A fatal case of propranolol poisoning

Propranolol hydrochloride is a beta-adrenergic blocking drug used in a variety of clinical conditions. Overdoses can result in severe hypotensive states usually associated with bradycardia or asystole or with profound myocardial depression. We report on an 18-year-old man who ingested a massive dose of propranolol HCl in a suicide attempt. The patient was brought to the hospital in an unresponsive state within 30 minutes of ingestion. He was initially stabilized but subsequently died nine hours after the drug was ingested. Invasive monitoring during this period revealed the shock to be secondary to marked depression of his systemic vascular resistance. Cardiac rhythm and left ventricular output were maintained throughout the attempted resuscitation. This hemodynamic picture suggests that decreased systemic vascular resistance may be another mechanism of shock in significant propranolol HCl overdoses.     

Acute potassium dichromate poisoning: a toxicokinetic case study

CASE REPORT: A 48-year-old man drank 150 mL of an aqueous solution containing potassium dichromate 22.5 g in a suicidal attempt and was admitted 7 hours after the ingestion. Hemodialysis was promptly undertaken and chromium concentrations in serum, erythrocytes, and dialysate were determined during the treatment. Chromium elimination in urine was monitored during hemodialysis and the subsequent 400 hours. The total chromium eliminated via hemodialysis and urine was calculated as 36.7 mg or 0.16% of the ingested dose. Spontaneous urinary elimination proceeded according to an open one-compartment model. The elimination half-life was 71.37 hours +/- 17.13 hours (95% CI). Chromium elimination from serum followed an open two-compartment model, with the half-lives of 3.16 hours +/- 2.63 hours for phase 1 and 50 hours +/- 27 hours (95% CI) for phase 2. Calcium-EDTA therapy had no influence on erythrocyte, serum, or urine chromium level. It contributed, however, to a significant increase in chromium elimination rate in the dialysate. Serum zinc was very low at admission and serum zinc, copper, and magnesium were controlled during the initial 30 hours.     

A case of fatal poisoning by rifampicin

The toxicologic findings of a fatal poisoning with rifampicin (Rimactan) are presented. The concentration of rifampicin and its two major metabolites 25-desacetylrifampicin and 3-formylrifamycin in post-mortem blood, urine, bile and liver at about 10 h after ingestion of 14–15 g was determined using a high-performance liquid chromatographic method. The results of the toxicological analyses were compared with findings in fatal and non-fatal intoxications and after therapeutic administration of the drug. Possible explanation for the fatal outcome is given.

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Zusammenfassung Es wird über die Ergebnisse der Obduktion und der toxikologischen Untersuchung einer tödlichen Vergiftung mit Rifampicin berichtet. Die Konzentration von Rifampicin und seinen beiden Hauptmetaboliten 25-Desacetylrifampicin und 3-Formylrifamycin wurde mittels Hochdruckflüssigchromatographie in Blut, Harn, Gallenflüssigkeit und Leber bestimmt.Der Tod war etwa 10 Std nach Einnahme von 14–15 g Rifampicin eingetreten. Die Ergebnisse der toxikologischen Analysen werden mit den Ergebnissen in anderen tödlichen und nichttödlichen Vergiftungen sowie mit den Ergebnissen nach therapeutischer Applikation des Arzneimittels verglichen. Für den tödlichen Ausgang wird eine mögliche Erklärung gegeben.

     

A case of sotalol poisoning with fatal outcome

The case of a 58 year old woman who died after ingestion of 14.4 g of sotalol and 50 mg of triazolam is described. Despite medical treatment, intracardiac pacing and hemodialysis, cardiovascular failure persisted and became irreversible. High sotalol concentrations were observed in plasma (65 micrograms/ml) and in post mortem tissues samples. Tissue to plasma ratios ranged from 2.5 to 6. The high drug concentration found in heart tissue (104.4 micrograms/g) explains the difficulties experienced in the sotalol poisoning.     

A fatal case of apparent water hemlock poisoning

A 14-y-o North American native boy died 20 h after ingesting "wild carrot". He was gathering edible plants with his family on Canadian Thanksgiving. A sample of the plant he ingested couldn't be positively identified but it contained cicutoxin on chromatography. Bioassay caused death in mice which demonstrated clinical signs similar to water hemlock (Cicuta maculata) poisonings. Cicutoxin could not be demonstrated in postmortem tissue or gastric lavage. The boy's clinical signs and laboratory tests were consistent with other reported cases of this poisoning.     

A case of fatal methyl bromide poisoning.

A case of preventable fatality and a nearly greater disaster as a result of methyl bromide fumigation of a restaurant is presented. Methyl bromide is a nearly odorless, volatile hydrocarbon used as a fumigant in the food industry. As a result of this episode, recommendations are made for worker and community notification of the hazards involved whenever fumigation takes place. Addition of a mucosal irritant or olfactory stimulant is recommended to provide warning for methyl bromide exposure.     

