[Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) blood levels in patients with acute carbon monoxide poisoning - a preliminary observations].

Background: Neurotrophins are the family of proteins which stimulate and regulate the process of neurogenesis. Several factors belong to the family, mainly nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT 3), and neurotrophin-4/5 (NT-4/5). Acute poisoning with carbon monoxide (CO), which usually is accompanied by neurologic symptoms, can potentially change the secretion profile of neurotrophins. Aim of the study. The main goal of the study is to assess the changes of NGF and BDNF plasma levels during an acute phase of CO poisoning as well as immediately after recovery. Additionally, the relationship among neurotrophin levels and selected aspects of clinical course of CO poisoning were studied. Materials and Methods: The study group consisted of 18 patients (mean age: 31.8±10.3 years) hospitalized in Toxicology Department of University Hospital in Cracow because of acute CO poisoning. There were 10 women (mean age: 30.2±6.9 years) and 8 men (mean age 33.9±13.7 years) in the group. The levels of NGF and BDNF were evaluated using immunoenzymatic method (ELISA) in plasma samples taken thrice in each patient. The sample 1. was taken during hospital admission, the sample 2. about 12-36 hours after admission, and the sample 3. just before the hospital discharging (usually, on the 3rd-4th day). The clinical data were collected from patients' anamnesis, physical examination and neuropsychological evaluation. The statistical analysis were performed using tools comprised in STATISTICA 12.0 PL (StatSoft Polska, Cracow, Poland) software. Results: The majority of NGF plasma levels were less than 14 pg/mL (values below the limit of quantification), contrary to the sole case of 34.3 pg/mL. BDNF plasma levels ranged from 4.8 ng/mL to above 48 ng/mL, i.e. they were higher than the upper limit of measurement range for the plasma dilution which had been used. The comparison of NGF and BDNF plasma levels in the study group with their analogues in healthy volunteers taken from the literature indicates that NGF level declines and BDNF level rises in patients with CO poisoning. The profile of BDNF concentrations in the majority of patients formed the characteristic pattern: BDNF sample 1. > BDNF sample 2. < BDNF sample 3. Taking all the values of BDNF higher than 48 ng/mL as equal to 48 ng/ mL, the statistically significant difference among 3 sample series was found according to BDNF levels. Maintaining the above mentioned assumption, the statistically significant negative correlation between the number of higher cognitive functions disturbed in one patient at the same time and the BDNF levels in sample series 2 was discovered, as well as the weak correlations between BDNF level in sample series 1 and carboxyhaemoglobin or lactate level. Moreover, weak but statistically significant correlations were present between the duration of CO exposure and BDNF levels in each sample series. Conclusions: The NGF plasma level is probably declined, while the BDNF plasma level is increased in patients with acute CO poisoning. The concentration­time curve for the plasma BDNF may sometimes undergo fluctuations with two peaks on its course. Plasma BDNF level may serve as a biological marker of disturbed higher cognitive functions in acute CO poisoning. Some clinical aspects of CO poisoning (duration of exposure, HbCO and lactate blood levels) may influence BDNF level.

Abnormal olanzapine toxicokinetic profiles--population pharmacokinetic analysis.

CONTEXT: Olanzapine is widely used in the treatment of schizophrenia and it is becoming more frequently responsible for overdoses. Standard pharmacokinetic models do not fit to the toxic concentration data. OBJECTIVE: The aim of present study is to investigate the reasons for an abnormal olanzapine plasma concentration time curve in the range of toxic concentrations. Two hypotheses were verified: entering the enterohepatic cycle, and drug deposition and its desorption from activated charcoal used for gastrointestinal decontamination. MATERIALS AND METHODS: One-hundred thirty-five plasma concentration data from 21 patients hospitalized for acute olanzapine poisoning were analyzed with the use of the population pharmacokinetic approach. A non-linear mixed-effects modeling approach with Monolix 4.3.1 was employed. RESULTS: A model assuming gallbladder emptying at irregular intervals was developed. Also, a model that describes desorption of olanzapine from the charcoal surface, in which the dose is divided into two absorbed fractions, was constructed. The analysis has found gastrointestinal decontamination and previous olanzapine treatment, as the significant covariates for toxicokinetic parameters of olanzapine. CONCLUSION: Our study provides interesting models for investigation of toxic concentration of olanzapine, which may also be used as the basis for further model development for other drugs as well. The investigated population was not large enough to reliably confirm any of the proposed models. It would be well worth continuing this study with more substantial data. Also, any additional information about olanzapine metabolite concentration could be vital.

