The Role of Bronchoscopy in Pulmonary Complications due to Mustard Gas Inhalation

Freitag, Lutz; Firusian, N; Stamatis, G; Greschuchna, D

doi:10.1378/chest.100.5.1436

Cited by 73 publications

(36 citation statements)

References 15 publications

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“…It was observed that a subset of these patients with COPD presented with signs and symptoms similar to asthma, in which airway obstruction was reversible by bronchodilators [8, 19]. Early reports of pulmonary complications of heavy exposure to sulfur mustard gas revealed severe bronchial stenosis and loss of ciliary kinetics that lead to chronic infections and bronchiectasis [20]. Zarchi et al [21 ]showed increasing pulmonary complication over time after exposure to sulfur mustard gas.…”

Section: Discussionmentioning

confidence: 99%

Airway Hyperresponsiveness to Methacholine in Chemical Warfare Victims

Mirsadraee

Attaran²,

Boskabady³

et al. 2005

Respiration

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Background: The lung is one of the most exposable organs to chemical warfare agents such as sulfur mustard gas. Pulmonary complications as a result of this gas range from severe bronchial stenosis to mild or no symptoms. Airway hyperresponsiveness (AHR) which is usually assessed as response to inhaled methacholine is the most characteristic feature of asthma. AHR is reported in chronic obstructive pulmonary disease patients and smokers, and may also show in chemical warfare victims. However, there are little reports regarding AHR in chemical warfare victims. Objective: Therefore, in this study, airway responsiveness to methacholine in victims of chemical warfare was examined. Methods: The threshold concentrations of inhaled methacholine required for a 20% change in forced expiratory flow in 1 s (FEV₁; PC₂₀) or a 35% change in specific airway conductance (PC₃₅) were measured in 15 chemical war victims and 15 normal control subjects. Results: In 10 out of 15 chemical warfare victims (two thirds), PC₂₀ and PC₃₅ methacholine could be measured and subjects were called responders. AHR to methacholine in responder chemical war victims (PC₂₀ = 0.41 and PC₃₅ = 0.82 g/l) was significantly lower than in normal subjects (PC₂₀ = 5.69 and PC₃₅ = 4.60 g/l, p < 0.001 for both cases). There was a significant correlation between FEV₁ and PC₂₀ methacholine (r = 0.688, p < 0.001). The correlations between PC₂₀ and PC₃₅ were statistically significant as well (r = 0.856, p < 0.001). Conclusion: Results showed increased airway responsiveness of most chemical warfare victims to methacholine which correlated with the FEV₁ value and which may be related to chronic airway inflammation or irreversible airway changes.

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Section: Discussionmentioning

confidence: 99%

Airway Hyperresponsiveness to Methacholine in Chemical Warfare Victims

Mirsadraee

Attaran²,

Boskabady³

et al. 2005

Respiration

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“…Respiratory effects of SM exposure have long been investigated, focusing mainly on chronic respiratory effects in survivors (1,2,(13)(14)(15)(16). Regarding the acute effects of SM on the human respiratory tract, scarce data are available other than a few case reports (2-4, 6, 8, 10, 11, 17).…”

mentioning

confidence: 99%

“…This can result in nasal mucosal injury, rhinorrhea, loss of smell and taste, pharyngeal mucosal injury, and laryngitis (2,3,7,10). Moderate SM exposure results in various degrees of tracheobronchial mucosal injury, leading to a painful and forceful cough (2,3,7,15). By contrast, highlevel SM exposure can often lead to more severely disabling respiratory lesions that may cause death (6,8,10,12).…”

mentioning

confidence: 99%

Airway Obstruction Due to Bronchial Vascular Injury after Sulfur Mustard Analog Inhalation

