Toxicological European research. Recherche europeenne en toxicologie最新文献

A collective nitrous fumes poisoning (five cases) is reported. Two patients (case 3 and case 4) were comatose, in severe respiratory distress. Shock and slate blue cyanosis were noted. Physical examination and chest X ray revealed acute pulmonary edema-Methemoglobin levels were 71,3% (case 3) and 58% (case 4). Despite treatment both of them died from severe hypoxia resulting in cardiorespiratory arrest. Post-mortem examination was performed upon these four men. On admission the last one (case 5) was conscious, and in good hemodynamic condition. Acute pulmonary edema and cyanosis were present. Methemoglobin level was 37,3%. This patient recovered appropriate therapy. For case 1 and 2 acute anoxia due to methemoglobinemia seems to be cause of death. For cases 3 and 4 death is due to hypoxemia associated with pulmonary edema.

The goal of this study is to appreciate the early and late sequelae caused by Chlorine Gas. 186 exposed patients have been admitted to our unit since 1962-119 had functional respiratory explorations (FRE) with an analysis of blood gases, 79 underwent a study of carbon monoxide transfer. The results are in accordance with the literature for example 25% of the CO transfer test were pathological. 56 occupationally exposed subjects having had at least three acute episodes of exposure have been compared to 197 control subjects (groups were classed in function of age, tobacco intake, and pulmonary antecedent). Chlorine exposure even when frequent has no the influence on the FRE results or the appearance of pulmonary pathology. The pre-existence of a pulmonary disease doesn't affect the prognosis.

Seven cases of acute intoxications by inhalation of metallic vapors are reported. The metals involved were zinc in three cases, tin in one case and mercury in three cases. The severity of the respiratory symptoms was dependent from the inhalated metal. The inhalation of zinc or tin vapors produced an acute limited pneumonitis. A lesional pulmonary oedema and acute interstitial fibrosis with lethal outcome was observed in two cases of intoxication by mercury vapors. The treatment by dimercaptopropanol used in mercury intoxications, increased urinary mercury excretion, but did not improve the pulmonary symptoms.

Rats have been exposed for periods of 120 to 240 minutes to an atmosphere containing 6 +/- 0.7 mg per cu.m mercury vapor. All rats developed an acute respiratory distress which lead to death within 2 to 210 hours (mean 53.5 h). Microscopical examination of the lungs showed an oedema rich in fibrin, an epithelial necrosis, hyaline membranes and in two cases an interstitial fibrosis. Mercury levels in the lungs ranged between 0.5 and 9.37 micrograms per gramme wet weight. The activity of pulmonary superoxide dismutase was decreased to 1.57 +/- 0.66 micrograms per mg of soluble proteins, compared with the level of 5.01 +/- 0.76 micrograms per mg in control rats. This study confirm the pulmonary toxicity of mercury vapors observed in human intoxication.

Twenty years after the publication of the first cases, the intoxication with the herbicide Paraquat still has a low prognosis because of no efficient treatment. But many studies have allowed the definition of prognostic factors. Nearly, BISMUTH and als(2) demonstrated that the following criteria are significant: the oral route, the gastric lesions, the organic renal failure, the plasma-Paraquat concentration. Through a series of cases collected in 1981 at the Poison Control Center of Paris, the following prognostic factors have been studied: route of administration, sex of patient, circumstances of the poisoning, ingested volume, concentration of the solution, existence of an emetic in the commercial solution, gastric content, lesions of the upper digestive tract (mouth, oesophagus, stomach), renal impairment, hepatic failure, blood gasometry, lung function tests, plasma and urine paraquat concentrations. Forty-one cases were collected during this period, with thirty-four concerning acute Paraquat poisonings in humans. We studied twenty-seven of them caused by acute oral poisoning, with accidental circumstances in nine cases (two died) and intentional circumstances in eighteen cases (all died) (other cases concerned two ocular projections, four inhalations and one skin projection). The interest of this new investigation is the particularity of our series. Because of our recruitment (larger geographic distribution of patients, larger diversity of circumstances, of routes of administration, of ingested quantities, of treatments...). This series of cases is quite different from others previously published. This study confirms the validity of prognostic factors defined by BISMUTH and als(2). The factors, which look significant, strictly depend on the ingested quantity.(ABSTRACT TRUNCATED AT 250 WORDS)

The authors report 7 cases of acute pulmonary edema in acute carbon monoxide poisoning. Hemodynamic data suggest existence of a myocardial failure as a possible cause of these pulmonary edema and indicate caution for volemic expansion during the treatment of shock in carbon monoxide poisoning.

Following an epidemic of sniffing petrol fumes and the death of a child, the authors review published findings of this little-known type of toxicomania. They envisage the Clinical and Toxicological problems. Researching and identifying the petrol remain problems. It is possible to detect the traces of petrol directly in the blood by gaz chromatography on a capillary column coupled to flame ionisation detector but it not possible to identify the product with complete certainly. The gas liquid on a packed column detected by Fournier transformed infra-red spectrography can be given to identification with total accuracy.

The authors report a case of methemoglobinemia following a suicidal attempts with a popper containing isobutyl nitrite. The toxic effects of this substances, either by ingestion or inhalation, are described as well as risks of use in "everyday life". Regulations, still incomplete has been suggested in USA. In France, preventive measures should be taken.

285 patients affected by carbon monoxide poisoning were admitted in our intensive care unit over a period of two years (from july 1980 to july 1982). 18 patients had a pulmonary edema (P.E.). The occurrence of P.E. was more frequent when coma was grade 2, 3 or 4 (p less than 10(-3]. The acute physiologic score (weighting of physiologic measurements) as proposed by Knauss is higher in patients with P.E. (p less than 10(-2]. However death is never due to P.E.; about 54 patients with coma, 5 died; death is related to neurologic aggravation. Neurologic sequelae are not related to the occurrence of P.E. but to a delay in hyperbaric oxygen therapy. These date show that prognosis of carbon monoxide poisoning is related to neurological status and is not influenced by the occurrence of P.E. when correctly treated and when hyperbaric oxygen therapy is early realized.