Cases reported "Poisoning"

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1/28. Anticholinergic toxicity associated with lupine seeds as a home remedy for diabetes mellitus.

    We describe a case of sparteine intoxication associated with using a preparation from lupine seeds. A female patient of Portuguese origin presented to the emergency department with classic anticholinergic signs after ingestion of a lupine seed extract. She took the preparation with the belief it represented a cure for her recently diagnosed diabetes. Analysis of the patient's lupine bean extract identified the preponderant compound as oxo-sparteine by gas chromatography/mass spectrometry. Intoxication by lupine seeds rarely occurs in human beings. To our knowledge, no medical or toxicologic evidence supports a belief that lupine extract could lower serum glucose levels. This case highlights the need for emergency care providers to be aware of the health hazards that can be associated with the use of such home remedies.
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2/28. Forensic toxicological implication of acute fatal poisoning cases due to benfuracarb ingestion.

    We describe here three cases involving acute fatalities due to benfuracarb ingestion and the forensic toxicological implications. Benfuracarb, a carbamate insecticide and its main metabolite carbofuran, were detected using thin layer chromatography (TLC) and gas chromatography/mass spectrophotometry (GC/MS) after extraction with ethyl acetate and then quantified using gas chromatography (GC) equipped with NPD. The blood levels of benfuracarb and carbofuran were in the range of 0.30-2.32 microg/ml and 1.45-1.47 microg/ml, respectively. Benfuracarb was not detected in urine, but carbofuran was detected in the range of 0.53-2.66 microg/ml.
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keywords = chromatography, extraction
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3/28. hemoperfusion is ineffectual in severe chloroquine poisoning.

    OBJECTIVES: To study the toxicokinetics in severe chloroquine poisoning, and to evaluate the efficacy of hemoperfusion. DESIGN: Case report on one observation. SETTING: Medical intensive care unit (ICU) of the University Medical Center Utrecht, The netherlands. PATIENT history: A previously healthy, 52-yr-old woman ingested 100 tablets containing 100 mg chloroquine base 1 hr before admission. At admission, she was drowsy, agitated, hypotensive, and in respiratory distress. Shortly thereafter, she was resuscitated from cardiac arrest. After hemodynamic and respiratory stabilization, the patient was transferred to the medical ICU. TOXICOKINETICS EVALUATION: During the course of her stay at the ICU, blood samples were taken for the determination of chloroquine and the metabolite desethylchloroquine concentration. hemoperfusion was started 3.5 hrs after ingestion of the chloroquine tablets. MEASUREMENTS AND MAIN RESULTS: The following toxicokinetics data during this severe chloroquine poisoning were calculated: apparent volume of the central compartment 181 L, apparent volume of distribution 1137 L, half-life in the distribution phase 6.4 hrs, half-life in the elimination phase 392.8 hrs, and total body clearance 2.01 L/hour. The average extraction ratio during hemoperfusion was 0.07, 0.28, and 0.25, in plasma, erythrocytes and whole blood, respectively. The total amount of chloroquine removed by hemoperfusion was only 480 mg (5.3% of the amount ingested). Simulation of a hemoperfusion session over 5 hrs by using a column with an optimal extraction ratio of 1.0 would have removed 1,816 mg chloroquine, only 18.2% of the amount ingested. This limited contribution of hemoperfusion to the total clearance makes it ineffective. CONCLUSION: hemoperfusion is not effective in severe chloroquine poisoning, even when started (relatively) early in the course of the intoxication. Toxicokinetic evaluation of a chloroquine poisoning should be based on the evaluation of plasma and whole blood concentrations.
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keywords = extraction
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4/28. Felbamate overdose complicated by massive crystalluria and acute renal failure.

    CASE REPORT: We report a 20-year-old woman who developed altered mental status, massive crystalluria, and acute renal failure following an intentional overdose of felbamate and sodium valproate. Peak plasma concentrations of felbamate and sodium valproate were 200 microg/mL and 470 microg/mL, respectively. Macroscopic urinary crystals formed approximately 18 hours after ingestion and were identified by gas chromatography as containing felbamate. Renal ultrasound revealed unilateral hydronephrosis. Following parenteral hydration, the crystalluria and acute renal failure resolved and the patient recovered. The frequency and significance of crystalluria in felbamate intoxication is unknown.
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5/28. Repeated measurements of aldicarb in blood and urine in a case of nonfatal poisoning.

    A nonfatal case of poisoning involving aldicarb, an extremely toxic carbamate pesticide, is presented. A 39-year-old female ingested an unknown amount of aldicarb, together with alprazolam and sertraline. On admission to ICU (T0), she displayed marked cholinergic symptoms and a deep coma. The patient was given pralidoxime and atropine. Her condition gradually improved on days 2 and 3 and she was discharged at T0 80 h. aldicarb was assayed by high-performance liquid chromatography on 21 blood and 8 urine samples successively taken during hospitalization. At the same time, serum pseudocholinesterase activity was followed on 21 successive samples. Blood aldicarb level was 3.11 microg/mL at T0 and peaked at T0 3.5 h (3.22 microg/mL), then followed a two-slope decay with a terminal half-life of ca. 20 h. aldicarb was detected in all urine samples (peak level: 6.95 microg/mL at T0 31.5 h) and was still present at the time of discharge. serum pseudo-cholinesterase activity remained low (< or = 10% of normal) until the 30th hour then rapidly increased and returned to normal after the 60th hour. The patient's clinical picture closely followed blood aldicarb levels and serum pseudo-cholinesterase activities. To our knowledge, this is the first report of an aldicarb poisoning documented by repeated measurements of the drug in the intoxicated person.
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6/28. status epilepticus from an illegally imported Chinese rodenticide: "tetramine".

