Bronchial damage and diffuse alveolar hemorrhage following chlorine gas inhalation: A case report

Uemura, Kazuhiro; Isono, Momoko; Kagohashi, Katsunori; Hasegawa, Ryuichi; Satoh, Hiroaki

doi:10.3892/etm.2017.5161

Cited by 1 publication

(1 citation statement)

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“…Treatments following halogen exposure are mainly supportive, focusing on symptom alleviating, such as bronchospasm, pulmonary edema, and airway obstruction, using humidified oxygen, β 2 agonists, and antibiotics for potential infections. [ 7 ] In severe cases with ARDS, respiratory support with intubation and positive-pressure ventilation may be necessary. [ 8 ] Thus, animal model of halogen inhalation provides us an opportunity to elucidate its basic mechanisms and to test novel therapeutic agents to reduce morbidity and mortality.…”

Section: Introductionmentioning

confidence: 99%

Halogen Inhalation-Induced Lung Injury and Acute Respiratory Distress Syndrome

Zhou¹,

Song

Shang

et al. 2018

Chinese Medical Journal

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Objective:Exposure to halogens, such as chlorine or bromine, results in environmental and occupational hazard to the lung and other organs. Chlorine is highly toxic by inhalation, leading to dyspnea, hypoxemia, airway obstruction, pneumonitis, pulmonary edema, and acute respiratory distress syndrome (ARDS). Although bromine is less reactive and oxidative than chlorine, inhalation also results in bronchospasm, airway hyperresponsiveness, ARDS, and even death. Both halogens have been shown to damage the systemic circulation and result in cardiac injury as well. There is no specific antidote for these injuries since the mechanisms are largely unknown.Data Sources:This review was based on articles published in PubMed databases up to January, 2018, with the following keywords: “chlorine,” “bromine,” “lung injury,” and “ARDS.”Study Selection:The original articles and reviews including the topics were the primary references.Results:Based on animal studies, it is found that inhaled chlorine will form chlorine-derived oxidative products that mediate postexposure toxicity; thus, potential treatments will target the oxidative stress and inflammation induced by chlorine. Antioxidants, cAMP-elevating agents, anti-inflammatory agents, nitric oxide-modulating agents, and high-molecular-weight hyaluronan have shown promising effects in treating acute chlorine injury. Elevated free heme level is involved in acute lung injury caused by bromine inhalation. Hemopexin, a heme-scavenging protein, when administered postexposure, decreases lung injury and improves survival.Conclusions:At present, there is an urgent need for additional research to develop specific therapies that target the basic mechanisms by which halogens damage the lungs and systemic organs.

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Section: Introductionmentioning

confidence: 99%