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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 concentration–time 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.

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.

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.

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.

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.

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.

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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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).

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.

Based on the hypothesis, that extracorporeal removal of endo- and egzogenic substances should be beneficial to the clinical course of the patient in liver failure or poisoned, treatment systems were evaluatedbased on the two concepts: (1) blood dialysis against albumin dialysate--Molecular Adsorbent Recirculating System (MARS), Single Pass Albumin Dialysis (SPAD), Continuous Veno-Venous Haemodiafiltration (CWHDF); (2) selective albumin filtration and adsorption combined with haemodialysis--Fractioned Plasma Separation and Adsorption-Prometheus. We present our own experiences with MARS and Prometheus procedures between 2003-2006 years.

Hymenoptera are the large group of insects which includes honey-bees, bumble-bees, paper wasps, hornets, ants. Female hymenoptera possess specialized stinging apparatus with which they inject their venom into prey's or intruder's body. It could be life-threatening for people sensitive to the venom. The hymenoptera venom consists of mixture of biologically active substances, eg. enzymes (phospholipases, hialuronidase), peptides (melittin, apamin, mastoparans, bombolitins) and low-molecular-weight compounds (biogenic amines, acetylcholine, carbohydrates, lipids, free amino acids). Several types of reactions are possible to develop after stinging by hymenopteran insects: (1) non-allergic local reaction (pain, small oedema, redness at the site of the sting); allergic reactions: (2) large local reaction (extensive local swelling, exceeding 10 cm, persisting longer than 24 hours) and (3) anaphylaxis (generalized urticaria, bronchospasm, hypotension, cardiovascular collapse, loss of consciousness); (4) systemic toxic reaction (oedema, vomits, diarrhoea, headache, hypotension, seizures, altered mental status); (5) unusual reactions (cardiac ischaemia, encephalomyelitis et al.). Therapeutic management after stings includes removing of the stinger (bee stings), local remedies (ice-packs, topical steroids) and prevention and treatment of an anaphylactic shock (epinephrine, general steroids, beta-mimetics, fluid resuscitation, oxygen therapy). In the present review types of reaction after hymenoptera stings were described with special interest of anaphylactic and toxic reactions as well as therapeutic management after stings.

Background: Carbamazepine (CBZ) is an antiepileptic drug with tricyclic structure which implies its potential cardinotxic properties, especially in acute poisoning., Aim: To evaluate some cardiovascular effects connected with CBZtoxicity and tofind the relation between them and CBZ plasma level., Material and Methods: 34 patients (18 males, 16 females; median age 24.5) hospitalized in our Department in 1996-1997 and 2005-2006 due to acute CBZ poisoning. Analysis included following parameters: systolic (SBP) and diastolic (DBP) blood pressure, ECG parameters: heart rate (HR), duration of QRS complex, PQ interval and corrected QT interval (QTc) calculated with Bazett's (QTc(B)) and Hodges's (QTc(H)) formulas. These parameters were compared with reference values for general population available in the literature. Relations between above mentioned parameters and CBZ plasma level were studied by means of Generalized Additive Model (GAM)., Results: The reference values were exceeded most often for QRS (62%), DBP and QTc(B) (53%, both) and SBP (50%). The mean number of parameters with exceeded norms was 3.1 per patient (SD = 1.71). We failed to find any significant correlation between CBZ plasma level and any of the studied parameters. Positive correlation between SBP and DBP (r = 0.68; p < 0.001) and negative correlation between QRS and HR (r = -0.50; p = 0.003) were found., Conclusion: CBZ could affect different cardiovascular parameters which should be monitored in cases of acute drug poisonings.

Hallucinogenic mushrooms, also called "magic mushrooms", are becoming a more frequent cause of abuse, especially among young people, who use them experimentally for recreational purposes. In the autumn of 2004, several people were admitted to and observed in the Department of Clinical Toxicology in Krakòw after they had used magic mushrooms to experience hallucinatory sensations. Three of them had visual hallucinations, and the fourth experienced both visual and auditory hallucinations followed by the exogenous psychosis after use of Psilocybe semilanceata. One person was hospitalised for several days while the others were observed in the emergency department. The main source of information for patients about hallucinogenic mushrooms was the internet. In the cases discussed the mushroom poisoning caused no organ damage and the symptoms disappeared in about 6 hours.

