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Transient and permanent myocardial damage is a vital element of toxicological practice. This applies both to poisonings in which heart injury is typical and to those in which it is only a rare complication. Vital signs of poisoned patients, especially unconscious ones, must be carefully monitored, because the consequences of late diagnosis or improper treatment can be potentially fatal. The following paper discusses the mechanisms leading to heart damage in the course of acute poisoning. It also presents clinical symptoms, treatment options and prognosis for myocardial injury in selected poisonings.

The heart muscle is particularly sensitive to the toxic effects of carbon monoxide. Cardiovascular complications are present in 30-40% poisoned patients. Currently, multiple ECG records and at least two-time determination of cardiac markers' concentration (mainly troponin I) are known as the gold standard practice in the diagnosis of cardiac injury especially with regard to medium and severe poisoning. So far there have not been any recommendations for further diagnostic steps in case of abnormalities in these examinations. This paper presents a review of cardiac imaging techniques as well as the analysis of their usefulness in carbon monoxide poisoning. According to the authors echocardiography is considered to be an extremely important examination which, thanks to its accessibility and non-invasive nature, should be performed on all patients with myocardium injury suspicion made on the basis of clinical image, ECG records and biochemical markers.

Gammabutyrolactone is included in the solvent such as wheel cleaners, pesticides, cosmetics, drugs. After ingestion GBL is converted to gamma-hydroxybutyrate. Both substances are classified as so called "club drugs" and their action is characterized by euphoria, sedation, and induction of retrograde amnesia of events. These activities were basis for the use of GHB and its lactone as rape pill. Acute poisoning with these compounds causes confusion, agitation, ataxia, nausea, vomiting, nystagmus, dyskinesia, hallucinations, coma, irregular breathing, hypothermia, bradycardia, hypotension, convulsions, respiratory paralysis and thus respiratory arrest. These substances carry a risk of development of physical addiction of the hard proceeding of abstinence syndrome. In the USA there is a ban on the sale and promotion of these compounds. In Poland despite the fact that GHB is a controlled substance, there is no regulation of GBL trading. The aim of this paper is to summarize current knowledge regarding the pharmacology, impact on the human body, toxicity, and the effects of chronic abuse of these substances.

Pulmonary edema is a severe, potentially fatal clinical condition. It happens, when interstitial fluid is accumulating in the alveoli, impeding proper gas exchange. Typically we distinguish cardiogenic and noncardiogenic pulmonary edema. The article describes the case of severe pulmonary edema, which occurred in a young woman, free of cardiac diseases, about 30 hours after a suicidal drug poisoning (clozapine, ketoprofen, thiethylperazine). Both clozapine and ketoprofen intoxication, may be severe. Complications in these poisonings affect not only the central nervous system, but also the circulatory or respiratory system and may even occur several hours after the overdose of these drugs. The study considered the causes and possible mechanisms of pulmonary edema in poisoning with these drugs.

Rhabdomyolysis and associated kidney failure is a medical problem, often faced by doctors working in the centers of toxicology. Its most common cause is mechanical damage to the muscles, but predisposing factors include a big group of other pathologies and clinical conditions, including: electrolyte imbalance, immobility, infections, drug or psychoactive substances poisoning. The article presents an example of a patient with severe rhabdomyolysis syndrome caused by an alcohol withdrawal syndrome. Based on our experience and scientific studies of other clinical centres the paper presents various causes of muscle damage, including the iatrogenic effects of ethanol intoxication treatment. The article explains the importance of a proper and quick treatment which prevents damage of internal organs, including kidney failure.

Doxepin is a tricyclic antidepressant from the group of dibenzoxepines. Apart from the antidepressant effect, it has also the sedative and anxiolytic effect, so it is used in the treatment of anxiety disorder in the course of psychosis, organic diseases and alcoholism. Doxepin increases concentration of norepinephrine and serotonin in the brain by preventing inactivation and blocking their reuptake. In addition, the drug has an antagonistic effect on receptors in CNS (muscarinic M1, histamine H1, alpha-1adrenergic, serotonergic 5-HT2) and also blocks sodium and potassium channels in cardiomyocytes. In this paper we present a case of severe poisoning by various drugs, including doxepin. The dominating symptom was prolonged toxic coma. Slow return of consciousness was observed from the fifth day after intoxication, logical verbal contact with the patient was possible on the seventh day. It seems that this symptom results from the pharmacokinetic properties of doxepin as well as the high drug dose and a synergistic effect of lorazepam and phenobarbital. Transient anisokoria was an unusual symptom that appeared in the course of intoxication. The patient was examined by a neurologist and underwent CT of the head twice - no organic causes were revealed. This phenomenon can be explained by physiological anisokoria, caused by asymmetry in the sympathetic innervation of pupil rectractor muscle, exacerbated by a complete parasympathetic conduction block as a result of anticholinergic action of doxepin. Tricyclic antidepressants are often used by patients for the purpose of suicide. Because of the serious cardiological and neurological symptoms the course of doxepin intoxication may be severe.

