Grob U, Schiltknecht M, Rentsch K, Kupferschmidt H. Department of Internal Medicine, Institute of Clinical Chemistry, Division of Clinical Pharmacology and Toxicology, Department of Medicine, University Hospital, Zurich, and Swiss Toxicological Information Centre, Zurich, Switzerland.
Background: The benzodiazepine antagonist flumazenil is not regarded as efficacious to reverse gammahydroxybutyrate (GHB)-induced CNS depression, although it interacts with the GABA receptor complex.
Case Report: A 36 year-old white caucasian male presented to our Emergency Department in frank coma (Glasgow Coma Scale 3) at time = 0. We only later learned that he had ingested GHB and some alcohol approximately one hour previously. His pupils were pinpoint, the physical examination was otherwise unremarkable, with no meningeal signs. At t = +5 min. blood was drawn for chemistry and an intravenous line was inserted. Because drug-induced coma was suspected, naloxone 0.4 mg was administered intravenously at t = +30 min. without effect. At t = +105 min. flumazenil 0.2 mg was given via the intravenous line, with a rapid and complete reversal of the coma (GCS rose from 3 to 14 within 5 minutes), with no relapse. Plasma GHB concentration was 137 mg/L; ethanol, benzodiazepines, zolpidem and zopiclone were non-detectable.
Conclusion: This well-documented report shows a striking effect of flumazenil on GHB-induced coma. The only alternative explanation is that arousal and flumazenil administration were coincidental. Against this view stands the close temporal relationship between the two events, the fact that plasma GHB concentration was very high 100 minutes earlier, and that the presence of flumazenil-sensitive drugs was excluded. The effect of flumazenil in this setting should be studied prospectively.
2002 North American Congress of Clinical Toxicology, Palm Springs, California, in: J Toxicol Clin Toxicol 2002, 40 (5), 615-616
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Curjuric I, Guirguis M, Kupferschmidt H, Meier-Abt PJ. Swiss Toxicological Information Centre, and Division of Clinical Pharmacology and Toxicology, University Hospital, Zurich, Switzerland.
Objective: Errors in medicine have received increased awareness in recent years. This is especially true for errors caused by medical professionals. In contrast, errors caused by non-professionals have received less attention. Therefore, the aim of this study was to compare frequency, type and severity of reported errors in drug-therapy between medical professionals (physicians, nurses, pharmacists) and non-professionals.
Methods: We reviewed retrospectively all calls to the Swiss Toxicological Information Centre between January 1997 and June 2001 for errors in drug-therapy and analysed these cases with regard to frequency, responsible party, type of error, involved ATC-drug-class and clinical outcome. We defined three types of errors: type 1, wrong patient/right drug; type 2, right patient/wrong drug; and type 3, right patient/right drug/wrong application (e.g. wrong dose, route of administration). Data on the outcome were based on feedback-reports from physicians. The clinical outcome was graded into asymptomatic, minor, moderate, severe, lethal.
Results: Among 38'535 cases with drug exposition, we found 2297 (6%) errors in drug-therapy. Among all errors (2297=100%), 912 cases (40%) were reported by physicians and 1385 (60%) by non-physicians. Medical professionals caused errors in 556 (24%) and non-professionals in 1707 (74%) cases. In 34 (2%) cases the origin of the errors remained unknown. Following types of errors were identified in professional (P; 556=100%) and non-professional (NP; 1707=100%) groups: Type 1 errors, P 20 (4%), NP 50 (3%); type 2 errors, P 126 (23%), NP 461 (27%), and type 3 errors P 361 (64%), NP 1086 (64%). In P 49 (9%)/NP 110 (6%) cases it remained unclear whether the patient or the drug was confounded. Type 3 errors (P; 361=100%/NP; 1086=100%) concerned wrong doses P 269 (75%)/NP 889 (82%), wrong route of administration P 63 (17%)/NP 158 (15%) and others P 29 (8%)/NP 39 (3%). In the P-group most errors were made with drugs acting on the central nervous system (44%) followed by anti-infective (17%) and cardiovascular drugs (7%). In the NP-group central nervous drugs were involved in 24% of errors followed by respiratory (22%) and anti-infective (8%) drugs. In 379 feedback-reports the clinical consequences of the errors were qualified as asymptomatic (P 117; NP 92), minor (P 51; NP 57), moderate (P 23; NP 21), severe (P 12; NP 4), lethal (P 0; NP 2).
Conclusions: The majority of drug therapeutic errors were caused by non-professionals (74%). In medical professionals and non-professionals types of errors, drugs involved and clinical consequences of drug therapeutic errors were surprisingly similar although the two lethal cases occurred exclusively in the medical non-professional group.
XXII International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT), Lisboa, Portugal, 22-25 May, 2002
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Koller M, Schnorf-Huber S, Kupferschmidt H, Meier-Abt PJ. Swiss Toxicological Information Centre, Zurich (STIC), and Division of Clinical Pharmacology and Toxicology, Department of Medicine University Hospital Zurich, Switzerland.
Objectives: MP is increasingly used for the treatment of attention deficit hyperactivity disorder (ADHD). In Switzerland, prescriptions of MP have doubled during the last 5 years leading to increasing concerns about MP poisoning. The aim of this study was to investigate the symptoms and the outcome of MP poisoning.
Methods: All feedback reports from physicians on patients with acute oral MP poisonings between 1968 and 2001 were analysed retrospectively. Only cases with MP monointoxications containing sufficient information regarding ingested dose and symptoms were included. Results were statistically analysed by logistic regression with age, dose and decontamination (no or late decontamination vs. early decontamination <1 hr) as independent variables. Intoxication severity was assessed according to the EAPCCT/EC/IPCS Poisoning Severity Score (Persson et al. J Toxicol Clin Toxicol 1998;36:205-213).
Results: Among 149 cases with MP monointoxications 39 cases were included into the study. 26 (67%) cases were male, and 13 (32%) cases were female. Age ranged from 2.5 to 68 years (median 13.0). 21 patients received gastrointestinal decontamination within 1 hr post-ingestion. The circumstances of poisoning were accidental in 12 (31%), intentional in 16 (41%), and others in 11 (28%) cases. 11 (28%) patients remained asymptomatic, whereas 72% of the patients developped either mild (16 cases, 41%) or moderate (12 cases, 31%) symptoms. The most frequent symptoms were neurological (51%), cardiovascular (46%) and/or ocular (13%). Symptoms included tachycardia (33%), agitation (26%), mydriasis (13%), hallucinations/disorientation/delir (8%), tremor (7%), and dizziness (7%). The doses of MP ranged from 0.9 mg/kg to 31.1 mg/kg with a median of 2.55 mg/kg. No significant associations were found between severity and dose (p=0.0535), age and/or decontamination.