Chloroquine is a derivative of 4-aminoquinoline, which is used in the malaria prophylaxis and treatment and the therapy of some connective tissue diseases. Its narrow therapeutic index causes that the medicine is relatively toxic, especially in the case of an overdose or an acute intoxication. In the recent study two cases of the acute chloroquine poisoning, hospitalized in the Toxicology Department in Kraków, were described and one of them was fatal. The first case was 16-year-old girl who ingested 5 g of chloroquine phosphate in the suicidal attempt. After about 2 hours general seizures appeared followed by ventricular fibrillation and cardiac arrest. After near 2-hour-lasted reanimation procedures she was resuscitated, but 14 hours later another cardiac arrest appeared because of the bradyasystole. Despite the institution of advanced reanimation methods including external pacemaker and electrostimulation, spontaneous circulation did not return and the patient was declared dead. Postmortem toxicological examination of blood, vitreous humour, bile and liver revealed extremely high concentrations of chloroquine (252.15 mg/l in blood). The second case was the 15-year-old girl who ingested 7.5 g of chloroquine phosphate. She developed significant hypotension requiring intravenous infusions of fluids and catecholamines and respiratory distress positively treated with endotracheal intubation and mechanical ventilation. In both cases a considerable hypokalemia and prolonged QTc interval were observed. According to the literature, a clinical picture, diagnosis and recommended therapy of an acute chloroquine poisoning were reviewed.

The aim of this study was to determine relations between the clinical state and the severity of liver damage comparing to the amount of ingested paracetamol, time since ingestion and serum concentration of paracetamol with patients after acute intoxication with this drug. A retrospective analysis of medical records of 95 patients hospitalized in the Toxicology Department in Kraków or treated in the Toxicological Admission Room in 2002-2004 years because of acute paracetamol intoxication was performed. The general clinical state connected with intoxication and the severity of liver damage were determined using the Poisoning Severity Score (PSS). The level of consciousness was determined with the Glasgow Coma Scale and Matthew's scale. The serum concentration of paracetamol during admission to the hospital, levels of biochemical markers of liver damage (AST, ALT), bilirubin and INR index were also performed. We found a statistically significant positive correlation between the ingested dose of paracetamol comparing to the gravity of poisoning, the severity of liver damage, levels of aminotransferases and bilirubin. A positive correlation between time since ingestion of paracetamol to hospitalization and the gravity of poisoning according to PSS scale was also statistically significant. A paracetamol concentration measured during admission to the hospital had no influence on neither the clinical state of patient nor the severity of liver damage. We conclude that the therapeutical approach should consider possibly shortening of the time since drug ingestion to hospitalization and institution of specific treatment (N-acetylcysteine) as well as minimalization of the paracetamol dose, which could be absorbed, by different methods of elimination from the GI tract (eg., gastric lavage, activated charcoal laxatives).

Unlabelled: Amanita phalloides is a direct life-threatening poisoning because of acute multiorgan failure. Urgent liver transplantation (LTx) is the last chance to save patient's life in severe cases. In many cases of mushroom poisoning the patient dies because of unavailability of a liver graft. Liver albumin dialysis (MARS) is a promising treatment to bridge the patient to LTx or stabilize his or her condition until spontaneous liver regeneration occurs., Case Report: Four family members (father, mother and two sons) were eating self-collected mushrooms (Russula vesca). Typically for the Amanita phalloides poisoning, the first symptoms appeared in all persons more than 12 hours after mushroom ingestion. Because they did not improve, the whole family was admitted to the Regional Hospital in Ketrzyn (24 hours after mushroom ingestion). Mycological examination of gastric washings was positive only in the mother, in whom the Amanita phalloides spores were found. During the first 48 hours of poisoning the biochemical indexes of liver injury were observed in all persons. The whole family members were sent to centers where liver albumin dialysis could be performed: the mother was admitted to the Department of Nephrology and Dialysis Therapy in Olsztyn, the father and the first son were admitted to the Clinical Toxicology Department in Krak6w, and the second son was admitted to the Department of Internal Medicine and Acute Poisonings in Gdańsk. Three albumin dialysis procedures were performed in the case of mother with complete liver recovery. After the first liver albumin dialysis, the father of the family was disqualified from the following procedures because of severe coagulation disturbances (GI bleeding), and died the fourth day after mushroom ingestion. The first son fulfilled the King's College criteria and was accepted for high urgency liver transplantation. After two albumin dialysis procedures had been able and the patient was urgently sent to the Department of General and Transplantation Surgery in Szczecin, where liver transplantation was successfully performed. The second son was treated conservatively with improvement of general condition and biochemical indexes and no albumin dialysis procedure was necessary., Conclusion: Liver albumin dialysis may be effective in severe Amanita phalloides poisoning to stabilize the condition of a patient until spontaneous liver regeneration occurs or as a bridge to LTx. In cases of a family poisoning, proper coordination and cooperation among toxicology departments and transplant centers is required.