Silibinin is the most active component of a complex of flavonoids -silymarin contained in fruit milk thistle (Sylibum marianum). Its mechanism of action is complex and highly beneficial in protecting hepatocytes. On the one hand this compound blocks the penetration of various toxins (for example amanitin) into the hepatocytes not allowing in this way for the cell death and on the other hand, it prevents apoptosis through intracellular. It protects the liver from oxidative intracellular free radicals by increasing the activity of enzyme superoxide dismutase and peroxidase, as well as by increasing the concentration of glutathione and the activity of the peroxidase. Silibinin strengthens and stabilizes the cell membranes, inhibits the synthesis of prostaglandins associated with the lipid peroxidation and promotes regeneration of liver through the stimulation of protein synthesis and effect on the production of new hepatocytes. A particularly interesting topic from the perspective of a toxicologist is the application of silibinin in Amanita phalloides poisoning. Clinical trials conducted in this respect are very encouraging. The other beneficial application of silibinin is in therapy of the alcoholic liver cirrhosis. The evidence shows that the use of silymarin leads to a significant reduction in liver-related mortality and even reduction in the number of patients with encephalopathy in the course of the disease. Application of silibinin goes beyond liver disease and expands in the direction of cancer and even diabetes. What is interesting is the fact, that the substance of herbal origin occurring in the environment is so strong, favorable, beneficial and multidirectional. Science has contributed to improving the bioavailability of silibinin thus making it more effective.

Sodium azide poisonings are a rare reason for hospitalization in toxicological units. They are observed as rarely as once within a number of years per hospital. Consequently, an algorithm for the optimum procedure of treating such intoxications does not exist and, as a result, there is a need to describe every single clinical case. A female, aged 55, was directed to the toxicological unit from a county hospital after swallowing four tablets of sodium azide, 150 mg each, in the form of preservative for fresh milk samples. Two hours after the incident a gastric lavage was performed and the tableting blend was retrieved. In the clinical examination higher concentration of lactic acid, ALAT and TSH were observed. In the ECG record unspecific aberrations in the ST segment were noticed. Due to the patient's general good condition and the fact that the tableting blend had been retrieved from the gastric rinse, further use of the antidote indicated in the therapy of cyanide intoxications was abandoned. Symptomatic treatment was used along with the patient's eight-day observation. In the described case the early decontamination prevented the development of acute poisoning.

This paper describes a case of now 49-year-old patient with alcohol dependence syndrome, hospitalized three times in the Center of Clinical Toxicology in 2009-2012 due to ethylene glycol poisoning. Twice, the course of poisoning was defined as severe. It was complicated by respiratory failure, severe metabolic acidosis, renal failure, disorders of the central nervous system; once referred to it as a medium, complicated by renal failure. He was treated with ethyl alcohol as an inhibitor of alcohol dehydrogenase, hemodialysess and intensive symptomatic and supportive therapy. This paper shows the great effectiveness of early hemodialysis and intensive therapy even in case of multiple and severe intoxication with toxic alcohols.

Tako-tsubo cardiomyopathy is a clinical syndrome induced by a strong mental or physical stress, characterized by a transient hypokinesia, akinesia or dyskinesia middle segments of the left ventricle and apical, with associated electrocardiographic changes of ST-T segment like in acute coronary syndrome, with no significant changes in coronary arteries in coronary angiography. Tako-tsubo cardiomyopathy is mainly found in women in the sixth and seventh decade of life and represents 1-2% of cases originally diagnosed as acute coronary syndrome. We present a case of tako-tsubo syndrome in the course of carbon monoxide poisoning in a 56-year-old patient, with a positive history of ischemic heart disease and hypertension. Moreover, the reasons for its occurrence were considered based on clinical course, laboratory tests and imaging, and available literature.

Carbon monoxide still remains one of the most common causes of fatal poisonings. Mechanisms of carbon monoxide toxic effects are complex and lead to hypoxia of body tissues. The most sensitive to tissue hypoxia are: the central nervous system and the cardiovascular system.The most characteristic cardiac symptoms of carbon monoxide poisoning are: stenocardial symptoms, hypotonia, myocardial dysfunction and arrhythmia (atrial fibrillation, tachycardia, bradycardia). Carbon monoxide connects with high affinity to metallo-proteins mainly to hemoglobin impairing oxygen transport in the body and to myoglobin, interfering with its function as oxygen reservoir among others in myocardium. Connecting to cytochrome oxidase in mitochondria it blocks the chain of electron transport which results in impairment of cellural respiration and formation of free radicals. Carbon monoxide has also relaxation effect against the smooth muscles of blood vessels, and thrombogenic effect. It is particularly adverse in patients with ischemic heart disease. In case of carbon monoxide poisoning one should always search for features of myocardial injury- as far as screening is concerned the most important ones are ECG and screening for cardiac troponin. Depending on the course of poisoning other laboratory (e.g. BNP) or imaging (echo-cardiography. scintiscanning, coronarography) tests may also prove to be useful.