A case of fatal poisoning by Gyromitra esculenta

A case of fatal poisoning by the mushroom Gyromitra esculenta (false morel) in a 53-year-old woman is reported. Clinical data were characterized initially by vomiting and diarrhea, and subsequently by hypotension, anuria, jaundice, hemiplegia, and coma. Death followed on the 3rd day. Prominent pathologic findings were brain edema, necrosis, fatty degeneration of the liver, nephrosis, scattered petechiae, and small hemorrhages. Gyromitrin was extracted in methanol, purified by thin layer chromatography, identified by I. R. spectrometry, and weighed. The relationship between O. D. at 277 m and the concentration (0.1–0.5mg/ml in absolute ethyl alcohol) was established.     

Human parathion poisoning. A toxicokinetic analysis

The mortality rate of suicidal parathion poisoning is particularly high, the onset of fulminant cholinergic signs, and the patients frequently present to the emergency physician with life-threatening symptoms. Despite this uniformity, subsequent clinical course differs significantly among patients, mostly not as a result of different delays in treatment or insufficiency of primary care. Probably, the differences depend on the amount of poison absorbed and/or the disposition of the active poison, paraoxon. We followed the toxicokinetics of parathion and tried to quantify the actual poison load. To this end, we monitored parathion-intoxicated patients (patients requiring artificial ventilation) for plasma levels of parathion and paraoxon along with the activity of erythrocyte acetylcholinesterase and its reactivatability. Plasma obidoxime concentrations were followed as well as the cumulative urinary para-nitrophenol conjugate excretion as a measure of total poison load. All patients received a standard obidoxime scheme of a 250 mg bolus dose intravenously, followed by continuous infusion with 750 mg per 24 hours as long as reactivation could be expected (usually 1 week). All other treatment was instituted as judged by the physician. It was recommended to use atropine at low doses to achieve dry mucous membranes, no bronchoconstriction and no bradycardia. Usually 1-2 mg/h were sufficient. Seven selected cases are presented exemplifying toxicokinetic peculiarities. All patients were severely intoxicated, while the amount of parathion absorbed varied widely (between 0.12 and 4.4 g; lethal dose 0.02-0.1 g) and was generally much lower than anticipated from the reports of relatives. It remains open whether the discrepancies between reports and findings were due to exaggeration or to effective decontamination (including spontaneous vomiting, gastric lavage and activated charcoal). Absorption of parathion from the gastrointestinal tract was sometimes retarded, up to 5 days, resulting in fluctuating plasma profiles. The volume of distribution at steady-state (Vdss) of parathion was around 20 L/kg. Post-mortem analysis in one patient revealed a 66-fold higher parathion concentration in fat tissue compared with plasma, 16 days after ingestion. Biotransformation of parathion varied widely and was severely retarded in one patient receiving fluconazole during worsening of renal function, while phenobarbital (phenobarbitone) sedation (two cases) had apparently no effect. The proportion of plasma parathion to paraoxon varied from 0.3-30, pointing also to varying paraoxon elimination, as illustrated by one case with particularly low paraoxonase-1 activity. Obidoxime was effective at paraoxon concentrations below 0.5 microM, provided aging was not too advanced. This concentration correlated poorly with the paration concentration or the poison load. The data are discussed in light of the pertinent literature.     

Mercaptoethanol poisoning: report of a fatal case and analytical determinations

A suicide due to oral intake of 2-mercaptoethanol is reported. High concentrations of 2-mercaptoethanol and its metabolite 2-mercaptoacetate were found by gas chromatography in the urine and gastric content of the victim. These compounds were also identified by gas chromatography/mass spectrometry. Increased amounts of inorganic sulfate were furthermore found in the urine. Case history and autopsy findings are presented, and the metabolism of 2-mercaptoethanol is discussed.     

Clinical course of a fatal ingestion of diquat

CASE REPORT: A 28-year-old male ingested the herbicide diquat. The patient rapidly developed severe gastrointestinal and metabolic disturbances, airway compromise, respiratory failure, renal failure, hemodynamic collapse, and seizures. We describe multiple metabolic abnormalities, an apparent artifact introduced by diquat in the laboratory assay for serum creatinine, serum diquat levels, and the need for emergency airway management.     

A fatal poisoning from Nicotiana glauca

A young adult male was found dead in a field. No cause of death was apparent at autopsy, and the only positive toxicological finding was the presence of a nicotine-like alkaloid isolated from the liver. Anabasine, the major, highly toxic alkaloid of the shrub, Nicotiana glauca (tree tobacco) was subsequently identified in all body specimens examined using gas chromatography/mass spectrometry. Concentrations of anabasine in blood, urine and other body organs are reported.     

A fatal copper sulfate poisoning.