Veress¹,

O’Neill²,

Hendry‐Hofer³

et al. 2010

Am J Respir Crit Care Med

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Rationale: Sulfur mustard (SM) is a frequently used chemical warfare agent, even in modern history. SM inhalation causes significant respiratory tract injury, with early complications due to airway obstructive bronchial casts, akin to those seen after smoke inhalation and in single-ventricle physiology. This process with SM is poorly understood because animal models are unavailable. Objectives: To develop a rat inhalation model for airway obstruction with the SM analog 2-chloroethyl ethyl sulfide (CEES), and to investigate the pathogenesis of bronchial cast formation. Methods: Adult rats were exposed to 0, 5, or 7.5% CEES in ethanol via nose-only aerosol inhalation (15 min). Airway microdissection and confocal microscopy were used to assess cast formation (4 and 18 h after exposure). Bronchoalveolar lavage fluid (BALF) retrieval and intravascular dye injection were done to evaluate vascular permeability. Measurements and Main Results: Bronchial casts, composed of abundant fibrin and lacking mucus, occluded dependent lobar bronchi within 18 hours of CEES exposure. BALF contained elevated concentrations of IgM, protein, and fibrin. Accumulation of fibrin-rich fluid in peribronchovascular regions (4 h) preceded cast formation. Monastral blue dye leakage identified bronchial vessels as the site of leakage. Conclusions: After CEES inhalation, increased permeability from damaged bronchial vessels underlying damaged airway epithelium leads to the appearance of plasma proteins in both peribronchovascular regions and BALF. The subsequent formation of fibrin-rich casts within the airways then leads to airways obstruction, causing significant morbidity and mortality acutely after exposure.

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“…In lungs dissected at thoracotomy from Iranian casualties of the Iraq-Iran conflict, bronchiectasis and severe chronic inflammation were demonstrated [30]. Pulmonary inflammation including neutrophil infiltration into the airspaces and interstitium were significant observations and alveolar spaces were filled with eosinophilic debris in SM-exposed animals.…”

Section: Discussionmentioning

confidence: 97%

The Protective Effect of Nigella Sativa on Lung Injury of Sulfur Mustard–exposed Guinea Pigs

Hossein

Vahedi

Amery

2008

Experimental Lung Research

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The lung is one of the most exposable organs to chemical warfare agents such as sulfur mustard (SM) gas. Airway hyperresponsiveness and lung inflammation are reported in chemical warfare victims. There is no definite treatment for respiratory disorders induced by SM exposure. However, the protective effect of Nigella sativa on inflammatory process was shown. In the present study, the protective effect of Nigella sativa on tracheal responsiveness and lung inflammation of SM exposed guinea pigs was examined. Guinea pigs were exposed to diluent's solution (ethanol, control group), 100 mg/m(3) inhaled sulfur mustard (SME group), and SME treated with Nigella sativa, 0.08 g daily (SME+N), n = 6 for each group. Tracheal responsiveness (TR) to methacholine, total white blood cell (WBC) count of lung lavage, and differential WBC were done 14 days post exposure. The weigh of animal were measured at the beginning, middle (day 7), and the end (day 14) of the study. The TR of SM-exposed guinea pigs was significantly (P < .001) and WBC nonsignificantly higher than those of controls. In SME guinea pigs, there was a weight loss but in the case of SME+N guinea pigs, no obvious weight change thought the study was seen. The eosinophl, monocyte, and lympocytes in SME animals were significantly changed compared to control group (P < .001 for all cases). Monocyte, lymphocyte, and neutrophil number were decreased in SME+N group compared to SME animals, which was significant only for neutrophil (P < .05). These results showed a preventive effect of Nigella sativa on TR of SM-exposed guinea pigs.

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The Role of Bronchoscopy in Pulmonary Complications due to Mustard Gas Inhalation

Cited by 73 publications

References 15 publications

Airway Hyperresponsiveness to Methacholine in Chemical Warfare Victims

Airway Hyperresponsiveness to Methacholine in Chemical Warfare Victims

Airway Obstruction Due to Bronchial Vascular Injury after Sulfur Mustard Analog Inhalation

The Protective Effect of Nigella Sativa on Lung Injury of Sulfur Mustard–exposed Guinea Pigs

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