Fatal suicidal poisoning with antituberculosis agents with ST elevation and acute coronary syndrome symptoms--a case report.

A 19-years old, previously healthy male, ingested the higher amount of rifampicin, isoniazyd, pyrazinamide, ketoprofene and alcohol. Within less than 20 hours he developed dyspnoe, pruritus, red man syndrome, and ECG changes suggesting acute coronary syndrome appeared - ST interval elevation. In the next few hours chest pain appeared and troponin I concentration was elevated (13.54 ng/ml). The performed echocardiography revealed global hypokinesis with the decreased left ventricular ejection fraction (approx. 30%). There was no significant pathological changes in coronarography, except for slowed blood flow. Further patient developed cardiogenic shock, pulmonary oedema and died within 32 hours from medication overdose.

[Metallic mercury poisoning caused by intravenous injection in vague circumstances--a case report]. / Zatrucie rtecia metaliczna podana dozylnie w niejasnych okolicznosciach--opis przypadku.

UNLABELLED: Mercury is a heavy metal found in nature in three forms: metallic mercury, organic and inorganic compounds. It is a general protoplasmatic toxin. The pathophysiology of mercury toxicity is related to its binding to sulfhydryl groups of different receptor proteins and cellular enzymes, interrupting cellular metabolism and in this way causing cell death. In the paper we present a case of 57-year-old woman, who was admitted due to suspicion of metallic mercury parenteral poisoning. The computed tomography (CT) scan of abdomen accidentally revealed multiple disseminated tiny metallic densities. The blood mercury level was high (41.9 microg/l), as well as mercury urine level (85.7 microg/g creatinine which was 42.8 microg/l). Neurologic examination revealed unobtrusive symptoms of cerebellum affection. Psychological examination revealed disturbances of cognitive abilities reliant on the efficiency of vision organ. The results of A. Benton's organic test were abnormal. Psychiatric examination revealed no abnormalities. Results of pulmonary function tests were within normal limits. CONCLUSIONS: The intravenous injection of metallic mercury did not cause serious clinical effects. Followup examination in order to reveal chronic toxic effects is necessary. Diagnostics and treatment of metallic mercury intoxications by parenteral injection should be carried out in the clinical toxicology departments.

[Massive lamotrigine poisoning--case report]. / Masywne zatrucie lamotrygina--opis przypadku.

Lamotrigine is a phenyltriazine derivative used as antiepileptic drug with pharmacological profile similar to phenytoin. It is chemically unrelated to the other antiepileptic drugs and mechanism of anticonvulsant action is that lamotrigine inhibits sodium channels, resulting in neuronal membrane stabilization and block of excitatory neurotransmitter release. Mean therapeutical dose of lamotrigine is 200 - 400 mg/day. Overdose experience with lamotrigine is limited. In severe cases of poisonings there were serious effects such as: coma, respiratory depression, recurrent seizures and intraventricular conduction disturbances. We report massive suicidal poisoning with lamotirigine unknown dose. Clinical course was severe--we observed deep coma, respiratory depression, epileptical state, ventricular disrhytmias, atrio-venticular heart block, cardiovascular shock, rhabdomyolysis and hypokalemia. There was ventricular fibrillation in course of poisoning. The patient was successfully resuscitated and discharged on 18 hospital day.

[Acute poisoning due to barium chloride--case report]. / Ostre zatrucie chlorkiem baru--opis przypadku.

We reported a case of 52-years-old male, suffering from alcohol dependence, who ingested 20-30 ml 10% barium chloride solution as a substitute of ethanol. We observed gastrointestinal disturbances (nausea, vomiting, diarrhea), numbness and paresthesias of limbs, severe hypokalemia (1.29 mmol/l) resulting in general paralysis of skeleton muscles, dysarthria and dysphagia, ventricular arrhythmias. This patient was treated successfully with potassium chloride supplementation and was discharged after 9 days.

[Acute poisoning due to chemical substances inducing methemoglobinemia--two cases report]. / Ostre zatrucie substancjami methemoglobinotwórczymi--opis dwóch przypadków.

Methemoglobin is an oxidized derivative of hemoglobin. It is generated by oxidization the ferrous form of iron (Fe2+) in the heme molecule to the ferric form (Fe3+). A molecule of methemoglobin is incapable of binding and carrying of oxygen. Methemoglobinemia, an increased concentration of methemoglobin in the blood above 2%, may be congenital due to deficiency or lack of specific enzymes protecting hemoglobin from oxidization or abnormal structure of hemoglobin molecule. More often methemoglobinemia is acquired as a result of accidental or intentional poisoning due to chemical substances oxidizing hemoglobin. Some of them may induce hemolysis. Cyanosis resistant to oxygen therapy and dyspnea occur in patients with the methemoglobin concentration above 20%. Consciousness disorders, respiratory and circulatory failure, liver and kidney damage may occur in patients with high methemoglobin levels greater than 50%. Fatal cases have also been reported. In the paper we present two cases of patients who were admitted to our hospital ward. First of them regards a 21-year-old woman with the methemoglobin level of 38.3% induced by accidental inhalation exposure to aniline. The other case concerns a 49-year-old man who developed methemoglobinemia of 42.7% after suicidal ingestion of an urea-substituted herbicide containing linuron. We observed hemolysis in both of these cases. They were treated symptomatically and with a specific antidote--methylene blue.

[Fatal colchicine poisoning--case report and review of literature]. / Smiertelne zatrucie kolchicyna--opis przypadku i przeglad literatury.

Colchicine is a natural pseudo-alkaloid found in plants such as the autumn crocus (Colchicum autumnale) and glory lily (Gloriosa superba), which is used to treat gout and some other rheumatological disease. Colchicine binds to tubuline and prevents its polymerization into microtubules. It is thus able to impair those cellular functions that involve microtubules, eg. it arrests mitosis in metaphase. Tissues with high mitotic activity are preferentially affected. We report suicidal colchicine poisoning leading to death after 61 hours. Clinical course was typical for colchicine action. We observed severe diarrhea, cardiovascular shock, ARDS, multiorgan system failure and DIC. Postmortem toxicological studies confirm colchicine poisoning.