The use of anexate (Ro 15-1788) in acute self-poisoning with benzodiazepines alone or combined with other drugs--preliminary results.
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Adolescent↗
Biomedical subjects
F J Baud
Publications and source records attributed to F J Baud.
Toxicokinetics of paraquat through the heart-lung block. Six cases of acute human poisoning.
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.
Adult↗
[Anaphylactic shock].
The anaphylactic shock is a life-threatening reaction produced by the release of pharmacologically active substances (histamine, leukotriene...) by most cells and basophils. The release of these mediators may be immunologically mediated (anaphylactic reaction a typical immediate hypersensitivity reaction mediated by IgE) or not (anaphylactic reaction when not mediated by an antigen-antibody process). These mediators in turn specific end-organ responses in the cardio-vascular system, (vasodilatation, change in inotropy, increased capillary permeability), the respiratory system (bronchospasm upper airway oedema) and the skin (urticaria). Because of its etiology (mainly drugs, contrast media and colloids) the treatment of anaphylactic or anaphylactic reactions must be prophylactic. When it occurs, its cure is based upon adrenaline and fluid loading and eventually bronchodilators.
Allergens↗
[Emergency treatment of overdose].
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Coma↗
Elimination of paraquat.
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.
Animals↗
Arterial-venous plasma concentration differences of meprobamate in acute human poisonings.
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.
Adolescent↗
Spontaneous toxicokinetics of lithium during a therapeutic overdose with renal failure.
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Acute Kidney Injury↗
Elimination of paraquat.
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.
Adult↗
Arterio-venous plasma concentration differences in amitriptyline overdose.
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.
Adolescent↗
Cyanide poisoning from propionitrile exposure.
A 55-year-old worker was exposed to propionitrile by both the inhalational and dermal routes. He rapidly lost consciousness and developed metabolic acidosis consistent with cyanide poisoning. Treatment with hydroxycobalamin and sodium thiosulfate produced complete symptom resolution within an hour. Serial blood cyanide and thiocyanate levels documented a rapid decrease in cyanide and concomitant increase in thiocyanate. Serious cyanide poisoning can occur from propionitrile exposure. Treatment with hydroxycobalamin and sodium thiosulfate can produce rapid clinical improvement.
Cyanides↗
Determination of hydroxocobalamin and cyanocobalamin by derivative spectrophotometry in cyanide poisoning.
Hydroxocobalamin (OHCo) and cyanocobalamin (CNCo) are determined directly in biological media, without extraction, by using first derivative spectrophotometry. We diluted 200 mL of plasma, urine, or standards with 1.8 mL of pH 6 buffer (boric acid, potassium dihydrogen orthophosphate, and potassium hydroxide). The first derivative spectra of the dilutions were plotted between 320 and 400 nm. At the exact zero-crossing point for hydroxocobalamin, the derivative values of cyanocobalamin concentration were determined. The same procedure was followed for hydroxocobalamin at the zero-crossing point for cyanocobalamin. The derivative values of the concentration curves are linear in the range 5-100 microM. The minimum detection limit is approximately 5 microM for hydroxocobalamin of cyanocobalamin on the determination of hydroxocobalamin or vice versa, although the spectra strongly overlap. The method is fast and simple to use, thus making it easy to assess the in vivo transformation of hydroxocobalamin into cyanocobalamin after the administration of high doses of hydrocobalamin in cyanide poisoning.
Cyanides↗
Morphine disposition in opiate-intoxicated patients: relevance of nonspecific opiate immunoassays.
The use of routine nonspecific immunoassays to detect or quantitate opiates in biological fluids raises the question of the relevance of such immunoassays in the investigation of opiate overdose disposition. We investigated the plasma disposition of morphine in 13 patients intoxicated by the intravascular (i.v.) (n = 5) or oral routes (n = 8) using both a highly morphine-specific antibody radioimmunoassay (RIA) and a nonspecific morphine RIA. Both RIAs showed a first-order elimination rate after i.v. intoxication (apparent plasma terminal half-life ranged from 2.9 to 4.7 hours for unchanged morphine and from 3.2 to 4.9 hours for total opiates) and a persistent opiate concentration with rebound after oral ingestion, suggesting a slow release of opiates from the gastrointestinal tract, in dealers and bodypackers. Moreover, i.v. and oral kinetic data were similar for the two RIAs, except for the ratio between total and unchanged morphine concentrations. The nonspecific morphine assay gave a threefold to 16-fold higher concentration than the specific morphine assay but with parallel kinetics for all patients. We conclude that the current, routine nonspecific morphine immunoassays could be a valuable analytical tool for investigating opiate toxicokinetics.
Adult↗
Paraquat poisoning. An overview of the current status.