Body-packing is the way of psychoactive substances smuggling by swallowing of carefully prepared packages with drugs into the gastrointestinal tract or by insertion them into the vagina or the rectum, especially in order to avoid finding them by the custom service. Cocaine, as well as opiates, is the one of the most often smuggled drugs by so called body-packers. In the present study the first case of the body-packer from Malopolska region in Poland, who was observed in the Toxicology Department of the Collegium Medicum UJ, was described. The 29-year-old man swallowed 60 packages containing cocaine with a total net weight of about 500 grams. The plain abdominal radiography revealed multiple shadows of foreign bodies in the gastrointestinal tract, but the results of blood and urine cocaine measurements were negative. During the 37-hours stay in our department the patient was monitored (blood pressure, heart rate, temperature), laxatives and oral fluids were administered. All the packages were evacuated through the natural way and it was followed up by the control abdominal radiography. No symptoms of acute cocaine intoxication or any other complications were observed. According to the case there is also the thorough review of literature presented including the kinds of body-packing, the diagnostic methods used in recognizing of body-packers and the ways of their treatment taking into consideration the conservative management as well as surgical methods.

Malayan cobra (Naja naja sputatrix) is the venomous snake of the Elapidae family which involves at least three species of Asian spitting cobras, according to the new taxonomy. This snake occurs naturally in southeastern Asia and in Poland it is kept only in the private breedings. Its venom mainly contains neurotoxins which have paralyzing activities to the nervous system and cardiotoxins which act cytolytically. The present study shows a case of the forty-one-year-old man professionally engaging in venomous reptiles who was bitten in his left ring finger by the Malayan cobra. No general symptoms, especially neurotoxic, were observed in the patient after the snake bite, but there was a significant local tissue injury including necrosis. In the bite site the infection with Morganella morganii developed with consequent phlegmon within the hand and the forearm. Additionally, features of haemolysis and injury of muscles with elevated level of serum creatine phosphokinase (CPK) were present. The local injuries of tissues were treated surgically including the amputation of the bitten finger which has undergone the necrosis. No specific antivenom was used in the treatment.

The aim of the study was to present the group carbon monoxide poisoning in Kraków in December 2003. Despite the reanimation procedure one fatal case was stated on the spot (HbCO--60% according to post-mortem toxicological examination). CO threshold limit values were significantly exceeded in the whole building. The inhabitants (15 persons) were transported to the Department of Clinical Toxicology Jagiellonian University Medical College. Also 4 staff members of the ambulance and 2 policemen called to the incident, were diagnosed and observed. Totally, toxicology medical care was given to 21 CO exposed persons. In 8 of them acute CO poisoning of minor grade was stated. Any clinical symptoms of poisoning in the rest of CO exposed persons were noted.

The only venomous reptile that naturally occurs in Poland is the adder or common viper (Vipera berus). Its bites are not of great epidemiological importance, but in some cases serious life-threatening symptoms may appear. The most common symptoms of adder envenomation are: local edema, reddening and pain of the bitten site and also the general symptoms coming from the alimentary tract (vomiting, diarrhoea, abdominal pain), the circulatory system (hypotension, shock, ECG abnormalities), the central nervous system (sleepiness, vertigo, disorientation, loss of consciousness), hematological symptoms (leukocytosis, hemolysis, coagulopathy) and allergic symptoms (fever, urticaria, angio-oedema). In the present study we described the case of a twenty-year-old patient hospitalized at the Toxicology Department of the Collegium Medicum UJ after a viper bite. Except for some above-mentioned symptoms he also developed ocular symptoms like ptosis and blurred vision. Such symptoms after the common viper bite have not been described in the literature till now. The cause of them seems to be an intense allergic reaction in the region of the orbit and eyelids all the more so because the patient had the positive allergy history. However, taking into account the latest reports from the literature, a neurotoxic action of some components of the Vipera berus venom may also play a role. Because of the developing general symptoms a specific equine antivenom was administered to the patient, apart from the supportive care, without any serious side effects that usually are observed after the use of such a kind of sera. It is thought that the sheep antivenom is better than the equine one considering a lack of allergic side effects. As a result of applied treatment the local and general symptoms including ocular symptoms subsided.