Biomedical subjects
Publications and source records attributed to A Buchter.
Whether chronic intoxication with arsenic can induce cancer of the urinary tract is an important question in urology and occupational medicine. Here, we consider potential exposure, and discuss the epidemiology and toxicology of arsenic. In addition, we conceptualize a possible strategy for clinical procedures.
CASE REPORT: A 34-year-old white male was executing blasting works in an operation of a quarry several times a month during a period of 1 year. Each time he worked with explosives, he complained of headache, vertigo and concentration failure which started shortly after beginning and continued several hours after. The results of the physical examination on a day without blasting works were normal. Because of the exact working parallel appearance of the symptoms we did further explorations at the workplace which showed the usage of nitroglycerin blasting agents without observance of the safety regulations. The symptoms only at blasting workdays with normal clinical findings at break led considering the relation with the occupational conditions to the diagnosis "headache due to exposure to nitroglycerin explosives". It was reported to the employer's liability insurance association as an occupational disease with the aim of improving occupational conditions. CONCLUSION: Occupational toxic agents as a potential trigger of unclear headache support the requirement of an exact anamnesis of working conditions and environment.
HISTORY AND CLINICAL FINDINGS: Two men and one woman developed typical symptoms of a thrombosis in the arms after unusual physical effort at their work place (a coal miner after a bad fall, a radiographer after having to catch a patient, a painter after jerkily moving a heavy piece of furniture). INVESTIGATIONS AND DIAGNOSIS: In all three patients a thrombosis of the subclavian vein was demonstrated by duplex scans or phlebography. In two patients tests for hypercoagulability were unremarkable. None of the patients had a thoracic outlet syndrome. TREATMENT AND COURSE: After initial local thrombolytic or heparin therapy alone, phenprocoumon treatment over several months was given in two cases, and in one case low-molecular-weight heparin was administered over several months. All three patients complained of strain-related residual symptoms in the affected arm (pain, swelling, easy fatigability). In all three cases, the accident insurer recognized the incident to be a work-related accident. CONCLUSION: Patients with a Paget-Schroetter syndrome resulting from a sudden and unusual physical effort at work, which is covered by statutory accident insurance, must be reported to the accident insurer as a work-related accident in order to safeguard individual medical claims of the patient and for general medical and epidemiological reasons.
The authors report 7 patients with thromboses in the upper extremity resembling Paget-Schroetter syndrome. According to their case histories, all patients had a temporal and causal relationship between partially unusual sports activities and the genesis of the thrombosis. The cause of this condition is a strain on the subclavian and axillary veins by retroversion or hyperabduction of the arm. This can entail microtraumatizations of the venous intima, consequently leading to a consecutive local activation of coagulation and to a possible thrombosis of the vessel. A mechanical compression of the vein by adjoining bone, ligament, and muscle structures can intensify the effects. Further primary diseases and risk factors as secondary causes for thromboses where taken into consideration when examining the patients. The Paget-Schroetter syndrome should be considered as a possible cause for unspecified trouble in the upper extremity reported by athletes. If such prolapses occur, they can be categorized as accidents by private and statutory insurance companies that cover accidents.
INTRODUCTION: Primary thrombosis of the upper extremity (Paget-Schroetter syndrome, effort thrombosis) is usually not accepted either as a work-related accident or an occupational disease by the industrial injuries insurance authorities. This study aims to look at the circumstances under which this kind of thrombosis may be recognised as an occupational hazard. MATERIALS AND METHODS: After thoroughly studying the clinical records of 82 patients with thrombosis of the upper extremity in the outpatient department for angiology during a 10-year period, we found that in 51 cases the thrombosis was caused by secondary reasons (i.e., central venous catheterisation, malignoma, hypercoagulability, postoperative). In the remaining 31 patients, we painstakingly conducted a general and occupational history and further clinical, laboratory or technical investigations to differentiate the aetiology. RESULTS: Twenty-eight of 31 patients with suspected primary thrombosis of the axillary or subclavian vein (Paget-Schroetter syndrome) showed unusual private or occupational physical exercise as the underlying cause. Sixteen patients reported only short physical exercise up to several hours or acute trauma. Longer physical exercise periods (several days, months or even more) were found in 12 patients. Ten of the 28 patients who acquired the thrombosis doing occupational tasks covered by the industrial insurance, may be eligible for compensation. In 4 of these 10 insured cases, we found strong hints for work accidents, 6 patients of this group apparently revealed criteria of occupational diseases. Four of the 28 patients had a combination of physical effort and additional thrombogenic risk factors (cardiac pacemaker, hypercoagulability). CONCLUSION: Primary thrombosis of the upper extremity (Paget-Schroetter syndrome) should be announced to and compensated by the industrial injuries insurance either as work-related accident or occupational disease if the patient's occupational history shows close relationship between thrombosis manifestation and extraordinary physical efforts or exercises during occupational strains. For this reason, we recommend the recognition of the Paget-Schroetter syndrome in the national list of occupational diseases.