Acute caffeine poisoning resulting in atrial fibrillation after guarana extract overdose.

UNLABELLED: Guarana (Paullinia cupana) is the climbing vine native to Amazon Basin, characterized by high caffeine content in its seeds. Guarana extract is a common ingredient of energy drinks used in order to boost energy and physical endurance and increase alertness. Severe caffeine intoxication is rare, but may be life-threatening mostly due to supraventricular and ventricular dysrhythmias. OBJECTIVES: We present the case of intentional caffeine poisoning after ingestion of tablets containing guarana extract, complicated by atrial fibrillation. CASE REPORT: A44-year-old man with no significant medical history was admitted to hospital about 21 h after ingestion of guarana extract containing 1.6 g of caffeine. Typical symptoms of caffeine toxicity, i.e. nausea, vomiting, anxiety and palpitaions, occurred shortly after ingestion. On admission, he was conscious, with blood pressure of 136/86 mmHg, heart rate of 106-113 beats per minute, fever of 37.8 °C, and symmetrically increased deep tendon reflexes. QTc interval in electrocardiogram was prolonged to 0.542 s. Laboratory tests revealed hypokalemia, hyperglycemia, leukocytosis, as well as elevated creatinine and creatine phosphokinase levels. Approximately 45 h post ingestion, the patient developed atrial fibrillation with fast ventricular rhythm. Tachydysrythmia subsided after infusion of amiodarone and restoration of electrolyte balance. Echocardiogram revealed presence of asymmetrical hypertrophy of the left ventricle with the systolic anterior motion of the mitral valve and normal left ventricular outflow tract gradient suggesting non-obstructive hypertrophic cardiomyopathy. CONCLUSION: Acute caffeine poisoning may result in atrial fibrillation, especially in predisposed patients with underlying hypertrophic cardiomyopathy.

Primary angioplasty in patient with ST-segment elevation myocardial infarction in the setting of intentional carbon monoxide poisoning.

BACKGROUND: ST-segment elevation myocardial infarction (STEMI) due to coronary artery occlusion in the setting of acute carbon monoxide (CO) poisoning is a very rare presentation. OBJECTIVE: Our aim was to report on the use of primary angioplasty in a patient with STEMI in the setting of CO poisoning. CASE REPORT: A 36-year-old man with retrosternal chest pain was admitted after exposure to CO. The initial electrocardiogram (ECG) showed ST depression in I, aVL, and V3-V4 with slight ST elevation in II, III, aVF leads. Toxic carboxyhemoglobin level of 22% and troponin I of 2.19 µg/L were confirmed. After oxygen therapy the chest pain diminished, but after about 15 h it returned. The repeat ECG revealed normalization of previous ST depression with persistent ST elevation in II, III, aVF leads. The troponin I concentration was 5.94 µg/L. An echocardiogram demonstrated an apex hypokinesia involving the adjacent segments of the anterior and lateral wall. On the coronary angiogram, an acute occlusion of the distal left anterior descending coronary artery was confirmed. Primary percutaneous coronary intervention (PCI) of the infarct-related artery was performed. After PCI, the patient was symptom free and had partial ST-segment elevation resolution. The patient was discharged home after 7 days, with persistent ST-T changes and mild hypokinesia of the apex suggesting myocardial injury. CONCLUSIONS: Patients with toxic CO exposure who have symptoms of STEMI should be carefully evaluated with serial ECG, cardiac necrosis marker measurements, and an echocardiogram. When there is evidence of myocardial injury, a wider use of coronary angiography can identify patients who could benefit from PCI.

