[Acute poisoning: general management and main causes].
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Acute Disease↗
Biomedical subjects
Frédéric Baud
Publications and source records attributed to Frédéric Baud.
[Acute hydroxychloroquine poisoning. The danger of rapid or excessive correction of initial hypokalemia].
INTRODUCTION: Toxic effects of hydroxychloroquine, like chloroquine, include membrane stabilization and hypokalemia, which is correlated with the severity of the overdose. Correction of hypokalemia can expose patients to the risk of ventricular arrhythmia. CASE: A 19-year-old woman who had ingested 6 grams of hydroxychloroquine was admitted to intensive care with severe hypokalemia (1.5 mmol/L on admission). Thirty-six hours after correction of the hypokalemia, circulatory arrest followed ventricular fibrillation. Her potassium level at that time was 5.8 mmol/L. Outcome was favorable after it returned to normal. DISCUSSION: Because its pathogenesis remains debatable, the hypokalemia following hydroxychloroquine poisoning must be corrected with care, even when severe. This correction is difficult, and extracellular transfer of the excess potassium after elimination of the toxin exposes the patient to the risk of ventricular arrhythmia.
Adult↗
Measurement of serum pralidoxime methylsulfate (Contrathion) by high-performance liquid chromatography with electrochemical detection.
Pralidoxime methylsulfate (Contrathion) is widely used to treat organophosphate poisoning. Despite animal and human studies, the usefulness of Contrathion therapy remains a matter of debate. Therapeutic dosage regimens need to be clarified and availability of a reliable method for plasma pralidoxime quantification would be helpful in this process. We here describe a high-performance liquid chromatography technique with electrochemical detection to measure pralidoxime concentrations in human serum using guanosine as an internal standard. The assay was linear between 0.25 and 50 microg mL(-1) with a quantification limit of 0.2 microg mL(-1). The analytical precision was satisfactory, with variation coefficients lower 10%. This assay was applied to the analysis of a serum from an organophosphorate poisoned patient and treated by Contrathion infusions (100 and 200 mg h(-1)) after a loading dose (400 mg).
Buffers↗
Development and validation of a gas chromatography-mass spectrometry method for the simultaneous determination of buprenorphine, flunitrazepam and their metabolites in rat plasma: application to the pharmacokinetic study.
Buprenorphine (BUP), a synthetic opioid analgesic, is frequently abused alone, and in association with benzodiazepines. Fatalities involving buprenorphine alone seem very unusual while its association with benzodiazepines, such as flunitrazepam (FNZ), has been reported to result in severe respiratory depression and death. The quantitative relationship between these drugs remain, however, uncertain. Our objective was to develop an analytical method that could be used as a means to study and explore, in animals, the toxicity and pharmacological interaction mechanisms between buprenorphine, flunitrazepam and their active metabolites. A procedure based on gas chromatography-mass spectrometry (GC-MS) is described for the simultaneous analysis of buprenorphine, norbuprenorphine (NBUP), flunitrazepam, N-desmethylflunitrazepam (N-DMFNZ) and 7-aminoflunitrazepam (7-AFNZ) in rat plasma. The method was set up and adapted for the analysis of small plasma samples taken from rats. Plasma samples were extracted by liquid-liquid extraction using Toxi-tubes A. Extracted compounds were derivatized with N,O-bis-(trimethylsilyl)trifluoroacetamide (BSTFA), using trimethylchlorosilane (TMCS) as a catalyst. They were then separated by GC on a crosslinked 5% phenyl-methylpolysiloxane analytical column and determined by a quadrupole mass spectrometer detector operated under selected ion monitoring mode. Excellent linearity was found between 0.125 and 25 ng/microl plasma for BUP, 0.125 and 12.5 ng/microl for NBUP and N-DMFNZ, 0.125 and 5 ng/microl for FNZ, and between 0.025 and 50 ng/microl for 7-AFNZ. The limit of quantification was 0.025 ng/microl plasma for 7-AFNZ and 0.125 ng/microl for the four other compounds. A good reproducibility (intra-assay CV=0.32-11.69%; inter-assay CV=0.63-9.55%) and accuracy (intra-assay error=2.58-12.73%; inter-assay error=0.83-11.07%) were attained. Recoveries were 71, 67 and 81%, for BUP, FNZ and N-DMFNZ, respectively, and 51% for NBUP and 7-AFNZ, with CV ranging from 5.4 to 13.9%, and were concentration-independent. The GC-MS method was successfully applied to the pharmacokinetic study of BUP, NBUP, FNZ, DMFNZ and 7-AFNZ in rats, after administration of BUP and FNZ.
Analgesics, Opioid↗
[Interactions between benzodiazepines and opioids].
Benzodiazepines and opiates or opioids are used concomitantly in various circumstances, for example in anesthesiology, for the management of acute or chronic pain and for substitution therapy in heroin addiction. There are numerous interactions between these two families of substances. The objective of this review is to present the interactions identified in clinical and experimental studies reported in the literature dealing with their effects on pain, anxiety, sedation and respiration. The exact mechanism of benzodiazepine and opioid interactions remains to be established. It may depend on pharmacokinetic or pharmacodynamic mechanisms. Certain arguments would support the pharmacodynamic hypothesis: the co-location of GABA and opiate receptors in the central nervous system, the existence of possible cross-reactivity and common pathways of intracellular transduction. The deleterious interaction of benzodiazepines and opioids on respiration may take place at the level of the central command of ventilation or may be related to additive actions on the different neuromuscular components of the respiration. A better understanding of the exact mechanisms implicated in these interactions would increase the safety of prescription of these drugs.
Anti-Anxiety Agents↗