine extent of airway injury. We utilized a 3-D endoscopic frequency-domain optical coherence tomography (FD-OCT) constructed with a swept-source laser to investigate morphological airway changes following smoke and cyanide exposure in rabbits. The thickness of the mucosal area between the epithelium and cartilage in the airway was measured and quantified. 3-D endoscopic FD-OCT was able to detect significant increases in the thickness of the tracheal walls of the rabbit beginning almost immediately after smoke inhalation injuries which were similar to those with combined smoke and cyanide poisoning.

Highlights

Airway injury due to smoke exposure and inhalation risks including thermal, chemical, and toxic injuries, as well as secondary infectious complications result in significant morbidity and mortality
Smoke inhalation injury is frequently accompanied by cyanide poisoning that may result in substantial morbidity and mortality, and methods are needed to quantitatively determine extent of airway injury
Quantification of acute and longer term thickness changes of mucosa area in the airway by using in-vivo 3-D endoscopic OCT may provide a more sensitive tool for investigation of the effectiveness of various therapeutic interventions in smoke inhalation and other airway injuries

Summary

Introduction

Airway injury due to smoke exposure and inhalation risks including thermal, chemical, and toxic injuries, as well as secondary infectious complications result in significant morbidity and mortality. Combined smoke inhalation injury (with carbon monoxide exposure) and cyanide toxicity limit some potential therapeutic options, such as methemoglobin induction. The effects of the approved cyanide treatment agent, cobalamin, and the recently described novel treatment agent cobinamide, which binds nitric oxide (NO) on concurrent airway injury process in smoke inhalation injury, are not known. Because NO has been reported to have a complex role in smoke inhalation airway injury process [8,9,10], these NO scavengers could potentially affect airway injury when administered to patients with combined smoke and cyanide exposure and these important questions need to be investigated

Methods

Results

Discussion

Conclusion