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. 2009 Jun 1;3(3):283-297.
doi: 10.1586/ERS.09.21.

Pathophysiology, management and treatment of smoke inhalation injury

Sebastian Rehberg  1 , Marc O Maybauer, Perenlei Enkhbaatar, Dirk M Maybauer, Yusuke Yamamoto, Daniel L Traber
Affiliations

Pathophysiology, management and treatment of smoke inhalation injury

Sebastian Rehberg et al. Expert Rev Respir Med. .

Abstract

Smoke inhalation injury continues to increase morbidity and mortality in burn patients in both the third world and industrialized countries. The lack of uniform criteria for the diagnosis and definition of smoke inhalation injury contributes to the fact that, despite extensive research, mortality rates have changed little in recent decades. The formation of reactive oxygen and nitrogen species, as well as the procoagulant and antifibrinolytic imbalance of alveolar homeostasis, all play a central role in the pathogenesis of smoke inhalation injury. Further hallmarks include massive airway obstruction owing to cast formation, bronchospasm, the increase in bronchial circulation and transvascular fluid flux. Therefore, anticoagulants, antioxidants and bronchodilators, especially when administered as an aerosol, represent the most promising treatment strategies. The purpose of this review article is to provide an overview of the pathophysiological changes, management and treatment options of smoke inhalation injury based on the current literature.

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Figures

Figure 1
Figure 1. Proposed pathophysiology of smoke inhalation injury
iNOS: Inducible nitric oxide synthase; NF: Nuclear factor; nNOS: Neuronal nitric oxide synthase; PARP: Poly(ADP ribose) polymerase; RNS: Reactive nitrogen species; ROS: Reactive oxygen species. Reproduced with kind permission from Frontiers in Bioscience [27].
Figure 2
Figure 2. Bronchoscopic finding after smoke inhalation injury
Erythema, edema and ulceration (view into the left and right main bronchi).
Figure 3
Figure 3. Isolated airway cast
The formation of mucus secretions, denuded airway epithelial cells, inflammatory cells and fibrin leads to subtotal or total occlusion of distal as well as main airways.
See this image and copyright information in PMC

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