Conclusion: MP poisoning is relatively benign in most cases. At doses up to 31.1 mg/kg MP, moderate symptoms such as agitation, hallucinations, disorientation and/or marked tachycardia occur in a minority of patients.
XXII International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT), Lisboa, Portugal, 22-25 May, 2002
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Fehr M, Kupferschmidt H. Swiss Toxicological Information Centre (STIC), and Division of Clinical Pharmacology & Toxicology, University Hospital, Zürich; Switzerland.
Objectives: Under increasing financial pressure poison control centres have to demonstrate their cost effectiveness in order to keep proper funding. The STIC is the only Poison Control Centre (PC) in the country and serves a population of seven million. In 2000 it received a total of 30'935 calls, 61.3% of which came from the public, 29.9% from physicians, and the remainder from veterinarians, pharmacists and various organisations. The aim of the study was to assess cost sparing effects in the public health care system of the public use of the PC.
Methods: A survey was performed by sending out a questionnaire to the public callers during February 2001. Calls on non-toxicology issues and calls from abroad were excluded. Besides questions concerning health care cost effects, the questionnaire included also questions covering user satisfaction and demographic data. The questionnaires were sent out one working day after the call took place. The callers were asked 1) what they would have undertaken if the PC had not been available, 2) whether they had already contacted the health care system (visited or telephoned emergency medical services, a physician or an emergency department), 3) if they had been advised by the PC not to contact the health care system (HCS), and 4) whether they did contact the HCS after the call to the PC.
Results: During the study period a total of 1336 calls from the public were answered. A total of 1047 questionnaires were sent out to the callers. The rate of return was 85% (n=888); 813 answers could be analysed.
(Table omitted)
Of 401 primary callers to the PC, 93% could be prevented successfully from contacting the HCS unnecessarily. The extrapolated annual number of these cases is 5000.
Conclusions: The services provided to the public by a poison centre do effectively decrease the cost in the HCS by preventing unnecessary measures in non-toxic exposures. Therefore the accessibility of a PC to the public should be broad, and the threshold to call a PC should be low by educating people about the services of the PC.
XXII International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT), Lisboa, Portugal, 22-25 May, 2002
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Rauber-Lüthy Ch, Lanzicher L, Guirguis M, Schnorf S, Kupferschmidt H, Meier PJ, Swiss Toxicological Information Centre; Division of Clinical Pharmacology and Toxicology, University Hospital; Department of Pediatrics, Stadtspital Triemli; Zurich, Switzerland.
Background: Acyclovir has been used widely for treatment of documented or suspected herpes simplex infection in newborn. It is generally well tolerated and acute renal failure in the newborn has not been reported so far.
Case report: A 1.5-day old, 3170-g girl had vesiculo-bullous skin lesions suspecting a herpes simplex infection. An intravenous treatment with acyclovir was started. An unusual increase in weight to 3660g was noted on day 4 and a serum creatinin of 211 mmol/L on day 5. At this stage a dosing error of acyclovir was discovered. The patient had been given 100mg/kg instead of 10mg/kg 3 times daily i.v. over 4 days. Acyclovir then was discontinued. The creatinin decreased to normal within 2.5 days. On day 5 a renal ultrasound showed a marked enlargement of the kidneys. The follow up revealed no pathologic signs on day 12. The acyclovir blood levels were then measured. The highest level was 277 mg/ml (20-fold elevated over maximal therapeutic level).
(Table omitted)
Conclusions: To our knowledge this is the first case of a newborn with transient renal failure caused by acyclovir poisoning. The child recovered fully with conservative treatment only. In comparison with two cases previously reported, that experienced no renal toxicity (1), our case showed much higher serum levels of acyclovir. Hence, the case report underlines the wide safety margin of acyclovir. Renal failure must be expected only after erroneous administration of very high doses and appears fully reversible after termination of acyclovir overdose.
(1) McDonald LK et al. Lack of toxicity in two cases of neonatal acyclovir overdose. Pediatr Infect Dis J.1989, 8, 529-32
North American Congress of Clinical Toxicology, Montréal, Québec, October 4-9, 2001
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Kupferschmidt H. Swiss Toxicological Information Centre, and Division of Clinical Pharmacology and Toxicology, University Hospital, Zuerich, Switzerland.
Background: Data collected by Poison Centers might give clues to temporal increases of particular types of poisoning thus enabling proper timing of preventive measures and campaigns. We hypothesized that such data will yield information about seasonal and diurnal accumulation of certain types of poisoning.
Methods: Calls to a poison center concerning human poisoning were recorded during a period of 2 years (1998-99) with regard to patient age (adults >16 years old), circumstances of poisoning (intentional vs. accidental) and class of poison (therapeutic drugs, technical and industrial products, household products, agrochemicals, drugs of abuse, plants, mushrooms, envenomations). 24 one-hour intervals of all 730 days were created to analize diurnal variations. Both years were divided into 2-week intervals for analysis of seasonal variations.
Results: 47554 calls were included (46% adults, 54% children; 76% accidental, 21% intentional). Call volume peaked during summer at the beginning of September for adult and pediatric poisoning. The seasonal variations were entirely due to accidental poisoning (increasing from 300 to 475 per week) whereas intentional poisoning remained stable (100 per week) throughout the year. Poisoning with therapeutic drugs decreased slightly during summer, whereas poisoning with plants and agrochemicals increased markedly (5-fold and 4-fold resp.). Diurnal variations of poisoning is almost entirely the result of accidental poisoning in children with a marked peak from 11 to 12 a.m. and from 5 to 8 p.m.
Conclusion: Seasonal and diurnal variations are almost exclusively due to accidental poisoning. This stresses the need for enhanced preventive activities, particularly in pediatric poisoning. In our geographical region campaigns for prevention of agrochemical poisoning are best carried out in March, for plant poisoning in June, whereas campaigns for prevention of therapeutic drug poisoning can take place all over the year.
North American Congress of Clinical Toxicology, Montréal, Québec, October 4-9, 2001
Kupferschmidt H. Swiss Toxicological Information Centre (STIC), and Division of Clinical Pharmacology & Toxicology, University Hospital, Zürich; Switzerland.
