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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

Unlabelled: Paracetamol is a widely known over-the-counter analgesic and antipyretic which, in acute poisoning usually causes liver damage, and less commonly damage to the kidney, heart, and pancreas. In the present paper we report a case of acute suicidal paracetamol intoxication complicated by acute hepatic and renal failure. The discussion covers the pathogenesis, clinical course, and treatment of acute renal failure in the course of paracetamol poisoning., Case Report: A thirty-four-year-old woman was admitted to hospital in the second day after ingestion of nearly 17 g of acetaminophen. During admission to the hospital, the maximum values of transaminases (AST 19 350 U/L, ALT 11 760 U/L) were found; they have gradually normalized over the next few weeks. Sequentially monitored serum creatinine showed an upward trend, reaching a value of 588 micromol/L in the fifth day after drug ingestion. The patient underwent 1 haemodiafiltration and 4 haemodialysis treatments resulting in an improvement in renal function., Conclusions: In acute acetaminophen poisoning, in addition to standard monitoring of liver function, the monitoring of kidney function is necessary because of the risk of acute renal failure due to acute tubular necrosis. Kidney damage is likely to be transient and generally will not need long-term renal replacement therapy.

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.

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.