[Brain death and transplantological issues in patients deceased due to poisonings]. / Smierc mózgowa oraz aspekty transplantologiczne u chorych zmarlych w wyniku zatruc.

The classical definition of human death, based on the statement of the definitive cessation of blood circulation, is still in use except the cases, where the death took the brain, but the blood circulation remained active for some time. In these cases, a "new definition of death" based on the statement of brain death, should be used. The diagnosis of brain death is made by performing of clinical tests and ancillary investigations in order to confirm patient's irreversible coma, lack of brainstem reflexes, lack of motor activity and apnea. Brain death results from the massive damage of brain tissue caused by various pathological processes including the direct and indirect effects of xenobiotics poisoning. Patients who deceased due to poisoning can be donors of tissues and organs for transplantation.

[Consciousness disturbances during poisonings: pathophysiology, clinical picture, and basic principles of diagnosis and management]. / Zaburzenia swiadomosci w przebiegu zatruc: podstawy patofizjologiczne, obraz kliniczny oraz zarys postepowania diagnostycznego i terapeutycznego.

Consciousness is the physiological state of the central nervous system, during which an individual maintain arousal (level of consciousness, vigilance) and realize the internal thoughts as well as the external stimuli (awareness, consciousness content). The toxicity of multiple xenobiotics may lead to impairment of both consciousness categories, presenting clinically as consciousness disturbances, quantitative and qualitative, respectively. Based on the behavioral criteria, different consciousness disorders are diagnosed, among others: brain death, coma, vegetative state, minimally conscious state, akinetic mutism. In the present paper, pathophysiology, clinical picture, as well as basic diagnostic and therapeutic principles of conscious disturbances are described, especially in poisoned patients.

[Toxicant-induced and drug-induced coma neurotoxicological issues of general anesthesia]. / Spiaczka toksyczna i farmakologiczna aspekty neurotoksykologiczne znieczulenia ogólnego.

Coma is a pathological condition of unconsciousness in which the patient cannot be awaken by any stimuli (lack of arousal), whose eyes are closed and who has no awareness of self or environment (lack of content of consciousness). Toxic coma is usually transient and disappears after elimination of xenobiotic, and possibly its active metabolites, from the body. Authors present the etiological factors, clinical features and principles of diagnosis and management of toxic coma. Additionally, mechanisms of altered consciousness induced iatrogenically by general anesthetics as well as a brief description of their toxicity are presented.

[Consciousness disorders: vegetative state and minimally conscious state]. / Zaburzenia swiadomosci: stan wegetatywny i stan minimalnej swiadomosci.

Brain injury due to hypoxia, trauma, stroke, poisoning, and other pathological conditions may result in chronic disorders of consciousness in the form of vegetative state (VS) or minimally conscious state (MCS). VS is a condition defining patients who have awaken from coma, open eyes spontaneously or on command, but still are not aware of themselves or their environment, showing only a reflex motor responses. MCS is a condition in which patients are not able to communicate consistently, but they are not already in the VS, because of evident signs of awareness of themselves and the environment. The paper discusses the diagnostic criteria, etiology as well as diagnostic procedures and treatment of VS and MCS

[Xenobiotic-induced seizures and epileptic states as a cause of consciousness disturbances]. / Napady i stany padaczkowe indukowane ksenobiotykami jako przyczyna zaburzen swiadomosci.

Poisoning with many xenobiotics may result in seizures, which are usually generalized. Seizures leading to unexplained disturbances of consciousness are usually generalized tonic-clonic, absence seizures and complex partial seizures Prolonged seizures without recovery of consciousness during interictal period are called status epilepticus. This paper presents the etiology, patomechanism, clinical characteristics, as well as diagnostic and therapeutic principles of toxic seizures. Additionally, the clinical description of nonepileptic psychogenic seizures is given, which often need to be differentiated with true seizures.