Nickel, a siderophilic metal forming the first transition series group VIIIb of the periodic table together with cobalt and iron, is an ubiquitous element, which is essential, at least in several animal species. There are water soluble (chloride, nitrate, sulfate), moderately soluble (carbonates, hydroxides) and water insoluble (metallic, sulfides, oxides) nickel species. Toxicity decreases from nickel carbonyl = Ni(CO)4 to soluble to insoluble compounds. Acute nickel toxicity can almost entirely be reduced to nickel carbonyl.
Symptoms of acute nickel poisoning: In case reports 325mg nickel sulfate (73mg elemental nickel) led to nausea, giddiness, decreased pulse. 0.5-2.5 g nickel (as sulfate and chloride in drinking water) produced nausea, vomiting, abdominal discomfort, diarrhea, lassitude, headache, cough, dyspnea for 1-2 days without sequelae. A 2.5 yo girl died of cardiac arrest after ingestion of 10-15g nickel sulfate (2.2-3.3 g elemental nickel) with erythema, mydriasis, stupor, nuchal rigidity, tachycardia, and pulmonal congestion. Postmortem changes included acute hemorrhagic gastritis. Nickel carbonyl is fatal after inhalation of 30 ppm for 30 minutes. A 47-yo male died of respiratory failure four days after massive nickel carbonyl exposure. His urine contained 535 µg Ni/L, and postmortem investigation revealed pulmonary and cerebral edema. The intoxication typically appears in two stages: The first immediate stage involves respiratory irritation and unspecific symptoms such as dizziness, frontal headache, weakness, nausea, and vomiting, followed by tightness of the chest, dyspnea and nonproductive cough. While in minor exposures these symptoms are moderate and resolve within 1 day, in more severe poisoning more pronounced pulmonary (pulmonary edema, pneumonitis) and gastrointestinal symptoms develop within 12-120 hours along with myalgias, fatigue, profound weakness, delirium, and convulsions. Additional complications include hepatorenal dysfunction, adrenal insufficiency, and hyperglycemia. Primary causes of death include diffuse interstitional pneumonitis, and cerebral edema and hemorrhage. A minority of the survivors of severe nickel carbonyl poisoning may develop pulmonary fibrosis, although most do not show respiratory impairment.
Effects of chronic exposure to nickel containing dusts include the development of allergic diseases of the respiratory tract, while skin sensitization occurs frequently after prolonged contact with metallic nickel. Nickel is a common sensitizing agent, and nickel and nickel compounds are recognized carcinogens (IARC 1990).
The intestinal absorption of soluble nickel compounds is rapid (1-2 h) with a bioavailability of 1-5%, while the absorption of metallic nickel and less soluble compounds is poor. Dermal absorption of nickel carbonyl after cutaneous exposure can be significant. In blood nickel is bound to albumin and nickeloplasmin. Animal studies indicate that highest concentrations of nickel after parenteral administration of soluble nickel salts occur in the kidney, and also in the lungs, liver, endocrine glands, cartilage, and connective tissue. After nickel carbonyl exposure highest concentrations are found in lung, brain, kidney, liver, and adrenals. Nickel is rapidly eliminated, mainly via urinary excretion and does not accumulate. Acute nickel toxicity is believed to be associated with its ability to bind to enzymes including hepatic microsomal enzymes, enzymes involved in carbohydrate metabolism and proteins transporting ions across cell membranes. Nickel competes with calcium intracellularly and may cause membrane disruption via lipid peroxidation, ultimately leading to cell death.
In unexposed individuals mean nickel concentrations in whole blood are 0.28 µg Ni/L (range <0.05-1.08), in serum 0.34 µg Ni/L (range <0.05-1.05), in plasma generally <2 µg Ni/L, and in 24-hour urine <2 µg/g creatinine. Serum concentration of >8-10 µg Ni/L indicate an excessive exposure to nickel. After exposure to sparingly soluble nickel compounds serum nickel concentrations reflect mainly the lung burden of nickel, while blood and 24-hour urine samples are good measures of exposure to soluble nickel compounds over the preceeding 1-2 days. After nickel carbonyl exposure the concentration of nickel in the urine correlates well with the severity of poisoning during the first three days postexposure. Levels peak at 24-48 hours postexposure and return to baseline within 1-2 weeks. According to Sunderman levels of 60-100 µg Ni/L are associated with mild, 100-500 µg Ni/L with moderate, and >500 µg Ni/L with severe poisoning (samples collected within 18 hours postexposure).
Treatment: Nickel carbonyl is the only nickel compound causing acute poisoning after inhalative exposure, while soluble divalent nickel salts may eventually lead to acute poisoning after ingestion.
Patients with significant exposure to nickel carbonyl should be removed immediately from the source of exposure. Contaminated clothes must be removed to prevent dermal absorption. Attention should be given to maintaining sufficient oxygenation. Symptomatic patients and individuals with heavy exposure should be brought to a health care facility for evaluation. On persons having ingested toxic amounts of soluble nickel compounds gastroenteral decontamination should be performed within 1-2 hours post ingestion. Supportive care is the mainstay of treatment.
Antidotes with potential efficacy in nickel poisoning include sodium dietyldithiocarbamate (DDC), disulfiram, D-penicillamine, N-benzyl-D-glucaminedithiocarbamate, meso-2,3-dimercaptosuccinic acid (DMSA), and dimercaptopropanesulfonic acid (DMPS). DDC is a investigational antidote forming lipophilic chelates with divalent nickel. In mice it reduces the accumulation of nickel in the lungs by redistribution to fatty tissue including the brain. It is more effective when administered parenterally and early. The protocol proposed by Sunderman for adult human poisoning with nickel carbonyl consists of the oral administration of 35-45 mg/kg DDC in divided doses during the first 24 hours followed by 400 mg every 8 hours until symptoms resolve and urine nickel concentrations are back to normal. In critically ill patients DDC may be given parenterally at a dose of 12.5 mg/kg. However, controlled data in human poisoning are lacking, and published case series are controversial. Disulfiram which is metabolized in the body to two molecules of DDC is used as a chelating antidote in nickel carbonyl poisoning. Because human data are almost absent for disulfiram, D-penicillamine, DMSA, and DMPS, these compounds cannot generally be recommended as treatment for nickel (carbonyl) poisoning.
