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Results for “GAS POISONING”

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At least 127 records · Page 7Linked to original sources
PubMed1987

[Lung parenchymatous changes following mustard gas poisoning].

The authors present a late sequel of poisoning with dichlorodiethyl sulphide, also known as mustard gas or Ypérite, in a patient of 22 years of age--a late sequel not described in the literature to date. After the poisoning, a severe pulmonary fibrosis with pulmonary artery hypertension developed. A mediastinal emphysema that had so far been observed only during the acute intoxication phase, was evident even two years after the intoxication. Perivascular collections of air in the left lung communicating via the left hilus with the mediastinal air point to the existence of bronchus or lung parenchyma fistulas.

Adult↗
PubMed1987

[Fire at the Viennese hotel "Am Augarten"--a contribution to the toxicology of combustion gas poisoning].

The fire at the Vienna hotel "Am Augarten" (28.9 1979) caused 25 deaths. 24 victims died as a result of inhalation of fire gases; 10 of them also suffered 2nd and 3rd degree burns. In one case, death was due to internal injuries (sustained when jumping from a window). The fact that none of the bodies was charred facilitated identification. In all cases autopsy revealed the typical symptoms of inhalation of fire gases (soot deposition in the respiratory tract, presence of carboxyhaemoglobin in the blood). In public discussion the question was raised whether the inhalation of hydrogen cyanide (liberated from nitrogen-containing natural or synthetic polymers by pyrolysis) was a contributory factor to the fatal outcome. The cyanide concentrations in blood samples measured by gas chromatography were below the toxic range in all cases. Chemical investigation comprised the determination of the carboxyhaemoglobin concentrations and the demonstration of volatile hydrocarbons in the air of the lungs.

Austria↗
PubMed1990

[Treatment of insecticide and nerve gas poisoning].

Organic phosphides such as insecticides and nerve gases are chemically and biologically akin. They have the same main structures and both act as cholinesterase inhibitors. The nerve gases are generally more reactively chemical and therefore far more toxic. Since both nerve gases and insecticides react to the same group of acetylcholinesterase the development of symptoms and the treatment of the intoxication are fairly similar. Intoxication may ensue from inhalation, from penetration of the skin, or from consumption of contaminated food or water. The latter mode of administration is the most common in cases of suicide.

Chemical Warfare Agents↗
PubMed2002

[A case suspected of acute gas poisoning by carbon monoxide (CO), presenting with progressive diffuse leukoencephalopathy associated with marked brain edema].

A 51-year-old man was found comatose in a decerebrate posture in a cottage. Brain MRI showed diffuse high-signal-intensity areas in the white matter on T 2-weighted and FLAIR images, and diffusion-weighted images showed marked diffuse high intensity areas in the white matter. Initially inflammatory demyelinating diseases were suspected and methylprednisolone pulse therapy was administered. However, no improvement was noted. On close inspection of the cottage, a gas generator was discovered in the poorly ventilated room. He was therefore suspected to have suffered from gas intoxication, including carbon monoxide (CO). Hyperbaric oxygen therapy was administered, but without any improvement. The diffuse white matter lesions and brain edema progressed with time and the patient died of cerebral herniation. Autopsy revealed no inflammatory processes. Most cases with CO intoxication show hyperintense lesions in the globus pallidus on both sides in T 2-weighted images, and some cases show lesions only in the white matter without any involvement of the globus pallidus. The progressive clinical course, diffuse leukoencephalopathy and brain edema may be due to apoptosis of oligodendrocytes. CO intoxication is thus important in the differential diagnosis of diffuse white matter lesions of the cerebrum.

Brain↗
PubMedDate not supplied

Delayed ocular complications of mustard gas poisoning and the relationship with respiratory and cutaneous complications.

BACKGROUND: This study was aimed to determine the correlation between ocular complications and respiratory or cutaneous complications in a group of 40 Iranian veterans with late complications of sulphur mustard (SM) poisoning. METHODS: Thorough ophthalmologic examination was performed on all severely SM-poisoned veterans in the province of Khorasan, Iran. Spirometric evaluation of pulmonary function, as well as estimation of the burned skin area, was performed for all the patients. The severities of ocular, respiratory and cutaneous complications were classified into four grades in each patient and were compared with each other, using Spearman's rank correlation test. RESULTS: Forty male patients (aged 43.8 +/- 9.8 years) with confirmed SM poisoning were studied 16-20 years after their initial exposure. Common symptoms were recorded as itching (42.5%), burning sensation (37.5%), photophobia (30%) and tearing (27.5%). Abnormal conjunctival and limbal findings were chronic conjunctivitis (17.5%), perilimbal hyperpigmentation (17.5%), vascular tortuosity (15%) and limbal ischaemia (12.5%). Abnormal corneal findings were subepithelial opacity (15%), corneal thinning (15%), diffuse corneal opacity (10%), neovascularization (7.5%) and epithelial defects (5%). A significant positive correlation was found between the severity of ocular and respiratory complications (r = 0.322, P = 0.043). Cutaneous complications revealed no significant correlation with either ocular or respiratory complications. CONCLUSIONS: SM causes delayed destructive lesions in the ocular surface and cornea, leading to progressive visual deterioration and ocular irritation. Late complications of SM poisoning in the eyes, respiratory system and skin are mainly due to SM's local irritant effects.

Adult↗