Paraquat is a bipyridyl compound with no known chronic toxicity or teratogenicity. It is poorly absorbed when inhaled, but causes severe illness when ingested orally, death usually occurring within 2 days of ingestion of 50 mg/kg. At lower doses death may be delayed for several weeks. The toxic compound accumulates in lung tissue where free radicals are formed, lipid peroxidation is induced and nicotinamide adenine dinucleotide phosphate (NADPH) is depleted. This produces diffuse alveolitis followed by extensive pulmonary fibrosis. The most important prognostic indicator is the quantity of paraquat absorbed, as shown by the plasma paraquat concentration. While renal failure will develop in the majority of those patients who eventually die, it may not, if present alone, indicate a fatal outcome. The absence of caustic burns in the upper digestive tract indicates a good prognosis. Treatment of paraquat poisoning remains ineffective, but Fuller's earth, activated charcoal and resins may prevent some absorption of the toxin. When tubular necrosis occurs, renal excretion of the compound decreases rapidly. A 3-compartment pharmacokinetic model has been described following ingestion of tracer doses including a 'deep' compartment for active pulmonary accumulation. Haemodialysis, haemoperfusion and forced dialysis have been attempted, with no clear improvement in survival rates. Superoxide dismutase, glutathione peroxidase, N-acetylcysteine and other 'free radical scavengers' have failed to alter the outcome in poisoned patients. Other theoretical treatments, such as deferoxamine, immunotherapy, NADPH repletion and lung transplantation still require clinical validation.
Charcoal↗
4-Methylpyrazole may be an alternative to ethanol therapy for ethylene glycol intoxication in man.
4-Methylpyrazole (4 MP) is a strong inhibitor of alcohol dehydrogenase. Its use in acute ethylene glycol (EG) or methanol intoxication has been suggested in experimental studies about its efficacy and safety. We report three cases of accidental intoxication with ethylene glycol in man treated orally with 20 mg/kg/day of 4 MP. The treatment was maintained until plasma EG concentrations became unmeasurable. The patients were admitted early during the course of the poisoning. Their neurological status was good. A slight metabolic acidosis observed in two cases was easily corrected and did not recur. Renal function remained normal in all cases. No patient underwent hemodialysis. On admission plasma EG concentrations were 24.2 mmol/l, 13 mmol/l and 9.7 mmol/l respectively. Plasma EG half-lives were 14.5, 11.5 and 14.75 hours respectively. Plasma oxalate concentrations and the rate of urine oxalate elimination, determined in two patients, were high on admission but quickly returned to normal. Concerning possible side effects of 4 MP, a skin rash was observed in one patient and a possible eosinophilia in the others. These three cases suggest that 4 MP may decrease the metabolic consequences of EG poisoning in man and may be of therapeutic value when administered early during the course of the intoxication before coma, seizures and organic renal failure have occurred.
Adult↗
[Lactic acidosis and multi-organ failure secondary to anti-retroviral therapy in HIV-infected patients].
A SERIOUS COMPLICATION: Antiretroviral therapy may induce severe lactic acidosis with multiorgan failure in HIV-infected patients. CLINICAL DESCRIPTION: Patients are admitted for onset of dyspnea, abdominal pain, nausea, vomiting or diarrhea, with weight loss and general fatigue over the past few days. Physical findings are usually not contributive except for constant presence of hepatomegaly. Laboratory examinations reveal severe metabolic acidosis with increased anion gap and serum lactate elevation. Perturbations of hepatic and pancreatic enzyme values may exist. Echotomography and CT scan demonstrate fatty liver, confirmed by histological examination of the biopsy. Outcome in the intensive care unit is generally multiorgan failure and death. Symptomatic treatments, mechanical ventilation, bicarbonate infusion or hemodialysis appear to be ineffective in most severe cases. PATHOPHYSIOLOGY: Antiretroviral nuceloside analogs are inhibitors of mitochondrial DNA polymerase gamma. This explains the dysfunction of the mitochondrial respiratory chain, leading to inhibition of lactate metabolism in the liver and enhancement of serum lactate and acetone body levels. Elevation of lactate/pyruvate and beta-hydroxybutyrate/acetoacetate ratios suggest mitochondrial dysfunction. Many other co-factors may be associated. THERAPEUTIC APPROACH: Several therapeutic strategies (thiamine, coenzyme Q, carnitine and riboflavin) have been tried. They rely on the pathophysiological hypothesis that sustained cellular dysfunctions cause this clinical syndrome.
Acidosis, Lactic↗
[Acute toloxatone poisoning. Apropos of 122 cases].
Toloxatone is a new monoamine oxidase inhibitor. One hundred and twenty two cases of poisoning with this drug are reported. In this series, the minimal toxic dose was 2 g. The first symptoms appeared about one hour after ingestion. In most cases, only drowsiness and mild adrenergic effects were observed. In a few cases of massive overdose, coma, pyramidal irritation, and myoclonic jerks occurred. In 3 cases of severe poisoning, toloxatone was associated with tricyclic antidepressants. Symptoms were similar to those reported in intoxications associating classical monoamine oxidase inhibitors and tricyclic antidepressants: muscular rigidity, hyperthermia and cardiovascular collapse. Two of these patients died.
Acute Disease↗
[Hypokalemia in massive chloroquine poisoning. 2 cases].
Two cases of hypokalemia which was deep (1.1 mmol/l), symptomatic and protracted were observed during the early course of acute massive chloroquine intoxication. Biochemical data suggest that the mechanism of hypokalemia in such cases is intracellular transport.
Acute Disease↗
Paraquat poisoning: biological presentation.
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Humans↗