References: 1) Barceloux DG. J Toxicol Clin Toxicol 1999; 37: 239-58. 2) Bradberry SM, Vale JA. J Toxicol Clin Toxicol 1999; 37: 259-64. 3) Sunderman FW. Ann Clin Lab Sci 1989; 19: 1-16. 4) Sunderman FW jr, et al. Toxicol Ind Health 1986; 2: 17-78. 5) Da Costa JM. Med News 1883; 43: 337-8. 6) Sunderman FW jr, et al. Am J Ind Med 1988; 14: 257-66. 7) Szathmary SC, Daldrup T. Fresenius Z Anal Chem 1982; 313: 48. 8) Webster JD, et al. Ann Intern Med 1980; 92: 631-3. 9) Jones CC. Arch Environm Health 1973; 25: 245-8. 10) Sunderman FW, Kincaid JF. JAMA 1954; 155: 889-94. 11) Vuopala U, et al. Ann Clin Res 1970; 2: 214-22. 12) Sunderman FW, Sunderman FW jr. Am J Med Sci 1958; 236: 26-31.
XXI International Congress of the EAPCCT, Barcelona, May 16-19, 2001
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Balmelli A, Kupferschmidt H, Rentsch K, Schneemann M. Department of Internal Medicine, Institute of Clinical Chemistry, Division of Clinical Pharmacology and Toxicology, University Hospital, Zurich, and Swiss Toxicological Information Centre, Zurich, Switzerland.
Objective: MDMA- (methylenedioxymethamphetamine, "ecstasy")-induced hyponatremia has been described in rare cases. Inadequate water-intake by ravers is invoked as possible cause as well as hormonal influences since >90% of the victims were young females. The role of interactions with other illicit drugs has not been clarified to date. 1-Benzyl-1-piperazine (street name: "A2"), a substance with amphetamine-like effects, is known since the 1970s, but there is no data on toxicity in humans. Benzylpiperazine has begun to be abused in Switzerland during the year 2000. We report a case of fatal use of MDMA and benzylpiperazine in a young woman.
Case Report: This 23-year-old female attended to a rave party where she consumed hard drinks and two capsules of benzylpiperazine. In the following 15 hours she drank 10 liters of water and took one tablet of ecstasy. Seven hours after the ingestion of benzylpiperazine and three hours after MDMA resp. she experienced minor malaise including frontal headache. Another three hours later she developed dizziness and somnolence (GCS = 8). In the Emergency Department she was found to be disoriented, deeply somnolent (GCS = 6), bradycardic (36 bpm), and hypothermic (core temp. 34.1°C). Her pupils were wide and nonreactive to light, and she did not react to painful stimuli. She seized twice 45 minutes after admission, and was intubated. Brain CT scan revealed massive brain edema with tonsillar herniation. The laboratory investigation revealed marked hyponatremia (115 mmol/L). Plasma osmolality was 246 mosm/L, and urine sodium concentration and osmolality were 23 mmol/L and 108 mosm/L resp. Blood ethanol was not detectable. Plasma MDMA concentration was 68 mg/L. Urine drug screen was positive for benzodiazepines, caffeine, nicotine, benzoylecgonine, MDMA and benzylpiperazine 5.7 mg/L (negative for amphetamines, barbiturates, cannabinoids, cocaine, opiates and phencyclidine). She was admitted to the MICU, serum sodium was corrected over 30 hours. Urine output increased consequently peaking at 1300 mL/h. The patient remained completely unresponsive (GCS = 3). Circulatory and neurologic condition further deteriorated, and she was declared brain dead 51 hours after admission. A post-mortem was refused by her relatives.
Conclusion: This is the first report of benzylpiperazine associated with the fatal outcome in a case of ingestion of illicit recreational drugs. Hyponatriemic hypotonic hyperhydration with cerebral edema is a rare but well-known complication of MDMA abuse. Young women are at particular risk. Therefore unrestricted water intake after MDMA ingestion (i.e. at rave parties) should be vigorously disencouraged. The role of coingested drugs (benzylpiperazine in this case) in the etiology of MDMA-induced cerebral edema is not known.
XXI International Congress of the EAPCCT, Barcelona, May 16-19, 2001
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Stäheli N, Guirguis M, Meier-Abt PJ. Swiss Toxicological Information Centre, Zurich, and Division of Clinical Pharmacology and Toxicology, Department of Medicine, University Hospital, Zurich, Switzerland
Objective: Chloral hydrate is still widely used in Switzerland as a sedative and hypnotic drug. In recent years an increasing number of chloral hydrate poisonings have been reported to the Swiss Toxicological Information Centre. The aim of this study was to analyse the cases with chloral hydrate monointoxications in regard to severity, dose dependent toxicity and effects of early decontamination.
Methods: We retrospectively analysed all feedback reports from physicians on patients with chloral hydrate poisoning between January 1980 and December 1999. Only cases with oral chloral hydrate monointoxication containing clinical detailed information regarding the severity of symptoms were included. Severity was assessed according to the EAPCCT/EC/IPCS Poisoning Severity Score.
Results: Among a total number of 402 cases with chloral hydrate overdose 95 patients (86 adults, 9 children) with clinically well documented monointoxications could be included in the study. 88 chloral hydrate poisonings were intentional and 4 accidental. In 3 cases the circumstances of intoxication were unknown. Nine (9.5%) individuals remained asymptomatic. 59 (62%) patients developed minor symptoms such as somnolence (52) and/or mild tachycardia (9). 17 (18%) patients showed moderate symptoms including sopor (9), agitation (5), moderate cardiac disturbances (2), single convulsion (1), gastric ulcer (1) and rhabdomyolysis (1). Eight (8.5%) patients where severely intoxicated with deep coma (6), ectopic ventricular beats (1), ventricular tachycardia (1), asystolia (2) and respiratory insufficiency (2). Two (2%) patients died because of septic-toxic shock after aspiration pneumonia and cardiac arrest. Ingested doses (± 10%) were known in 50 cases (4 asymptomatic, 34 mild, 9 moderate, 3 severe) and ranged between 0.6g and 30g. Moderate and severe symptoms where observed only above ingested doses of 2.4g and 7.5g chloral hydrate, respectively. While late primary decontamination (gastric lavage and/or activated charcoal) after one hour of intoxication had no influence on the dose-dependent severity of poisoning, early (<1 hour) primary decontamination (14 patients, ingested doses between 3g and 30g) prevented the development of severe symptoms and increased the dose-limit for moderate symptoms to 6g.