[Rare consciousness disturbances in toxicological practice: akinetic mutism, somnambulism, locked-in syndrome, and psychogenic coma]. / Rzadkie zaburzenia swiadomosci w praktyce toksykologicznej: mutyzm akinetyczny, somnambulizm, zespól zamkniecia i spiaczka psychogenna.

The toxicity of xenobiotics can result inrare disorders of consciousness, such as akinetic mutism and somnambulism as well as syndromes mimicking consciousness disturbances, such as locked-in syndrome and psychogenic coma. Akinetic mutism is a condition characterized by a lack of spontaneous movements and little or no vocalization. Somnambulism include performing of complex motor activity in an automatic manner during deep sleep, without any awareness of its execution. The locked-in syndrome is a state with quadriplegia coexisting with cranial nerves palsies and mutism, but with fully preserved consciousness. Psychogenic coma is a condition in which the patient has preserved level of consciousness and awareness, but does not communicate with theenvironment and does not exhibit the external manifestations of consciousness. This paper presents the etiology, clinical characteristics, as well as diagnostic and therapeutic issues for the above syndromes.

[Seafood poisonings. Part I. Shellfish and crustacean poisonings]. / Zatrucia zywnoscia pochodzenia morskiego. Czesc I. Zatrucia mieczakami i skorupiakami.

Seafood is a valuable source of nutrients, therefore, it constitutes an important part of diet in some geographical regions. The consumption of some shellfish and crustacean species may be a cause of food poisonings in humans, mainly due to simultaneous ingestion of biotoxins produced by algae, cyanobacteria, and bacteria. These toxins are accumulated in higher links of a food chain, i.e. mollusks and crustaceans, that consume toxins filtering phytoplankton. In the present paper the etiology, pathogenesis, symptomatology and treatment of some shellfish poisonings are presented.

[Seafood poisonings. Part II. Fish poisonings]. / Zatrucia zywnoscia pochodzenia morskiego. Czesc II. Zatrucia rybami.

Fish plays a significant role in human life, mainly as part of a balanced healthy diet and a good source of many of nutrients. However, contact with fish may be harmful or even life-threatening to man. Toxic effects, that fish exerts toward men (ichthyotoxism), result from envenomations by poison. ous fish equipped in venom apparatus (ichthyoacanthotoxism), direct contact with venom produced by skin glandules (ichthyocrinotoxism), or consuming fish containing toxins for nutritional purposes (ichthyosarcotoxism). In the present review, different fish-borne food poisonings are presented including their etiology, pathogenesis, symptomatology and treatment. In fact, the majority of fish poisonings are intoxications with toxins primary produced by bacteria, cyanobacteria and algae. These are consumed and accumulated in the food chain by herbivorous and predatory fish, that in turn may be a cause of poisonings in humans.

[Toxicology of Hymenoptera venoms]. / Wlasciwosci jadów blonkówek (Hymenoptera).

Hymenoptera venom is a secretion of special poison glands of insects. It serves both as a defensive substance against aggressors, as well as weapon used to paralyze the victim during gaining food. Chemically, the venom is a mixture of biologically active substances of high-, medium-, and small molecular weight with a variety of physiological functions. Individual substances may have toxic effects on stung human contributing to certain clinical signs and symptoms of venom poisoning. In the present paper, chemical structure, physiological role and toxicity of particular components of Hymenoptera venom are described.

[Electrocardiographic abnormalities in acute olanzapine poisonings]. / Zaburzenia elektrokardiograficzne w ostrych zatruciach olanzapina.