An 11-year-old female died within hours of accidentally ingesting a solution of copper sulfate. A postmortem blood sample was found to contain 66 micrograms/mL copper. The initial qualitative identification of this poison in the body organs and fluids was by means of SEM-microprobe analysis (SEM-MPA) and X-ray fluorescence (XRF). The samples were quantified by atomic absorption spectrometry.     

A fatal case of acute hydrogen sulfide poisoning caused by hydrogen sulfide: hydroxocobalamin therapy for acute hydrogen sulfide poisoning

A patient committed suicide with hydrogen sulfide (H(2)S) by combining two commercial products. The patient was given hydroxocobalamin as an antidote in addition to treatment with cardiopulmonary resuscitation, but died approximately 42 min after his arrival at the hospital. The patient's cause of death was attributed to acute hydrogen sulfide poisoning. Serum concentrations of sulfide before and after administration of hydroxocobalamin were 0.22 and 0.11 μg/mL, respectively; serum concentrations of thiosulfate before and after hydroxocobalamin administration were 0.34 and 0.04 μmol/mL, respectively. Hydroxocobalamin is believed to form a complex with H(2)S in detoxification pathways of H(2)S. Although H(2)S is rapidly metabolized and excreted, the decreased sulfide concentration may be also associated with this complex formation. The decreased sulfide concentration suggests that hydroxocobalamin therapy may be effective for acute H(2)S poisoning. The decreased thiosulfate concentration seems to be associated with formation of a thiosulfate/hydroxocobalamin complex, because hydroxocobalamin can form a complex with thiosulfate. The thiosulfate concentration decreased to a greater extent than did sulfide, suggesting that hydroxocobalamin has a higher affinity for thiosulfate than for H(2)S. Therefore, prompt administration of hydroxocobalamin after H(2)S exposure may be effective for H(2)S poisoning.     

A toxicokinetic analysis in a patient with acute glufosinate poisoning.

Incidents of poisoning in humans caused by the ingestion of the glufosinate ammonium containing herbicides are gradually increasing in Japan. This poisoning is characterized by various neurological symptoms such as disturbances of consciousness, convulsions and apnea which appear after an asymptomatic interval of several hours. We studied the toxicokinetics of glufosinate in a patient with this poisoning successfully treated without extracorporeal hemopurification. A 65-year-old male ingested BASTA, which contains 20% w/v of glufosinate ammonium, about 300 ml, more than the estimated human toxic dose. Four and a half hours after ingestion, he showed speech ataxia and systemic tremor. He was prophylactically intubated before the occurrence of serious respiratory failure. After 5 days of artificial ventilation he was extubated and discharged without any sequelae. We studied the serial change of serum glufosinate concentration every 3-6 h and assessed the urinary excretion of glufosinate every 24 h. The absorbed amount of glufosinate was estimated from the cumulative excreted in urine. Toxicokinetic analysis was performed using the two-compartment model. The changes in serum glufosinate concentration exhibited T1/2alpha of 1.84 and T1/2beta of 9.59 h. The apparent distribution volume at beta-phase and the total body clearance were 1.44 l/kg and 86.6 ml/min, respectively. Renal clearance was estimated to be 77.9 ml/min. The indication for extracorporeal hemopurification for this poisoning has been discussed.     

A fatal episode of accidental methomyl poisoning

Three fatalities from the accidental ingestion of methomyl, a carbamate pesticide, are reported. The methomyl had been stored in an unlabeled tin can and was accidentally used in preparing "roti," an Indian dish. The identification of the source of the poison through animal tests and further chemical identification is described. The lethal dose of methomyl was estimated to have been between 12 and 15 mg/kg body weight.     

Disseminated intravascular coagulation in a case of fatal lindane poisoning

After an accidental or intentional ingestion of lindane, clinical manifestations of poisoning may include rapid onset of nausea and vomiting, coma, seizures, respiratory failure, and death. While rhabdomyolysis, secondary renal failure, and aplastic anemia have also been reported, coagulopathies have not been observed following poisoning with this pesticide. In this case report we describe a 43-year-old female who intentionally ingested 8 oz of a 20% lindane solution. Her serum lindane concentration reached 1.3 mcg/ml and her clinical manifestations included seizures, coma, rhabdomyolysis, secondary renal failure, and disseminated intravascular coagulation. The coagulopathy presented early in her clinical course and resolved when serum lindane levels fell. The patient died 11 days after the ingestion.     

Toxicological findings in a fatal case of acebutolol self-poisoning.

A fatal case of acebutolol self-poisoning is presented. After single-step liquid-liquid alkaline extraction, acebutolol was identified by using an HPLC/DAD screening procedure. By means of a specific HPLC method, acebutolol was then quantified in a large range of postmortem samples. The blood acebutolol concentration was 34.7 micrograms/mL. The tissue distribution of the drug is discussed in the light of the existing literature.