Conclusions: Chloral hydrate is an important cause of moderate and severe acute poisoning in Switzerland. Patients with ingested doses above 2.4g chloral hydrate should receive primary decontamination with activated charcoal within one hour after intoxication in order to prevent the development of moderate and severe symptoms. Primary decontamination after one hour of intoxication appears to be ineffective, and the patients should be transferred to an intensive care unit for monitoring and rapid therapy of potentially life-threatening symptoms.
XXI International Congress of the EAPCCT, Barcelona, May 16-19, 2001
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Feser M, Kupferschmidt H. Swiss Toxicological Information Centre (STIC), and Division of Clinical Pharmacology & Toxicology, University Hospital, Zürich, Switzerland
Objectives: Poison Information Centres serve as a potential source of information on environmental toxicology issues for the public and for medical professionals. The aim of our study was to describe the reasons and motivations of the public and of physicians to call our poison information centre with problems related to environmental toxicology.
Methods: All calls to the Swiss Toxicological Information Centre (STIC) in 1997 and 1998 labelled as environmental-related were included in this retrospective study. Environmental exposure was defined as any unvoluntary exposure to any substance mediated by the inanimate nature (i.e. soil, water, air). This included theoretical requests as well as problems after real exposures.
Results: Within the two years the STIC received 588 calls related to environmental problems including 313 theoretical questions (53%), 159 calls regarding chronic exposures (27%) and 116 acute exposures (20%). The exposed individuals were 198 adults, 58 children, 6 without known age, and 8 animals. The substances or substance groups of interest or exposed to are presented in the table. Motivation for calling the STIC (n=588) were: interpretation of symptoms 164 (29%), information about a substance or a product 131 (23%), question whether a relevant exposure has taken place 118 (20%), bad smell with or without symptoms 21 (4%) and 39 (7%) respectively, exposure followed by typical symptoms 30 (5%), interpretation of a laboratory result 23 (4%), other 48 (8%).
Conclusions: The STIC receives calls regarding environmental toxicology issues on a regular basis, the frequency being approximately one per day. More than half of the calls were theoretical questions without exposure. Pesticides, industrial chemicals and gases/vapors are the most important substance classes. The main motivation to call our poison centre for an environmental issue is the interpretation of symptoms suspected to be a result of an environmental exposure and theoretical information about environmental poisons. Calls regarding symptomatic cases after a specific exposure are rare events (5%). Thus poison information centres play an important role with the information of the people, in theoretical risk assessment, and with prevention regarding environmental contaminants.
XX International Congress of the EAPCCT, Amsterdam, May 2-5, 2000.
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Betschart T, Rauber-Lüthy Ch, Guirguis M, Kupferschmidt H, Meier PJ. Swiss Toxicological Information Centre (STIC), Zurich, and Division of Clinical Pharmacology and Toxicology, Department of Medicine, University Hospital, Zurich, Switzerland.
Objectives: From 1990 to 1998, the number of inquiries to the Swiss Toxicological Information Centre concerning dextromethorphan poisoning increased by 376% as compared to 26% with therapeutic drugs in general. The aim of this study was to investigate the severity of dextromethorphan poisoning and its dose dependent toxicity.
Methods: We retrospectively analyzed all feedback reports from physicians on patients with dextromethorphan poisoning between January 1997 and June 1999. Only cases with dextromethorphan monointoxications containing sufficient information regarding ingested dose and severity of symptoms were included. Severity was assessed according to the EAPCCT/EC/IPCS Poisoning Severity Score (Persson et al. J Toxicol Clin Toxicol 1998; 36: 205-213).
Results: 108 patients (59 children and 49 adults) were included in the study. 44 ingestions were suicidal, 33 accidental and 17 abusive. In 14 cases the circumstances were unknown. The most frequent symptoms were somnolence (36%), tachycardia (25%), ataxia (23%), mydriasis (21%), agitation (14%), vomiting (13%), confusion (11%), nystagmus (7%), hypertension (6%) and hallucinations (6%). Ingested doses of dextromethorphan ranged from 1.6 mg/kg to 64.6 mg/kg. There was a large variability of doses within the same degree of severity. The association between increasing doses and the severity of symptoms was statistically significant (p < 0.05). Severe symptoms included seizures, coma and hypertension (>160 mmHg in children). Single seizures were observed at a minimum dose of 10 mg/kg, coma and multiple seizures at 22.5 mg/kg, and hypertension at 5.5 mg/kg. As severe complications one patient developed psychosis at 4.3 mg/kg, another rhabdomyolysis at 64.6 mg/kg. No fatalities were reported in our series.
Conclusions: Dextromethorphan poisoning seems to be relatively benign since only a small percentage of patients develop severe symptoms. In our series poisoning with dextromethorphan showed a dose dependent toxicity, whereas the poisoning severity at comparable doses varied considerably. A genetic polymorphism (CYP2D6) in dextromethorphan metabolism may explain why some patients develop severe symptoms at doses which lead to only minor or even no symptoms in others with poor metabolizers running a greater risk of serious toxicity.
XX International Congress of the EAPCCT, Amsterdam, May 2-5, 2000.
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Kupferschmidt H. Swiss Toxicological Information Centre (STIC), and Division of Clinical Pharmacology & Toxicology, University Hospital, Zürich; Switzerland.
Objectives: OTC drugs are generally believed to be less toxic than prescription drugs, but data supporting this assumption are virtually non-existent. Some of the more toxic substances such as acetaminophen (paracetamol) or salicylates are widely used as OTC medications. Therefore the aim of our study was to test the hypothesis that OTC medications in general lead to less severe symptoms in overdose than prescription drugs.
Methods: All cases of human toxic exposure with therapeutic drugs registered by the Swiss Toxicological Information Centre (STIC) during 1997 and 1998 were included in the study. Data acquisition was prospective. In multidrug ingestions, the toxicologically most relevant substance determined the classification of the case. For the assessment of severity, cases without written follow-up reports from treating physicians including detailed description of symptoms and findings, and cases with low causal relationship between symptoms and exposure were excluded. In multidrug exposures only cases with exclusively OTC-medications (no combination with prescription drugs) were considered as OTC cases(no combination with prescription drugs). Severity was classified according to the Poisoning Severity Score (PSS) of the EAPCCT/EC/IPCS (Persson et al. J Toxicol Clin Toxicol 1998; 36: 332-7). Statistic calculations were made using logistic regression, with p<0.05 considered statistically significant. Drugs were classified according to their ATC codes.