BACKGROUND: Olanzapine is an atypical antipsychotic used for many years in the treatment of schizophrenia and bipolar disorder. Poisonings with this medicine can results with cardiotoxic effects in the form of ECG abnormalities. AIM OF THE STUDY: To evaluate the nature and incidence of electrocardiographic abnormalities in patients with acute olanzapine poisoning. MATERIAL: 23 adult (mean age 38.4 +/- 15.5 years) patients with acute olanzapine poisoning, including 10 men (30.4 +/- 8.1 years) and 11 women (45.7 +/- 17.2 years), where 1 man and 1 woman were poisoned twice. The toxic serum level of olanzapine (above 100 ng/mL) was confirmed in each patient. METHODS: Evaluation of electrocardiograms performed in patients in the first day of hospitalization with automatic measurement of durations of PQ, QRS and QTc and the identification of arrhythmias and conduction disorders on the basis of visual analysis of the ECG waveforms. Statistical analysis of the results using the methods of descriptive statistics. RESULTS: The mean durations of PQ, QRS and QTc in the study group were as follows: 135 +/- 23 ms, 91 +/- 12 ms, and 453 +/- 48 ms, respectively. The most common ECG abnormalities were prolonged QTc and supraventricular tachycardia (including sinus tachycardia) - each 22%; less common were ST-T changes (17%) and supraventricular premature complexes (9%), and only in individual cases (4%) ventricular premature complexes, bundle branch block, sinus bradycardia and atrial fibrillation were present. CONCLUSIONS: In the course of acute olanzapine poisonings: (1) prolonged QTc interval is quite common, but rarely leads to torsade de pointes tachycardia; (2) fast supraventricular rhythms are also common, but rarely cause irregular tachyarrhythmias, eg. atrial fibrillation; (3) conduction disorders (atrioventricular blocks, bundle branch blocks) are not typical abnormalities; (4) the observed ECG abnormalities emphasize the need of continuous ECG monitoring in these patients.

[Sulpiride poisoning--case report confirmed with the quantitative determination of the xenobiotic serum level]. / Zatrucie sulpirydem--opis przypadku potwierdzony ilosciowym oznaczeniem stezenia ksenobiotyku w surowicy.

Despite above 40 years the presence of sulpride on the pharmaceutical market, the acute poisonings are poorly reported in the medical literature. The discussed case of sulpiride intoxication concerns ingestion probably dose of 12 g, that exceeded 10-fold maximum therapeutic dose. 16-year-old girl, with no previous sulpiride treatment, was admitted to the Toxicology Department about 3 hours after ingestion. In clinical picture she presented quantitative consciousness disturbances with maximum 10 scores in GCS scale, with tendency to low BP (minimum 88/45 mmHg) and episode of orthostatic hypotension. The ECG demonstrated: normogram, sinus tachycardia with a heart rate of 125 beats/min, PQ = 120 ms, QRS = 80 ms, prolongation of QTc to 519,6 ms and unspecific changes of ST-T syndrome. The qualitative toxicological test confirmed the presence of chlorprothixene in urine, but the serum therapeutic concentration (0.126 microg/ml) excluded the overdose. The quantitative determination of sulpiride serum concentration confirmed acute sulpiride poisoning. The measured sulpiride toxic concentration on admission and in the consecutive hours were from 13.2 to 8.2 microg/ml. Sulpiride toxicokinetic parameters such as t max = about 3 h, t 1/2 = 24.02 h, k(el) = 0.029 h(-1) were also estimated. They point out that the absorption rate is similar and the elimination is prorogated in sulpiride acute poisoning compared to therapeutic doses.

[Laboratory investigations in acute olanzapine poisonings]. / Badania laboratoryjne w ostrych zatruciach olanzapina.