    INTRODUCTION: The following case report demonstrates the severe consequences of refractory convulsive status epilepticus from an unfamiliar imported toxin, tetramethylenedisulfotetramine (TETS), and the difficulties of identifying the offending agent. CASE REPORT: A previously healthy 15-month-old girl was found by her parents playing with a white rodenticide powder brought from china. Fifteen minutes later, the child developed generalized seizures and was brought to an Emergency Department (ED). Her initial fingerstick blood glucose was 108 mg/dL. In the ED, the child was intubated for status epilepticus. Despite aggressive therapy with lorazepam, phenobarbital, and pyridoxine, she had 4 h of intermittent generalized seizure activity. She was extubated on the third hospital day, but appeared to have absence seizures and cortical blindness. Continuous electroencephalogram monitoring, performed weeks later, revealed severe diffuse cerebral dysfunction with multiple epileptogenic foci. The child remains developmentally delayed and is on valproic acid therapy for seizure control. Translation of the Chinese package labeling did not clarify its contents. Tetramethylenedisulfotetramine was finally confirmed by gas chromatography-mass spectrometry (GC-MS) in this rodenticide product and then quantified against a TETS standard that was synthesized in our laboratory. CONCLUSION: Tetramethylenedisulfotetramine is grouped with other "cage convulsants," such as picrotoxin, since they have a similar intercalating cyclical molecular structure and cause seizures through non-competitive gamma-aminobutyric acid (GABA) antagonism. The oral lethal dose 50% (LD50) in humans is estimated to be as low as 100 microg/kg. Our patient has severe diffuse cerebral dysfunction likely secondary to prolonged seizure activity after exposure to TETS.
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7/28. role of laboratory in the management of phenylbutazone poisoning.

    We report a rare case of intentional overdose of phenylbutazone in a 15-yr-old female. The patient exhibited symptoms of phenylbutazone toxicity and the presence of the drug was confirmed by gas chromatography mass-spectrometry (GC-MS) analysis of the initial urine sample. The patient underwent plasmapheresis to remove the drug from the circulation. Semiquantitation of sequential serum samples by GC-MS revealed elimination of phenylbutazone by day 5 of admission at which time the plasmapheresis was discontinued. Elevated blood urea nitrogen (BUN) and creatinine returned to normal. Analysis of biomarkers for liver necrosis and regeneration in sequential serum samples revealed the restoration of normal liver function by day 5. This case further confirms our previous observations that biomarkers for liver necrosis and regeneration can predict the outcome of patients with liver damage due to toxins.
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8/28. GC/MS identification of toxic pyrrolizidine alkaloids in traditional remedies given to two sets of twins.

    Neo- and perinatal mortality is high in most of africa. twins are at particular risk of perinatal mortality. The contribution of traditional remedies is seldom addressed. The case histories of two sets of twins who were treated with traditional remedies are described. The herbal remedies were analysed using gas chromatography-mass spectrometry. In one family, both siblings survived, albeit with hepatic damage. In the other family, one twin died within 24 h and the second one month after admission with a diagnosis of veno-occlusive liver disease (VOD). In both cases, the presence of the toxic pyrrolizidine alkaloid retrorsine, which is known to lead to VOD, was identified. health-care workers should be aware of the possibility of traditional medicine administration as a cause of illness, specifically in twin births.
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9/28. Usefulness of multi-parameter opiate analysis in hair of drug users and victims of fatal poisonings.

    The results of a multi-parameter analysis of opiates in the hair of drug users and victims of fatal poisonings with these xenobiotics have been presented. The analysis was carried out with the use of liquid chromatography coupled with mass spectrometry (LC-MS). The article discusses the monitoring of the drug users' adherence to pharmacotherapy and the usefulness of hair analysis for medico-legal purposes. The authors evaluate the differences in the contents of particular opiates in the hair as related to the origin of a sample (untreated drug user, drug user in the course of treatment, victim of fatal poisoning). The report presents differences between the Polish and American profiles of abuse, providing confirmation that a great part of drug users undergoing methadone treatment do not abstain from opiates and/or amphetamine, the latter as a rule being very often taken with opiates.
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10/28. Toxicological and histopathological analysis of a patient who died nine days after a single intravenous dose of methamphetamine: a case report.

    A man in his late twenties collapsed shortly after intravenously injecting himself with methamphetamine (MA). He slipped into a deep coma and remained in this condition for 9 days, until his death. autopsy revealed severe brain edema and localized subarachnoid hemorrhages in the cerebrum and cerebellum. Histopathological examination revealed myocardial necrosis in the left ventricle, rhabdomyolysis and bronchopneumonia. Blood derived from the cadaver was found to have high levels of blood urea nitrogen and creatinine, suggesting he experienced acute renal failure probably due to rhabdomyolysis. Most of the postmortem findings were consistent with MA poisoning. The patient's bronchopneumonia may have represented a hypostatic pneumonia that developed as a result of his deep coma. While the patient's brain edema, myocardial necrosis and rhabdomyolysis were diagnosed soon after admission, his bronchopneumonia and acute renal failure only occurred 6 and 8 days later, respectively. Although MA was not detected in the cadaver's blood, urine or liver, analysis of the decedent's hair using gas chromatography-mass spectrometry confirmed its presence at a concentration of 1.1 ng/mg. Based on these findings, we concluded that the patient's cause of death was multiorganopathy resulting from MA poisoning. This case suggests that the postmortem diagnosis of MA poisoning in patients who survive for relatively longer periods after drug injection should include toxicological hair analysis in combination with histopathological and postmortem physiochemical examination.
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