Results: In 1997 and 1998 the STIC registered 16179 calls related to therapeutic drugs 4852 of which related to OTC medications. The majority were drugs for the nervous system (43.3%, prevalent in the prescription group) and the respiratory tractus (15.2%, prevalent in the OTC group). 70% of the patients were children (<16 years-old) in the OTC group as compared to 35% in the prescription group. 87% of the calls were related to monointoxications in the OTC group (69% in the prescription group). 55% were calls from the public in the OTC group (33% in the prescription group). The ratio between intentional and accidental poisoning was 0.39 in the OTC group and 1.50 in the prescription group. 4657 cases with follow-up reports were included (OTC 14%). The severity in the OTC/prescription cases was none in 227/711 (34%/18%), mild 340/2260 (51%/57%), moderate 90/677 (13%/17%), severe 13/327 (2%/8%), and fatal 0/12 (0%/0.3%) respectively. There was an independent statistically significant correlation of severity with prescription status (p=0.0073), multidrug poisoning (p<0.0001), age (p<0.0001), intentional poisoning (p=0.015), and sex (p=0.017) (severe or fatal vs. moderate or mild or asymptomatic).
Conclusions: OTC medications are less dangerous in overdose than prescription drugs. Other factors contributing to the difference of severity are sex, age, and circumstances of poisoning (deliberate vs. accidental).
XX International Congress of the EAPCCT, Amsterdam, May 2-5, 2000.
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Kunz MW, Rauber-Lüthy Ch, Meier PJ, Kupferschmidt H. Swiss Toxicological Information Centre (STIC), Zürich and Division of Clinical Pharmacology & Toxicology, University Hospital Zürich, Switzerland
Objective: The abuse of mushrooms containing the hallucinogenic psilocybin is increasing and serious adverse effects requiring hospitalization are not uncommon. The aim of this study was to analyze the health risk of abusive "magic mushroom" ingestion between January 1995 and July 1999.
Cases and Methods: All cases recorded by the STIC between January 1995 and July 1999 were included in this retrospective study. Cases with written feedback reports of treating physicians and hospitals were analyzed with respect to type and severity of symptoms. Symptom severity was classified according to the Poisoning Severity Score (PSS) of the EAPCCT/EC/IPCS (Persson et al. J Toxicol Clin Toxicol 1998; 36:332-7).
Results: Within the analyzed period (55 months) 161 acute exposures to psilocybe mushrooms (107 males, 41 females, 13 sex unknown; median age 20y (range 14-56)) were reported to the STIC. The reported cases increased from 12 in 1995, 13 in 1996, 24 in 1997, 65 in 1998 to 47 until July in 1999. Detailed written follow-up reports were obtained in 67 cases. 26 of these 67 exposures were mixed intoxications (18 (69%) with concomitant cannabis consumption). Symptoms included hallucinations in 29 (43%) and panic attacks in 21 (31%) patients. Additional symptoms were mydriasis, gastrointestinal upset, and tachycardia. Severity was assessed as mild in 23 cases (34%), moderate in 41 cases (61%), and severe in 3 cases (4%). There were no letal intoxications. Reasons for hospitalization were marked hallucinations, hyperexcitability, panic attacks, coma and convulsions. Concomitant cannabis ingestion did not increase severity. However, concomitant opiate and ethanol ingestion induced coma (GCS 3-4) in one patient, and concomitant LSD consumption resulted in convulsions in another patient. A 19-year-old male jumped from a tree in a while having hallucinations resulting in paraplegia. Delayed reactions (flashbacks) were reported in 3 patients.
Conclusions: The data indicate that in Switzerland the number of hallucinogenic mushroom poisoning has increased during the last five years, with a sharp increase in 1998-1999. In most cases magic mushroom ingestion alone results in mild or moderate self-limited psilocybin poisoning. Severe complications can occur with the concomitant ingestion of other substances of abuse such as opioids, ethanol and/or LSD, or following self-inflicted injury due to the nature of the psychedelic effects of psilocybin.
XX International Congress of the EAPCCT, Amsterdam, May 2-5, 2000
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Ch Rauber, M Guirguis, ASt Meier-Abt, B Gossweiler, PJ Meier
Objective: Angel's trumpet (Datura suaveolens) is a plant that grows naturally in South and Middle America, but is also found as an ornamental plant in the United States and in Europe. It contains the tropane alkaloids atropine, scopolamine and hyoscyamine. The use of Angel's trumpet as a hallucinogen goes back to the precolumbian time. Since a few years, however, reports of its abuse as a hallucinogen have increased in the United States as well as in Europe. Here we report the cases with Angel's trumpet poisonings reported to the STIC since 1993, including a group poisoning with a lethal outcome in the city of Zurich during the summer 1998.
Case series: The STIC registered an increasing number of cases with Angel's trumpet abuse since 1993 (1993, 6 cases; 1994, 9 cases; 1995, 19 cases; 1996, 26 cases; 1997, 29 cases; 1998, 67 cases). Until 1998 no severe anticholinergic intoxications occured. However, on July 23, 1998, a group of eight adolescents consumed a magic drink prepared from the Angel's trumpet. Subsequently all 8 patients became agitated and developed tachycardia. Three patients experienced severe hallucinations. One 20 year old woman, which was under substitution therapy with methadone, was found comatose 1-2 hours after Angel's trumpet intoxication. She developed tonic-clonic seizures that were treated with midazolam. All patients had to be hospitalized and received primary care treatment including physostigmine application in two cases. While 7 patients completely recovered from their anticholinergic poisoning within 24 hours, the 20 year old woman developed rapidly central hyperthermia of 42.9° C. The pulse rate increased to above 200/min and the blood pressure decreased to 70/30 mmHg. Finally, the patient developed ventricular tachycardia and fibrillation. Despite massive external cooling, fluid and electrolyte replacements, administration of physostigmine and vasopressors and cardiodefibrillation the woman finally died approximately 4 hours after ingestion of the Angel's trumpet extract.
Conclusions: The data demonstrate that intoxications with magic drinks prepared from extracts of the Angel's trumpet are an increasing clinical toxicological problem also in Switzerland. Most importantly, severe Angel's trumpet poisoning resulted in a lethal anticholinergic intoxication in one patient. The exact cause of death remains unknown. It is possible that the patient ingested other drugs (to be determined) and/or experienced an idiosyncratic hypersensitivity against the natural tropane alkaloids of the Angel's trumpet.
