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Ingestion of household products and plants are the leading cause for calls to the poison control centres as far as children are involved. Severe intoxication in children has become infrequent due to childproofed package and blister packs for drugs. Chemical accidents in adults give rise to hospital admission in only 5 %. Suicidal selfpoisonings are still a challenge for paramedics, emergency and hospital doctors. Natural toxins as amatoxins, cholchicine and snakebites can lead to severe intoxication. Sedatives, antidepressants and analgesics are the drugs which are often used for suicidal intent due to their availability. Quetiapine and paracetamol are the drugs which are ingested for attempted suicide/ suicide mostly. The treatment of poisoning centers on the severity which can be judged by the poison severity score, the Reed classification or the GCS.Most intoxicated patients can be treated symptomatically or by intensive care measurements. Antidotal treatment however is needed for some specific poisonings.Exact sample drawing is essential for diagnostic and forensic purposes. There is no evidence based proof for the effectiveness of primary detoxification from the gastrointestinal tract like forced emesis, gastric lavage or the use of cathartics. Early after the ingestion of a harmful substance the administration of activated charcoal seems advisable. Hemodialysis can remove water soluble substances with a small volume of distribution. Multiple charcoal administration may exhibit some influence on secondary detoxification. Provision of evidence of the efficacy for newer antidotes like hydroxocobalamin in smoke inhalation, fomepizol for toxic alcohols and silibinin for amanita poisoning are emerging. Two recently recommended therapeutic principles have still to demonstrate their ability: Firstly the treatment of patients with calcium receptor antagonistic and beta-receptor antagonistic agents poisoning by high dose of insulin plus glucose, secondly the treatment for severe intoxication with cardiotoxic and psychotropic drugs with a lipid emulsion (Lipid rescue).It is essential for all doctors to contact a poison control center whenever they are confronted with an intoxicated patient. There they can get advice about which dose is toxic and about the newest therapeutic procedure.

A patient with severe organophosphate intoxication received Neostigmine 1 mg IV during the intermediate syndrome. This dose resulted clinically and neurophysiologically in a marked deterioration of neuro-muscular transmission. This effect of neostigmine on the neuromuscular block during the intermediate syndrome (deterioration) differs from its effect on a similar pattern (improvement), which is seen in the delayed neuropathy following organophosphate exposure. The administration of therapeutic doses of cholinesterase inhibitors in patients with a reduced safety margin due to inhibition of endplate acetylcholinesterase may be dangerous.

The effect of organophosphate intoxication with diisopropylfluorophosphate (DFP), paraoxon and parathion on the activity of some ATPases of rat hearts was examined. Biochemical and histochemical methods were employed to determine the activities of the transport ATPase, of the myofibres and mitochondrial ATPases using different doses and antidote application. The organophosphates studied here had an inhibitory effect on the activities of enzymes. Biochemical measurements showed that the ATPase activities are dependent upon the duration of poisoning, the dose of poison and the applied organophosphates. DFP caused the highest restriction in activity of the examined ATPases. The Ca2+-stimulated ATPase was more sensitive than the Na+/K+-ATPase to the application of organophosphates. The antidote therapy determined the grade of influence on activity. Combined treatments of organophosphate poisoning with atropine and obidoxime chloride in the high doses of 7.5 mg/kg and 12.5 mg/kg body weight i.m. proved to be the most effective against the organophosphate intoxication. Antidote combination of small doses and also single application of atropine or obidoxime chloride might cause a stimulation of activity of the Na+/K+-ATPase and a significant decline of the Ca2+-ATPase.

The preparation of ditertiary aliphatic diamines 3 designed as drugs protecting CNS acetylcholinesterase against organophosphate inhibition, is described. Owing to the radicals at the basic nitrogen atoms, these compounds should exist in appreciable amounts both as base and as diammonium ion at biological pH's.

Repetitive stimulation of the median nerve elicited a so far unknown course of the muscle action potentials in four patients with organophosphate intoxications. The amplitude of the initial muscle action potential decreased with the second stimulus and gradually increased to normal values by subsequent stimuli. With the second stimulus a loss of the repetitive muscle action potentials occurred. The Decrement-increment phenomenon was seen in early and/or late stages of severe intoxications when fasciculations were prominent. We suppose that the repetitive muscle action potential following the first stimulus results from backfiring. The second orthodromic nerve action potential collides with this antidromic activity leading to a partial extinction. Loss of backfiring with the second stimulus abolishes the phenomenon of collision and enables a recovery of the muscle action potential amplitudes.

A case of lethal suicidal intoxication with demeton-S-methyl is reported. Capillary chromatography on wide-bore columns (CP-sil 5, 0.53 mm ID, 1 micron film thickness) was used for the quantitative determinations of this substance in the body fluids and tissues.

By means of cranial computer tomography, it is possible to demonstrate the cerebral consequences of severe intoxications in vivo. A variety of different toxic agents produce similar disease patterns, which are thought to be due to fall in blood pressure caused by the toxin. The lesions are mainly localised in the basal ganglia at the borders of contiguous vascular territories. Six patients observed by the authors are described.

For investigation of intoxications with organic phosphates contents of stomach and intestines are the best analytical material. Phosphates are destroyed by metabolism in liver, so liver tissue should not be used as proof for organic phosphates.

In order to improve or supplement the currently used therapy of poisoning with phosphoric acid esters, a protein free extract from calf blood containing low-molecular subtances (Actihaemyl, Solcseryl) has been tested in female Wistar rats. After poisoning with paraoxon, DFP and soman, a combination of Solcoseryl, Toxogonin and atropine sulfate prolonged the time until exitus, improved the overall rate of survival and considerably shortened the phase of regeneration of the experimental animals even when they had been intoxicated with high doses of poison.

In this case report, a congestive cardiomyopathy caused by long-term organic phosphoric acid ester exposure is described. The cardiotoxicity and the role of such poisons in the genesis of cardiomyopathy are also discussed.

In a case of severe poisoning with the organophosphorous insecticide methidathione standardized forced diuresis and peritoneal dialysis were performed for the first time in addition to the usual therapeutical procedures (e.g. repeated gastric lavage, induced diarrhea, atropine and intensive care). The course of the illness as well as the duration of the acute phase were significantly shorter than in comparable cases. No hazardous situation occurred after the first hours of treatment. The presence of the organophosphorous cholinesterase inhibitor or of its metabolites in the urine and the dialysate was proved by thin-layer chromatography.

A 26-years-old man injected himself intramuscularly with 3.75 gram of demeton methyl in an attempt to commit suicide. After 36 hours severe symptoms of poisoning developed with loss of consciousness and respiratory arrest. As symptomatic treatment failed to improve his condition has given injections of purified serum cholinesterase. This was followed by a rise in the cholin esterase levels and the increased activity was accompanied by a rapid and definite improvement in the clinical findings. The results clearly indicate the usefulness of this method of treatment. Transfusions of fresh blood to counteract the cholin esterase deficiency are inadvisable because of the risks of complications. Substitution therapy with serum cholinesterase must be accompanied by administration of large doses of atropine.

Neuromuscular transmission was studied in 11 patients with organophosphate intoxication. The compound muscle action potential (MAP) was recorded from the thumb after single, repetitive (1-50 Hz) and paired stimulation. All patients showed a prolonged MAP. The duration increased with the severity of intoxication. The number of peaks varied only slightly. In all cases repetitive stimulation reduced the later components of the MAP. There was no correlation with tetanic fade of the initial negative component. One patient had a pronounced tetanic fade but a slight reduction of repetitive components. In view of experimental studies a combined pre- and postsynaptic effect seems to be responsible.