BACKGROUND: Olanzapine is an atypical antipsychotic with multireceptor affinity and different pharmacological effects, which can result with abnormalities in laboratory investigations. AIM OF THE STUDY: To assess the nature and frequency of laboratory tests abnormalities in patients with an acute olanzapine poisoning. MATERIAL: 26 adult cases (mean age 37.7 +/- 15.3 years) of an acute olanzapine poisoning (serum level above 100 ng/mL). Group consisted of 11 men and 13 women, but 1 man and 1 woman were poisoned twice. METHODS: Prospective analysis of the following laboratory parameters: complete blood count (CBC), coagulation tests (APTT, INR), serum concentration of sodium, potassium, chlorides, glucose, BUN, creatinine and bilirubin, serum activity of AST, ALT, GGTP and CPK, urinalysis. RESULTS: The most common laboratory abnormalities in the study group were: hyperglycaemia (96%), hyper-prolactinaemia (83%), elevated CPK (80%), hypokalaemia (75%), hyperbilirubinaemia (60%), leukocytosis (55%). Less frequent parameters were: elevated AST (20%), hyponatraemia (15%), elevated ALT(10%) and thrombocytopenia (5%). The onset of some parameters was as follows: 1st day of hospitalization hyperglycaemia, leukocytosis and hypokalaemia, 2nd - hyperbilirubinaemia and elevated CPK, and 3rd - hyperprolactinaemia. CONCLUSIONS: In acute olanzapine poisonings: (1) muscle and liver injury, serum glucose and electrolytes abnormalities, and changes in CBC can be present; (2) the valuable parameters for the monitoring of the course of poisonings are: serum activity of CPK and transaminases (AST, ALT), serum level of bilirubin, glucose, potassium and sodium, and CBC; (3) hyperprolactinaemia probably lacks of practical importance, but the further investigations are needed in this area.

[The clinical picture of acute olanzapine poisonings]. / Obraz kliniczny ostrych zatruc olanzapina.

BACKGROUND: Olanzapine is a second generation antipsychotic of thienobenzodiazepin group, which is used in the treatment of schizophrenia, bipolar disorder, and others, mainly psychiatric. Its multireceptor action (antagonism to dopaminergic D1, D2, D4, serotoninergic 5-HT2A, 5-HT2C, histaminergic H1, cholinergic M1-5, and a1--adrenergic receptors) results in multiple clinical symptoms in the course of acute poisoning. AIM OF THE STUDY: Evaluation of incidence and intensity of clinical symptoms in patients with of acute olanzapine intoxication. The pathophysiological mechanisms of particular symptoms are also described. MATERIAL: 26 patients (mean age 37.7 +/- 15.3 years) hospitalized in 2005-2008 in toxicological centers in Krakow and Gdansk because of acute olanzapine poisoning (all patients had the toxic serum level of olanzapine above 100 ng/mL). The study group consisted of 11 men (29.3 +/- 8.5 years) and 13 women (44.9 +/- 16.4 years); 1 man and 1 woman were poisoned twice. METHODS: Prospective analysis (using descriptive statistics) of data taken from medical anamnesis and results of physical examination, considering the following ones: consciousness disturbances (Glasgow Coma Scale, Matthew's scale, qualitative disturbances), vital signs (arterial blood pressure, heart rate, breathing rate, temperature), neurological findings (muscular tension, tendon reflexes, extrapyramidal symptoms, pupils) and others (oral and bronchial secretion, Poisoning Severity Score). RESULTS: The mean dose of ingested olanzapine in the study group was 352.5 +/- 220.0 mg, while the mean time since ingestion to hospital admission was 4.4 +/- 3.5 h. The half of the patients took other medicines together with olanzapine, and 23% consumed alcohol, as well. The following intensity of quantitative consciousness disturbances according to Matthew's scale were observed: grade 0 - 8%, I - 15%, II - 23%, III - 50%, and IV - 4%. The minimal and maximal values of blood pressure were: 102/63 +/- 16/14 and 163/ 97 +/- 27/18 mmHg, respectively; heart rate: 77 +/- 15 and 138 +/- 22 beats/min; temperature: 36.3 +/- 0.5 and 37.9 +/- 0.8 degrees C; breathing rate in non-intubated patients: 14 +/- 2 and 22 +/- 7 breaths/min. The mean duration of consciousness disturbances, endotracheal intubation and mechanical ventilation were: 44.9 +/- 31.3; 22.0 +/- 33.3 and 7.0 +/- 25.9 h, respectively. The study revealed tachycardia (85%), psychomotor agitation (81%), hypertension (73%), miosis (65%), and coma (54%) as the most common symptoms of poisoning. The hospitalization of poisoned patients lasted on average 5.7 +/- 3.6 days and the half of them were poisoned severely (PSS 3). CONCLUSIONS: In the course of acute olanzapine poisoning: (1) the prevailing symptoms come from circulatory and central nervous systems; (2) some symptoms are mutually opposed, eg.: coma - psychomotor agitation, hypertension - hypotension, tachycardia - bradycardia, hyperthermia - hypothermia, miosis - mydriasis; (3) rarely consciousness disturbances may persist for up to 6 days after olanzapine overdose; (4) the course of poisoning can be severe, sometimes complicated, but fatal outcomes are rare.

