[Inhalation of smoke causes hydrocyanic acid intoxication].
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Biomedical subjects
Publications and source records attributed to C Bismuth.
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A technique is described in which the toxicokinetics of paraquat on passage through the heart and lung were studied by means of blood samples drawn simultaneously from the pulmonary and radial arteries in six cases of acute human life-threatening paraquat intoxications. There was a trend for the radial plasma concentrations of paraquat to be greater than or equal to the pulmonary concentrations. This data suggests that from a clinical point of view the distribution of paraquat into the lungs is not a slow process. There may also exist some efflux of the paraquat into the circulation. This efflux of paraquat may result from direct lung and/or heart injury induced by massive paraquat poisoning.
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There is a striking discrepancy between the efficacy of the kidneys, haemodialysis and haemoperfusion in removing paraquat from the body and the poor prognosis of paraquat poisoning even when the blood and urine concentrations (which are good indices of concentrations in lung and other tissues) are very low. Extracorporeal elimination techniques have been used world-wide in paraquat poisoning. Do they remove paraquat effectively? Certainly. Do they increase the survival rate? Probably not. The reason being that when these techniques of elimination are initiated, potentially lethal concentrations of paraquat have already been attained in the highly vascular tissues of vital organs and in pneumocytes. The data presented here suggest that the successful treatment of paraquat poisoning will not be achieved by modification of toxicokinetics.
A non-exponential mathematical equation was used to extrapolate the 'predictive line' for plasma paraquat concentrations beyond 24 h. Plasma paraquat concentrations were measured in 30 patients who were admitted more than 24 h after overdose. The extrapolated line accurately predicted the outcome in 27 of these 30 patients. Urine paraquat concentrations were measured in 53 patients. All patients with urine paraquat concentrations of less than 1 mg/l (colourless or light blue test result using the colorimetric test) within 24 h of overdose survived. In contrast, patients with urine paraquat concentrations of more than 1 mg/l had a high probability of death. Even if plasma paraquat concentrations have a higher predictive value, urine data may contribute to a more rapid evaluation of prognosis.
Although it is many years since a haemodialysis and haemoperfusion over uncoated and later coated charcoal columns have been used for the treatment of intoxicated patients, the clinical efficacy of these extracorporeal techniques in the treatment of severely poisoned patients remains a matter of debate. Some of the reasons for this controversy may be the indiscriminate use of haemoperfusion in any form of intoxication, the lack of well-controlled studies and the wrong interpretation of the high haemoperfusion clearance values sometimes obtained. Simple pharmacokinetic principles are applied to this type of treatment and some practical guidelines as to how and when haemoperfusion should be applied or presented are reviewed. The limited place of haemoperfusion in the treatment of severe poisoning, its further declining use in the future, at least in its present design, and some promising new treatments are emphasized.
Arterial-venous plasma concentration differences of meprobamate were studied on admission of acute overdose in man. The patients were divided in two groups. In the control group (n = 25) two successive blood samples were collected from the same vessel. In the study group (n = 35) femoral arterial and venous blood samples were collected simultaneously. In the control group the differences were not significant. In the study group the differences were statistically significant (P less than 0.01). The present study suggests that the origin of blood samples should be stated for toxicological studies and that the toxicokinetics may be more complex than those recognized previously.
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There is a striking discrepancy between: the efficacy of the kidneys, haemodialysis (HD) and Haemoperfusion (HP) in removing paraquat from the body and the poor prognosis of paraquat poisoning even when the blood and urine levels (which are good indices of concentrations in lung and other tissues) are very low. Extra-corporeal elimination techniques have been used worldwide in paraquat poisoning. Do they remove paraquat effectively? Certainly. Do they increase the survival rate? Probably not. The reason being that when these techniques of elimination are initiated, potentially lethal concentrations of paraquat have already been attained in the highly vascular tissues of vital organs and in pneumocytes. The data presented suggest that the successful treatment of paraquat poisoning does not depend on modification of toxicokinetics.
The aim of this study was to determine whether femoral arterio-venous plasma concentration differences (AVD) of amitriptyline exist during acute intoxication in man. All patients studied were comatose and were divided into a control group who had two successive blood samples drawn from the same vessel and a study group who had samples drawn from the femoral artery and vein simultaneously. Serial plasma concentrations of amitriptyline were measured by gas liquid chromatography. In each group the differences were assessed by means of the Wilcoxon matched pairs test. In the control group (n = 13) there were no differences (T = 31, n = 12). In the study group (n = 24) the AVD were significantly different (T = 52, n = 23). For amitriptyline, the arterial or venous origin of blood samples for toxicological studies must be stated.
From January 1974 to June 1983, the Paris Poison Control Centre collected 84 cases of overdosage with orphenadrine alone or in combination. Prior papers emphasized fatalities related to orphenadrine poisoning. This retrospective study suggests an underestimated incidence of anticholinergic drugs abuse in our country. The clinical picture of orphenadrine poisoning associates drowsiness, agitation, confusion, delirium and seizures. Anticholinergic symptoms are often noted: mydriasis, sinus tachycardia, dryness of the mouth and urinary retention. No severe cardiac disturbance was found in these patients.
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A retrospective study of 25 cases of cyanide poisoning has brought to light the following points: cardiorespiratory arrests are frequent (7/25) and often inaugural; in severe intoxications (7/25), deep metabolic acidosis is the rule, and cyanide poisoning should always be suspected in cases of coma with severe acidosis; mild intoxications are frequently symptomless. Anxiety and agitation should not be considered as evidence of cyanide poisoning; they are merely due to fear in most cases. The present treatment of acute cyanide poisoning relies basically on symptomatic measures: sodium bicarbonate, cardiac massage and, above all, assisted ventilation with 100% oxygen. Our experience does not support the concept of a lethal cyanide blood level when patients can rapidly be transferred by a medical team to an intensive care unit. Survival depends more on prompt medical care than on the accessibility to sophisticated antidotes.
The Neuroleptic Malignant Syndrome (NMS) is a rare but severe affection (spontaneous mortality 30 to 50 per cent), associating fever, hypertonia with myolysis, and respiratory impairment. Its mechanism remains debatable: The origin of the hypertonia might be central (as phenothiazines and butyrophenones induce a blockade of dopaminergic receptors in the hypothalamus) or it might be muscular (with an impairment of the sarcoplasmic reticulum uptake of calcium in a genetically abnormal muscle, as is proven in malignant hyperthermia). Whatever the actual mechanism, the oral or intravenous administration of sodium dantrolene, a peripheral muscle relaxant agent which does not affect the neuromuscular transmission but prevents the calcium-dependent contraction of actin and myosine, has proved to be effective in three recent cases of NMS.