Unlabelled: Serotonin syndrome is caused by excess serotonin in the central nervous system. It usually occurs as adverse drug-therapy (neuroleptic agents, monoamine oxidase inhibitors, serotonin reuptake inhibitors and others)., Case Presentation: a 50-year-old woman with a history of depression, was admitted to our hospital, due to suicidal drug poisoning (moclobemide- 4500 mg, venlafaxine 1050 mg, mianserin 300 mg and cytisine 30mg). She was also drunk. The patient was unconscious and sweaty, on the ECG tachycardia (120/min) was observed. In addition, several hours after admission, the patient developed acute respiratory failure, we observed myoclonus, lockjaw, body temperature increased to 37.3 degrees Celsius, and blood pressure was 170/80 mmHg. During the neurological examination there was a tendency to bilaterall Babinski sign and the nystagmus was present. The patient was intubated, and we started an intravenous infusion of Relanium. In laboratory studies: ethanol: 2.52 g/l, tests for benzodiazepines and tricyclic antidepressants were negative, WBC 13.1 tys/microl, CPK was elevated to 372 U/L, other parameters (electrolytes, transaminases, serum total protein, glucose, CRP, creatinine) were normal. The patient required intensive care and treatment during the next two days. The diagnosis of serotonin syndrome was based on the Hunter's criteria, which are more sensitive and more specific than Sternbach's criteria. The patient was discharged from hospital in good condition.

The carbon monoxide poisoning still remains a main cause of fatal poisoning. The carbon monoxide poisoning occurs after inhalation of carbon monoxide. Carbon monoxide binds strongly to molecules, such as cytochrome oxidase, myoglobin, hemoglobin, causing hypoxia of tissues and organs. Carbon monoxide converts hemoglobin to carboxyhemoglobin and makes transport of oxygen through the body impossible and causes severe hypoxia. The only treatment is administering 100% oxygen or providing hyperbaric oxygen therapy. The central nervous system and heart are the most sensitive to hypoxia. We present the cases of two young people with no history of chronic diseases (a 24-year-old man and a 39-year-old woman) who were diagnosed NSTEMI in the course of severe carbon monoxide poisoning. Both poisoning cases were severe, both patients were unconscious when they were admitted to our hospital. We observed elevation of serum troponin level and changes in ECG (e.g. atrial fibrillation) significant for myocardial infarction.

The paper presents the case of a female, 36, hospitalised in the Lublin Regional Center of Clinical Toxicology, diagnosed with heavy ethylene glycol intoxication. The patient suffered from metabolic acidosis with pH at 6.6, bases shortage - 35,5 mmol/l, renal failure, acute respiratory failure, symptoms of CNS damage such as prolonged coma, followed by dysphasia and the lower limbs paresis persisting for a few weeks. During the treatment, ethanol was used as a competitive inhibitor of alcoholic dehydrogenase along with hemodialyses, intensive symptomatic treatment, care and rehabilitation. In spite of the severe course of the intoxication, the procedures employed with the patient resulted turned out to be effective, with total renal failure regression, lower limb paresis regression, speech function regain and regular motor apparatus function regain and the regaining of speech and regular motor apparatus functions. The case description proves that intensive therapy might lead to recovery even in cases of extreme metabolic acidosis.

The aim of this paper is to present a case of a 61-year-old male transferred to the Regional Center of Clinical Toxicology from the Department of Endocrinology with suspected methanol poisoning. The patient presented symptoms of diabetes with extreme hyperglycemia >1600 mg/dl and nonketotic hyperosmolar coma. Laboratory tests showed metabolic/respiratory acidosis, methanol 80 mg/dl, ethanol 0.47 g/l, creatinine 3.5 mg/dl, urea 140 mg/dl, lactic acid 4.11 mmol/l, myoglobin >1000 ng/ml, HbA1C >14.5%. During a few days prior to the hospitalization the patient was drinking a great amount of fruit juices and milk (a dozen or so litres per twenty four hours). The eventuality of metabolizing glucose and aspartame into methanol is known from professional literature. The possibility of excessive consumption of aspartame and its metabolites causing methanol poisoning in the presented patient was considered.

26 of serious inedible alcohol (ethylene glycol and methanol) intoxications have been observed in Lublin Regional Center of Clinical Toxicology during 2010/2011 (18 mounths). As a result of such intoxications, metabolic acidosis and acute renal failure and other organs injury develop. The writings inform that it is possible to survive a pH spectrum between 6.8 and 7.8, whereas beyond these values protein denaturation and death proceed. The paper presents two cases of intoxication with ethylene glycol and ethylene glycol, methanol together where the lowest pH values in capillary blood were recorded below 6.8. The first case is of a male, 45, who was diagnosed glycol concentration at 283.3 mg/dl, with the lowest pH value obtained in the gasometric examination of capillary blood at 6.712. The other case is of another male, 54, who had probably drunk condenser liquid. Ethylene glycol and methanol's concentration were 535 mg/dl and 37.5 mg/dl correspondingly, whereas the lowest capillary blood pH value was recorded at 6.745. Both men had been addicted to alcohol for many years. The treatment demanded multiple hemodialyses, respiratory therapy, catecholamine intravenous injections as well as intensive pharmacological treatment resulting from multi-organ complications. The intoxication in either case was non-lethal.