[Toxicity of sulpiride]. / Toksycznosc sulpirydu.

Sulpiride is a benzamide neuroleptic used in the treatment of some psychiatric and gastroenterological disorders. Its antipsychotic, antiautistic, activizing and antidepressive properties result from antagonistic action to dopaminergic D2, D3 and D4 receptors in the central nervous system (CNS). The oral bioavailability of sulpiride is poor and it does not appear to have an extensive first-pass metabolism, nor is it extensively protein-bound. Elimination of sulpiride appears to depend primarily on the kidneys. The acute sulpiride poisoning includes mainly neuropsychiatric (i.e., agitation, hallucinations, and CNS depression) as well as cardiac effects (i.e., hypotension, dysrhythmias, and sinus tachycardia). The life-threatening conditions with sometimes fatal outcome after sulpiride poisoning are prolongation of QTc interval with consequent torsade de pointes (TdP) and neuroleptic malignant syndrome (NMS). The quantitative methods for the measurement of sulpiride blood concentration are not routinely available and the toxic blood concentration is probably higher than 2 mg/L. Treatment of acute sulpiride poisoning includes standard protocols of gastrointestinal decontamination and further symptomatic and supportive measures, among them TdP (magnesium sulphate, isoproterenol, electrotherapy) and NMS treatment (benzodiazepines, bromocriptine, dantrolene, physical cooling).

[The review of acute risperidone poisoning]. / Ostre zatrucie risperidonem--przeglad zagadnienia.

Risperidone (RIS) is a benzisoxazole derivative, an atypical neuroleptic used in the treatment of schizophrenia and other psychoses. The therapeutic action of RIS depends not only on the parent compound but also its major active metabolite, 9-hydroxyrisperidone (9-OH-RIS), and the pharmacokinetics is modified by the genetic polymorphism of CYP2D6, the main site o RIS metabolism. Diverse symptoms of an acute RIS poisoning result from its interaction with multiple receptors, i.e. serotoninergic 5-HT2A and 5-HT7, dopaminergic D2, adrenergic alpha1 and alpha2, as well as histamine H1. The clinical picture of acute RIS poisoning consists predominantly of central nervous system and cardiovascular effects and the most severe symptoms are: hypotension, dysrrhythmias, consciousness disturbances, seizures and respiratory failure. No specific antidote for RIS poisoning is known and the treatment is only symptomatic and supportive. Quantitative determination of RIS blood concentration seems to be helpful in confirmation and monitoring of acute poisoning, nevertheless further investigations are needed to evaluate the relation between drug concentration and clinical symptoms.

[Acute lethal poisoning with venlafaxine]. / Ostre, smiertelne zatrucie wenlafaksyna.

The case of acute venlafaxine poisoning with fatal outcome is shown. The 52-year-old woman with depression disorder ingested 56 pills of Symfaxin ER 150 venlafaxine as a suicidal attempt. Initially she was observed in the Neurology Department because of seizures, but after her husband found empty packages of medicine she was sent to the Toxicology Department being suspected of venlafaxine poisoning. The qualitative toxicological test confirmed the presence of venlafaxine in urine. In the course of poisoning rhabdomiolysis, hypotension and consecutive acute renal failure were observed. Finally, severe ventricular tachyarrhythmia occurred leading do cardiac arrest. Despite intensive symptomatic and supportive treatment the patient died.