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Effectiveness of morphine in non-cardiogenic pulmonary edema due to chlorine gas inhalation.
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We report the case of an 11-yr-old boy who developed a non-cardiogenic pulmonary edema following inhalation of chlorine gas at a swimming pool. Rapid clinical improvement was noted after i.v. administration of morphine.
Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide.
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Chlorine gas is a widely used industrial compound that is highly toxic by inhalation and is considered a chemical threat agent. Inhalation of high levels of chlorine results in acute lung injury characterized by pneumonitis, pulmonary edema, and decrements in lung function. Because inflammatory
Positive pressure oxygen therapy in treatment of pulmonary edema caused by chlorine gas.
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[Action of cortisone on pulmonary edema following chlorine poisoning].
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Effect of morphine, aerosol mixtures, and other agents on experimental pulmonary edema in rats following exposure to chlorine gas.
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Chlorine gas exposure increases susceptibility to invasive lung fungal infection.
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Chlorine (Cl₂) is a highly irritating and reactive gas with potential occupational and environmental hazards. Acute exposure to Cl₂ induces severe epithelial damage, airway hyperreactivity, impaired alveolar fluid clearance, and pulmonary edema in the presence of heightened inflammation and
[The participation of the kallikrein-kinin system in edema formation in glomerulonephritis].
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Involvement of the kallikrein-kinin system in the pathogenesis of renal edemas may be mediated by increase of vascular permeability, proteinuria, diuresis and natriuresis. Proceeding from these points, in 27 patients with morphologically proved chronic glomerulonephritis and the nephrotic syndrome,
[Radiographic and computed tomographic manifestations of chest in patients with acute chlorine gas poisoning].
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OBJECTIVE
To investigate the radiographic and computerized tomographic features of chest in patients with acute chlorine poisoning and its diagnostic value.
METHODS
Twenty-eight cases of chlorine poisoning were reviewed. And their radiographic and computerized tomographic features were compared and
Inhalation of chlorine causes long-standing lung inflammation and airway hyperresponsiveness in a murine model of chemical-induced lung injury.
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Chlorine is highly irritating when inhaled, and is a common toxic industrial gas causing tissue damage in the airways followed by an acute inflammatory response. In this study, we investigated mechanisms by which chlorine exposure may cause reactive airways dysfunction syndrome (RADS) and we
Lessons learned from chlorine intoxications in swimming pools: the challenge of pediatric mass toxicological events.
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BACKGROUND
The classical doctrine of mass toxicological events provides general guidelines for the management of a wide range of "chemical" events. The guidelines include provisions for the: (1) protection of medical staff with personal protective equipment; (2) simple triage of casualties; (3)
Phosgene-induced acute lung injury (ALI): differences from chlorine-induced ALI and attempts to translate toxicology to clinical medicine.
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BACKGROUND
Phosgene (carbonyl dichloride) gas is an indispensable chemical inter-mediate used in numerous industrial processes. There is no clear consensus as to its time- and inhaled-dose-dependent etiopathologies and associated preventive or therapeutic treatment
Acute respiratory changes and pulmonary inflammation involving a pathway of TGF-β1 induction in a rat model of chlorine-induced lung injury.
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We investigated acute and delayed respiratory changes after inhalation exposure to chlorine (Cl2) with the aim to understand the pathogenesis of the long-term sequelae of Cl2-induced lung-injury. In a rat model of nose-only exposure we analyzed changes in airway hyperresponsiveness (AHR),
Chlorine-induced damage documented by neurophysiological, neuropsychological, and pulmonary testing.
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Chlorine causes acute pulmonary edema and damages airways, thus producing obliterative bronchiolitis. In the case series in this study, its adverse effects were extended to visual and central nervous system impairment. Twenty-two patients exposed briefly to undiluted chlorine at home or work were
Myocardial infarction, acute ischemic stroke, and hyperglycemia triggered by acute chlorine gas inhalation.
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Chlorine is one of the most common substances involved in toxic inhalation. Until now, several accidental exposures have been reported. The damage to the respiratory tract in the immediate phase after exposure to chlorine is well defined. Death occurs particularly due to pulmonary edema with
Histopathological effects of acute exposure to chlorine gas on Sprague-Dawley rat lungs.
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It is now recognized that acute inhalational exposure to irritant gases such as chlorine can cause an asthma-like abnormality known as reactive airways dysfunction syndrome (RADS). The aim of this study was to evaluate the effects of exposure to various levels of chlorine on airway mucosa and lung
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