A fully grown plant is shown here:
http://www.meb.uni-bonn.de/giftzentrale/engelstrompete.html
XIX International Congress, EAPCCT, Dublin, Eire, June 22-25, 1999.
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M Guirguis, B Gossweiler, H Kupferschmidt, JP Lorent, Ch Rauber, PJ Meier-Abt
Objective: To present the experience of the STIC in computerised data collection and evaluation and to show the practical usefulness of the newly developed TOXI system in clinical toxicological situations.
Methods: TOXI was realised in two steps: First, a relational database was designed to obtain detailed informations on products (ATC) and clinical case characterizations (EAPCCT guidelines with a few modifications). For optimal user-friendliness, synoptically viewing of four full pages on large monitors, as well as unrestricted free-text searching is provided. The second specified core feature is the definition of quality control, i.e. quality assurance of outgoing information by senior residents and the structured evaluations concerning the evolution of the poisoning cases. In addition, the TOXI system requires poisoning severity scoring based on EAPCCT guidelines (none, minor, moderate, severe or fatal) and a causality assessment (definite, likely, possible, conditional, doubtful or unrelated) of all registered cases.
Results: The physicians on duty at the STIC actually have immediate access to more than 120'000 case informations and 10'000 structured and evaluated feedback reports. Additionally, they can use 40'000 product data and 40'000 literature excerpts. Their everyday work is quality-controlled and based on the written feedback report obtained from the treating physicians. These clinical judgements are an essential quality-controlled basis for better risk assessment with particular emphasis on dose-response relationships. The usefulness of the TOXI-system is illustrated by two examples: First, the two-year experience with structured data regarding intoxications with non-steroidal antiinflammatory drugs demonstrated severe intoxications exclusively for mefenamic acid with a minimal dose for induction of convulsions of 3.5 g. Second, the analysis of 131 monointoxications with selective serotonin reuptake inhibitors (SSRI) (citalopram 50 cases, fluvoxamine 34, fluoxetine 23, paroxetine 15, sertraline 9) demonstrated moderate and severe cases in 14% for citalopram, 9% for fluoxetine, 6% for fluvoxamine and 0% for paroxetine and sertraline.
Conclusions: These results and our experience with the TOXI system demonstrate a marked improvement in the efficiency and reliability of quality-controlled collection and evaluation of clinical toxicological data. Most importantly, the TOXI system permits the rapid screening for dose-dependent and differential toxicities of newly introduced drugs and other chemical products. Hence, the TOXI system should be of considerable help in a more efficient and more adequate identification of the toxicological risk of new chemical agents introduced into the market and thus further contribute to overall drug and chemical safety and to reliable risk assessment in human pharmacology and toxicology.
XIX International Congress, EAPCCT, Dublin, Eire, June 22-25, 1999.
B Gossweiler, B Truttmann, M. Guirguis, PJ Meier, D Radovanovic, Ch Rauber-Lüthy
Objective: The ingestion of button batteries by small children is a frequent emergency problem in pediatric medicine. The actual management of this situation is controversial. While some authors recommend initial radiological evaluation in all children (e.g. Litovitz et al. 1992, Rumack et al. 1992), other clinical toxicologists suggest a radiological evaluation only in symptomatic children (e.g. Marcus et al. 1993). To improve the evidence for the most economic procedure, we evaluated further the frequency of late gastrointestinal complications after button battery ingestions.
Methods: All children cases with button battery ingestions registered at the Swiss Toxicological Information Centre (STIC) between 1985-1998 were analysed in regard to initial symptoms and late gastrointestinal complications.
Results: During the investigated time period the STIC was involved in a total of 1095 children cases with button battery ingestion. 339 (31%) cases required medical evaluation whereas the other 756 (69%) children could stay at home without any further complications. Detailed medical reports from treating physicians and hospitals were available in 236 cases. Among these medically evaluated cases, 220 (93%) children remained without any initial symptoms. The batteries were excreted in the feces and none of the children had any late gastrointestinal complications. 16 children (7%) had mild initial symptoms such as eating difficulties, nausea, dysphagia, vomiting, abdominal cramps, diarrhea and/or black stools. Among these symptomatic patients only one child with ingestion of a lithium disc battery (diameter 20 mm) had a severe outcome. The battery was radiographically localized in the esophagus from which it had to be removed endoscopically. Nevertheless, the transient impaction of the battery in the esophagus caused esophageal perforation and mediastinitis. Some weeks later an esophageal stricture developed, so far without any need for dilatations. The 1.5 year old boy continues to have problems with swallowing of solid food, but otherwise his growth and development is normal.
Conclusions: Our data provide further evidence that severe complications after button battery ingestions are in general very rare events. More specifically, none of our initially asymptomatic patients developed late gastrointestinal complications, indicating that asymptomatic patients do not require extensive medical evaluation and treatment. Thus, our data support the concept that radiological evaluation after button battery ingestion is only indicated in symptomatic patients. Because of the very rare complications radiologic evaluation of asymptomatic patients appears not to be cost effective and cannot be recommended as a general advice by poison information centers.
XIX International Congress, EAPCCT, Dublin, Eire, June 22-25, 1999.
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HHT Kupferschmidt, JP Kévorkian, T Yang, S Dawling, DL Seger, DM Roden, FJ Baud, TJ Meredith
Objective: Valproic acid (VPA) is a branched chain fatty acid with anticonvulsant properties thought to be mediated by altered central nervous system GABA metabolism and neuronal ion channel function. We recently reported a patient with VPA poisoning who exhibited marked prolongation of the QT interval [1]. QT prolongation to > 500-550 msec is a risk factor for the development of torsade de pointes. The aims of the present study were to determine whether QT prolongation is likely to be VPA-related, and to investigate the effect of VPA on the rapidly activating delayed rectifier (IKr) potassium current, which is blocked by most drugs causing torsade de pointes.
Methods: We retrospectively analyzed consecutive cases of VPA poisoning at our institutions (Nashville, Paris) between 1989 and 1998. We assessed heart-rate-corrected QT intervals (QTc according to Bazett's formula) at the acute stage (high VPA concentrations) and at baseline (low VPA concentrations). Cases without sufficient documentation of plasma drug concentrations and/or EKG changes, and cases with co-ingestion of substances known to affect the QT interval were excluded. IKr in the absence and presence of VPA was recorded in atrial tumor myocytes (AT-1 cells, n=4) using the whole-cell configuration of the patch clamp technique according to a standard protocol [2].
