[Poisoning by hypochlorite-containing disinfectants. A retrospective analysis of 594 cases of poisoning]. / Vergiftungen durch hypochlorithaltige Sanitärreiniger. Eine retrospektive Analyse von 594 Vergiftungsfällen.

Hypochlorite-containing disinfectants or bleaching fluids, if inhaled, may lead to life-threatening poisoning (56% of moderately severe cases, 5% of severe cases) through the immediate liberation of chlorine gas, if they are used together with another cleansing fluid which is very acid. A rough estimate suggests that there must be about 700 cases of such poisonings per year in the Federal Republic of Germany. The characteristic symptom is a respiratory distress syndrome when the liberated chlorine gas is inhaled. Toxic pulmonary oedema and cardiovascular failure can occur if the poisoning takes a fulminating course.

Methyltin intoxication in six men; toxicologic and clinical aspects.

Neurologic and psychiatric symptoms such as headache, tinnitus, defective hearing, changing desorientation and aggressiveness are initial symptoms of methyltin chloride intoxication. Some patients also developed epileptic equivalents, such as dreamy attacks and central ventilation transaminases. Laboratory findings included low levels of serum potassium, leucocytosis and elevated transaminases. The excretion rate of tin in the urine correlated with the severity of the intoxication. There was no measurable effect of plasma separation or d-penicillamine therapy on tin excretion in the urine or on the clinical picture. The long-term prognosis of severely intoxicated persons is poor. Neurohistopathologic findings confirm the animal studies by Brown et al and the severe damage and cell necrosis in the hippocampus area. To prevent such events workers need to be warned of the risk and dangers of working with organo-metallic compounds. The effectiveness of protective clothes and gas masks should be checked. In exposed workers regular testing is advised of tin concentrations in the urine.

Effect of disulfiram on N-nitroso-N-methylbenzylamine metabolism. Biochemical aspects.

The present biochemical experiments show that disulfiram inhibits N-nitroso-N-methylbenzylamine metabolism in the rat. More N-nitroso-N-methylbenzylamine may therefore reach extrahepatic tissues. The pathological lesions observed in the lungs in the present system can be explained by the finding that alkylation of lung DNA is increased and repair processes are impaired by enhanced cell proliferation in this organ.

[Poisoning with leather-impregnation sprays. A retrospective analysis of 224 cases of poisoning]. / Vergiftungen durch Leder-Imprägniersprays. Eine retrospektive Analyseüber 224 Vergiftungsfälle.

Annually, there are about 100-200 intoxications in the Federal Republic of Germany caused by inhalation of leather impregnation sprays. The course of these intoxications is moderately severe in 60% and severe in 18% of the cases. The signs and symptoms are characterized by a respiratory distress syndrome which sets in about 15-60 min after spraying and which requires several days of hospitalisation in severe cases. The sprays contain about 7-11 components; their toxicity is not exclusively associated with one substance only. Lower toxicity can be achieved by preparing a basic formulation adjusted to the low-hazard components.

Acute toxicity of pyrazolones.

Pyrazolone intoxication accounts for most (52 percent) mild analgesic poisonings in West Germany. Severe and fatal intoxication with pyrazolones is, however, rare. In the German literature, only 50 cases have been described in the past 62 years; 80 to 90 percent of these were caused by aminopyrine, which was withdrawn from the West German market in 1978 and replaced by propyphenazone. Up to now, no fatal poisoning with propyphenazone has been reported. However, the signs and symptoms of severe intoxication are similar for both propyphenazone and aminopyrine. The acute toxicity of dipyrone is slightly lower than that of propyphenazone, whereas phenylbutazone and oxyphenbutazone clearly cause less severe reactions. Characteristic symptoms include impaired consciousness progressing to coma, and convulsions. In addition, arrhythmia and cardiogenic shock may occur. Severe aminopyrine intoxication may also be complicated by sudden apnea. Liver damage may develop after a latent period of about 24 hours, especially after phenylbutazone and oxyphenbutazone poisoning. Therapy involves supportive measures as well as gastric emptying by emesis or lavage, installation of medical charcoal, and induction of diarrhea or gut lavage. Although exact clinicotoxicologic data on hemoperfusion are not available as yet, distribution volumes, plasma half-lives, and endogenous plasma clearances as well as results of in vitro trials all suggest the efficacy of this procedure. Hemoperfusion with uncoated amberlite XAD-4 resin is, therefore, recommended for patients with severe pyrazolone intoxication.

Successful treatment of paraquat poisoning: activated charcoal per os and "continuous hemoperfusion".

Ingestion of paraquat results in an extremely dangerous poisoning. The first aim is to clear the gastrointestinal tract by inducing emesis and performing gastric/gut lavage; as much activated charcoal as possible should be administered per os and as quickly as possible. The best measure to eliminate paraquat from blood and tissue is hemoperfusion with coated activated charcoal; it has to be performed in the sense of "continuous hemoperfusion" about 8 h/d over a period of 2-3 weeks. These measures give a chance to lower the lethality of paraquat poisoning.