Untractable fecalith's and hypercalcemia, both associated with Fuller's earth therapy in fatal case of paraquat poisoning.
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Biomedical subjects
Publications and source records attributed to F Colardyn.
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Animal experiments have suggested that diquat is less toxic than the more widely used paraquat. In this paper, nine previously reported cases of diquat intoxication are reviewed, together with the description of our personal observations in two additional patients. These two patients, like four other patients described in the literature, died from complications involving the gastrointestinal tract, brain and kidneys. Thus, diquat intoxication is apparently not as innocent as was originally thought. In this paper, special attention has been given to the major clinical differences between diquat and paraquat intoxication. In contrast with the latter, severe diquat intoxication induces gastrointestinal fluid sequestration and is associated with cerebral hemorrhagic lesions and a higher incidence of severe acute renal failure. Despite an asymptomatic clinical interval of up to 48 hours after ingestion, hemoperfusion should be started as soon as possible to prevent toxic levels of diquat in tissue.
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An open, comparative, randomized study was performed in two medical intensive care units to compare the efficacy of the combination of aztreonam and either cloxacillin or oxacillin [(cl)oxacillin] with that of the combination of tobramycin and a cephalosporin. Of the 92 patients who were included in the study, 76 were evaluable. All patients suffered from severe, mostly pulmonary, infections and received ventilatory support. The aztreonam combination yielded an 80% rate of clinical cure; mortality was 15%. Use of the aminoglycoside combination resulted in a 51% rate of clinical cure; mortality was 23%. The difference in cure rate between the two combinations was statistically significant. Adverse effects were negligible in patients who received the aztreonam combination, and superinfection was seen in only 2%. Of the patients who received the aminoglycoside combination, 20% developed a superinfection and 11% developed a new renal insufficiency. Therefore, the combination of aztreonam and (cl)oxacillin is a valuable alternative to the combination of an aminoglycoside and a cephalosporin.
The peripheral vascular effects of calcium entry blockers have been scarcely investigated. Therefore we examined the effects of different doses of tiapamil and nifedipine in two groups of volunteers. The measurements were done by plethysmography. At a lower dose there is a significant increase in venous capacity. At a higher dosage there is an increase of the arterial flow, eliciting a reflex sympathetic stimulation with heart rate increase and venoconstriction. Therefore calcium entry blockers can be considered as arterial and venodilators.
We present here the analysis of the activities of the mobile intensive care unit of the university hospital of Ghent in 1984. The call for medical intervention from the unit originated in most cases from the 900 centre. Trauma and cardiac arrest were the most frequent reasons for intervention. The majority of the interventions of the mobile unit were needed for patients at home. These data illustrate the need for orienting the medical emergency care systems towards patients at home.
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Venous occlusion plethysmography is a useful tool to investigate the effect of a vaso-active medication on the venous circulation in man. However, room temperature can be very critical when small changes have to be detected. Therefore several authors induce a preconstriction of the veins for example with norepinephrine. When the conditions of the experiment are carefully controlled and a very sensitive plethysmograph is used, a significant effect on forearm veins can be shown even after small doses of nitrates and a high room temperature; matching with placebo is critically needed. It is likely that by lowering room temperature the response would be exaggerated. Taking these restrictions in mind, venous occlusion plethysmography can be a very valuable, non-invasive tool to study the effect of vaso-active treatment on the veins in men.
We report three cases of fatal hyperthermia in the course of neuroleptic drug treatment. One patient developed his symptoms within hours after a single drug dose whereas the two others had a prolonged symptomatology which lasted for several days after the administration of different neuroleptic drugs. Biochemical events included diffuse intravascular coagulation, muscle cell necrosis and acute renal failure. Rhabdomyolysis was proved pathologically in two patients but brain lesions were atypical in all three cases. We conclude that the biochemical and pathological abnormalities seen in these patients are those which have been described by some authors in the malignant hyperthermia syndrome after anaesthesia. The symptomatology however can be insidious and the syndrome can develop after withdrawal of the drugs.