Results: Sixteen cases were included in the study. Peak total plasma VPA concentrations ranged from 184 to 1640 µg/mL (median 410 µg/mL). Low total plasma VPA concentrations ranged from 22 to 156 µg/mL (median 56 µg/mL). Twelve of 16 patients exhibited a longer QTc during the acute stage than at baseline. Acute QTc values were greater by 62±73 msec0.5 (mean±S.D.) than at baseline (p<0.01). Nine of 16 cases had acute QTc values >450 msec0.5 (6 cases >500 msec0.5). VPA (50 µmol/L; 7.2 µg/mL) completely abolished IKr in vitro.
Conclusion: Significant prolongation of the QT interval occurs commonly in VPA poisoning. The inhibitory effect of VPA on IKr in AT-1 cells was marked at low therapeutic concentration. This result suggests that VPA-related QT prolongation may be mediated by diminished potassium currents in cardiomyocytes. This is consistent with known alterations in cardiac potassium currents in acquired and congenital long QT syndromes.
VPA conversion: 1 µg/mL = 6.93 µmol/L
References:
1. Kupferschmidt H, et al. Clin Toxicol 36: 471, 1998.
2. Yang T, et al. Circ Res 75: 870-8, 1994
XIX International Congress, EAPCCT, Dublin, Eire, June 22-25, 1999
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HHT Kupferschmidt, DL Seger, TJ Meredith
Objective: Valproic acid (VPA) is a branched-chain fatty acid introduced in the 1970s to treat epileptic seizures. Indications for its use were extended in the 1990s to non-epileptic conditions including migraine prophylaxis and mood disorders. This led to an increase in the number of individuals treated with the drug. More importantly, the group of individuals to whom its use was extended included those who theoretically are at greater risk of taking an overdose. The aim of our study was to assess changes in frequency of VPA poisoning over the last 10 years and to determine the indications for VPA treatment in those individuals who overdosed with the drug.
Methods: We undertook a retrospective chart review of all cases of VPA poisoning seen at Vanderbilt University Medical Center (VUMC) between 1989 and 1998. We determined whether the patients were treated with VPA prior to their overdose and, if so, for what indication. Data obtained were contrasted with figures recorded for VPA poisoning in AAPCC TESS Annual Reports (1986-1997).
Results: Between 1989 and 1998, 37 patients with VPA poisoning were seen at VUMC. Only six presented between 1986 and 1995. Subsequently, the number of cases of VPA poisoning increased markedly (1996: 5; 1997: 10; 1998: 16). Of the 37 VUMC cases, 76% (28) were being treated with VPA for non-epileptic conditions, mainly bipolar disorders; 19% (7) of patients were being treated with VPA for seizure disorders; and only 5% (2) were not being treated with VPA. TESS data indicate an almost exponential increase in VPA exposures between 1986 (n = 402) and 1997 (n = 8085). The total number of exposures registered during the same period only doubled (1.1 million in 1986; 2.2 million in 1997). Intentional and adult exposures rose disproportionately. In striking contrast, the frequency of lithium poisoning has decreased steadily since 1994.
Conclusion: The marked rise in the frequency of VPA poisoning is probably secondary to its changed indications for use. The introduction of VPA therapy into a population with a high risk of self-harm appears to have led to an increased number of suicide attempts with this substance. This conclusion is supported by the fact that the countrywide number of intentional overdoses and of adult cases increased disproportionately, and that the majority of VUMC cases with VPA poisoning were patients with newer indications for treatment with VPA (mood disorders). The observed national trend is associated with a decrease in frequency of lithium poisoning.
XIX International Congress, EAPCCT, Dublin, Eire, June 21-25, 1999.
Neueste Literatur / Littérature nouvelle / Latest literature
M. Guirguis, B. Gossweiler, H. Kupferschmidt, J.P. Lorent, Ch. Rauber, P.J. Meier-Abt
Oral presentation (Abstract available on demand).
Third Meeting on computer as an aid in Poison Centres, Lille Dec. 9-12, 1998
H. Kupferschmidt, D. Seger, S. Dawling, L. Murray, T. Meredith
Oral presentation (abstract available on demand).
North American Congress of Clinical Toxicology, Orlando, Florida, Sept. 10-15, 1998
Neueste Literatur / Littérature nouvelle / Latest literature
H. Kupferschmidt, B. Gossweiler, J. P. Lorent, P. J. Meier-Abt
Oral presentation (abstract available on demand).
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
M. Guirguis, M. Strassel, J. P. Lorent
Oral presentation (abstract available on demand).
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
D. Radovanovic, H. Kupferschmidt, P. J. Meier-Abt
Poster
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
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H. Kupferschmidt
Keynote review
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
M. Schwendinger, H. Kupferschmidt, P. J. Meier-Abt
Poster
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
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C. Rauber-Lüthy, P. J. Meier-Abt, H. Kupferschmidt
Oral presentation (abstract available on demand).
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
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J. G. Koller, B. Graf, B.Gossweiler, H. Kupferschmidt, P. J. Meier-Abt
Oral presentation (abstract available on demand).
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
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E. Liggenstorfer, H. Kupferschmidt, P.J. Meier-Abt
Oral presentation (abstract available on demand).
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
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D. Radovanovic, H. Kupferschmidt, P.J. Meier-Abt
Oral presentation (abstract available on demand).
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
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V. Enderlin, H. Kupferschmidt, P. J. Meier-Abt
Oral presentation (abstract available on demand).
Examples of Ecstasy pills found in Switzerland:
http://www.eve-rave.ch/er_test1999.htm
Examples of Ecstasy pills found in Germany:
http://www.meb.uni-bonn.de/giftzentrale/xtcuebs3.html
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
Neueste Literatur / Littérature nouvelle / Latest literature
P. J. Meier-Abt
Keynote lecture
XVIII EAPCCT Congress, University Zurich-Irchel, March 24-28, 1998
P. J. Meier-Abt
Lecture
Continuing education in clinical toxicology, University Zurich-Irchel, March 24, 1998
K. Fattinger
Lecture
Continuing education in clinical toxicology, University Zurich-Irchel, March 24, 1998
P.J. Meier-Abt
Lecture
Continuing education in clinical toxicology, University Zurich-Irchel, March 24, 1998