[Poisoning with weever fish venom: a case report]. / Zatrucie jadem ostrosza (Trachinus draco)--opis przypadku.

Poland's access to the EU causes that there is the risk of poisoning from sources outside Poland. This is confirmed by the case reported below. The Weeverfish Trachinus draco lives in the coastal waters of West Africa and Europe (including those of the Mediterranean Sea) and belongs to the most poisonous fish species. The venom of Trachinus draco contains proteins that cause cellular membrane depolarisation, and haemolysis. A 35-yr. man was admitted to the Toxicological Department of the Nofer Institute of Occupational Medicine for symptoms, such as: a strong pain, swelling and reddening of the left leg, that had appeared after contact with an unidentified fish when he had been enjoying a bath in the Mediterranean Sea. In the additional examinations, slight abnormalities were detected only in the results of blood agglutination test. The patient was discharged from the hospital 7 days later in good condition.

[Sodium azide--clinical course of the poisoning and treatment]. / Azydek sodu--przebieg kliniczny zatrucia i leczenie.

Sodium azide poisonings occur very rarely. The mechanism of sodium azide toxic effect has not yet been fully explained. Despite the lack of an explicit procedure for the cases of sodium azide poisonings, in vitro tests and rare case reports suggest that treatment with antidotes for cyanide poisoning victims can be effective. This study describes two cases of suicidal sodium azide ingestion. Case 1. 30-year-old male ingested ca. 180 mg of sodium azide. On admission to hospital, within 4 hours from poisoning, the man complained of dizziness and anxiety. Physical examination revealed horizontal nystagmus, flapping tremor, HR 135/min. In laboratory tests, higher blood concentration of lactates (3 mmol/l) was detected, as well as lower potassium concentration (3.4 mmol/L) and increased transaminase activity (ALT 74 U/l, AST 90 U/l). Electrocardiographic tests showed a negative T wave in limb lead III. Other results were within normal. As the patient ingested a toxic dose of sodium azide, he was treated according to the therapy prescription for cyanide poisoning (amyl nitrite inhalation followed by intravenous administration of sodium nitrite and sodium thiosulphate). ECG record of the last day of hospitalization (7th day of treatment) showed negative T waves in lead III, V4-V6. He was discharged from hospital in good condition. Case 2.23-year-old male ingested 10 g of sodium azide 1.5 hours prior to admission to hospital. At the beginning, the patient's condition was good, but it changed to critical state within the first hours of hospitalization. He developed a deep coma, respiratory and circulatory insufficiency, metabolic acidosis, cardiac dysrrhythmias and anuria. Cardiac activity monitoring showed alternating tachycardia (140 beats per minute) and bradycardia (48 beats per minute), numerous additional supraventricular and ventricular extrasystoles and sinus dysrrhythmia. Cardiac arrest (asystolia) occurred twice, the second incident with fatal outcome. The patient received supportive therapy, he was also treated according to the therapy prescription for cyanide poisoning. Circulatory disturbances observed in both cases have been described in literature as symptoms of sodium azide poisoning. However, available literature data are scarce and lack systematization, most of them coming from several decades ago. The lack of patient's consent for detailed examination of circulatory system and liver made it impossible to gather further knowledge on the subject. The efficacy of treatment with antidotes for cyanide poisoning has not been unequivocally determined for this kind of intoxication.

[Clinical presentation of ST-elevation acute coronary syndrome in the course of intoxication with megadose of rifampicin. A case report]. / Obraz ostrego zespolu wiencowego z uniesieniem odcinka ST w przebiegu zatrucia megadawka rifampicyny. Opis przypadku.

We present a case of 29-year-old male, with coronary artery disease in mother's history, after suicidal poisoning with 30 g of rifampicin, who presented severe chest pain, ST elevations in ECG, low values of blood pressure and elevated troponin I. Echocardiography revealed generalised hypokinesia, and depressed contractility--left ventricle ejection fraction was 7%. Urgent coronary angiography has shown normal epicardial arteries with slow contrast inflow. The toxic properties of rifampicin as well as hypotension due to dehydration are considered reasons of symptoms in the presented case.

[Carbamazepine "CR"--clinical picture of intoxication: the kinetics of extracorporeal elimination]. / Karbamazepina "CR"--obraz kliniczny zatrucia: kinetyka eliminacji pozaustrojowej.

Carbamazepine (CBZ) intoxication is an important issue in acute poisonings practice. Pathological reflexes, central breathing depression and cardiac disturbances are the characteristic features of carbamazepine poisoning. The clinical picture is variable and does not always correlate with CBZ serum concentration. Controlled-release formulations of CBZ have a delay of over 48h between the time of ingestion and peak serum CBZ concentrations. Peristalsis paralysis makes the extracorporeal elimination a treatment of choice in this case. Unfortunately, the effectiveness of this procedure is not clearly established -the results are often contradictory which makes it difficult to set standards for elimination treatment. In this research we report 2 cases of controlled-release CBZ poisonings. Deterioration in the clinical state characterized mainly by central breathing depression appeared after 51 hrs (patient I) and 74 hrs (patient II) from CBZ ingestion. Charcoal hemoperfusion (HP) improved patients clinical state. During the HP procedure the mean CBZ plasma half-life (T(1/2)) was 6.67 h and 12.66 h. Those values were a few times lower then those measured after the cessation of HP. The mean charcoal column clearances (with blood flow 180 ml/min) were 77.2 and 108.9 ml/min. CBZ pharmacokinetics makes the drug move rapidly between the compartments during the HP. This movement may cause a reduction in CBZ concentrations in receptors' vicinity. Probably this mechanism accounts for the improvement of the patients' clinical state despite low kinetic values of the procedure.