Tetrahydrofuran poisoning after occupational exposure.
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Biomedical subjects
Publications and source records attributed to R Garnier.
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Voluntary ingestion of concentrated anticoagulant rodenticides leads to prolonged hypocoagulability sometimes accompanied by haemorrhage. The authors report 11 cases referred to the Paris Anti-Poisons Centre. The products implicated were chlorophacinone, bromadiolone, and warfarin. The time interval before medical intervention ranged from 90 minutes to 3 weeks. The absence of early clinical signs probably explains the number of late admissions. Haemorrhage of variable severity was observed in 8 cases. The prothrombin time varied with the administered dose of Vitamin K and/or coagulation factors. Three patients were lost to follow-up at days 9, 24 and 68. The other patients were treated for several weeks (27 to 82 days). Massive overdose with these rodenticides justifies stomach washout when the patients are seen early, daily check-ups of coagulability and treatment with Vitamin K at a dosage adapted to the biochemical abnormalities. Severe haemorrhage requires transfusion and the administration of factors of coagulation. The duration of the abnormalities is unpredictable; the prothrombin time should therefore be checked 48 hours after stopping Vitamin K therapy to detect any recurrence.
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Pattern reversal, brain stem auditory and somatosensory evoked potentials (PREPs, BAEPs, SEPs) have been recorded on 13 patients occupationally exposed to inorganic lead compounds, in 9 patients occupationally or accidentally exposed to inorganic mercury compounds and in 26 chronic alcoholics. The results were compared to those of a normal control group. Peripheral conduction velocities were decreased in lead exposed workers and in alcoholics, but not modified in the mercury exposed patients. In the three exposed groups, an amplitude increase (PREPs and upper limb SEP cortical components), more important in the mercury group and an increase of central conduction time in case of lower limb stimulation, could be interpreted as early signs of nervous cortical impairment.
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Thirty-one patients with isocyanate-induced asthma were studied 6-54 months after diagnosis. Four had the same work conditions and unchanged or worse respiratory symptoms; seven had an alternative job or safer work conditions at the same work-place and suffered from mild to severe symptoms. The remaining twenty subjects were definitely removed from exposure; of these, ten (50%) remained symptomatic after being removed from exposure for an average of 19 months. Asymptomatic patients appeared to be younger and to have shorter durations of total and symptomatic exposures, while symptomatic patients were more reactive to acetylcholine at diagnosis. For patients removed from isocyanate exposure and for those re-employed at the same work-place, quality of the new work site seems to play a role in the evolution of isocyanate-induced asthma.
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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.
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.
Fifty women who were subfertile received artificial insemination from donors (A.I.D.) with ultrasound monitoring of ovulation. They were compared with an identical number of women who were inseminated without ultrasound control. The series side by side showed that there was a lower fertilisation rate in those who were monitored (4.2% compared with 6.2%) per month on an average over six months as compared with those who were not monitored by ultrasound, and those who were monitored took significantly longer to become pregnant than those who were not monitored. Because of these results the authors wonder whether ultrasounds are harmful for ovulation.
In vitro tests of mutagenicity help detect carcinogenic substances. A variation of the Ames test may be used to study the mutagenicity of urine after exposition of the organism in vivo. Saccharin is a widely used artificial sweetener excreted in the urine which can induce dose-dependent tumours of the bladder in the animal. We studied the mutagenicity of the urine of healthy volunteers after the ingestion of a single dose of saccharin. The results show a mutagenic effect related to the dose ingested in two types of Salmonella typhimurium (TA 98 and TA 38). These results are difficult to interpret as saccharin is not mutagenic in vitro alone or in the presence of control urine which eliminates a direct carcinogenic or cocarcinogenic effect; we were unable to detect impurities or metabolites. This study underlines the difficulty of prophylactic detection of chemical carcinogens.
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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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Five cases of acute accidental poisoning with White Hellebore are reported. All cases occurred several minutes after the ingestion of home-made gentian wine. The clinical signs were nausea, vomiting, abdominal pain, hypotension and bradycardia. The initial ECG showed sinus bradycardia in 4 cases. In one patient, complete atrioventricular block with an ectopic atrial bradycardia and an intermittent idioventricular rhythm was recorded. Symptomatic treatment and/or atropine led to recovery within a few hours. These symptoms suggested poisoning with a veratrum alkaloid. The White Hellebore (Veratrum Album L.) and the Yellow Gentian (Gentiana Lutea L.) often grow side by side in the fields; it is easy to confuse the two plants before they flower if one is not a botanist. Each gentian wine was analysed by thin layer chromatography and chemical ionisation spectrometry. All the wines contained Veratrum alkaloids.
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.