Upper extremity thrombosis (Paget-Schroetter syndrome) hints already at physical strains with regard to the synonymous term "effort thrombosis". We report two cases of upper extremity thrombosis caused by wrestling. Wrestling as an example of martial arts activity leads to traumatic venous intima lesions with resulting local activation of coagulation as a main reason in pathogenesis of these thromboses. The possibility of a Paget-Schroetter syndrome should be considered in differential diagnosis if upper extremity complaints of unknown origin occur after wrestling matches. This kind of subclavian vein thrombosis should be reported to the accident insurance.
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We report the case of a 29-year-old man without immunodeficiency who acquired Pseudomonas aeruginosa pneumonia complicated by pulmonary abscess. The source of infection could be identified as aerosolized metalworking fluid at his workplace contaminated with Pseudomonas aeruginosa. A high titer of specific IgG antibodies (type-III-sensitization, Gell & Coombs) against Pseudomonas aeruginosa has been identified in the patients serum as an indicator for longstanding occupational airborne exposure to contaminated metalworking fluid. This community-acquired pneumonia has been reported to the industrial injuries insurance as an occupational disease for discussion of legal consequences and development of effective measures of prevention.
Acute acrylonitrile intoxications are followed by loss of consciousness, convulsions, respiratory arrest, and may end fatally. Common cyanide antidotes have not proved to be effective. In previous animal experiments we could demonstrate that the cyanide antidotes show some protective effect only after oral acrylonitrile application. Only a minimal amount of inhaled acrylonitrile will be transformed into cyanide, in contrast to pharmacokinetics after oral intake. After acrylonitrile inhalation the toxic effect of the whole molecule ( cyanethylation ) is important, and sulfhydryl compounds show antidotal effects. Further animal experiments demonstrate the superior antidotal effects of N-acetyl-cysteine after acrylonitrile inhalation. Intravenous injection of N-acetyl-cysteine in high doses is recommended according to the treatment of paracetamol poisoning.
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On the basis of previous determinations of pharmacokinetic parameters for inhaled vinyl chloride in men, rhesus monkeys, and rats, and on improved pharmacokinetic models a pharmacokinetic treatment of the problem of "peak concentrations" of vinyl chloride, as occurring in industrial practice, became possible. For the calculations, metabolic elimination kinetics of vinyl chloride was assumed to be first order as experiments in different species including rhesus monkeys showed "linear" pharmacokinetics up to atmospheric exposures of 200-300 ppm. The distribution of vinyl chloride between atmosphere and organism under different conditions was evaluated using "'steady-state-kinetics". After treating the processes of "influx", "efflux", and "metabolism", the numerical values for the parameters derived from a human kinetic experiment were used to theoretically calculate the time courses of concentration of vinyl chloride in the organism and of the cumulative amount of vinyl chloride metabolized, under the conditions of (a) a 2h constant exposure to 5 ppm vinyl chloride and (b) two subsequent "peaks" of 50 ppm with a duration of 5 min each. This model calculation suggested that, regardless of the exposure profile, the amount of (reactive) metabolites formed from vinyl chloride would solely be a function of the mean atmospheric vinyl chloride concentration over time. The general validity of this suggested rule could subsequently be demonstrated. As the concentration of the reactive metabolite of vinyl chloride responsible for the carcinogenic effect at the target site must be a resultant of both formation and inactivation, an evaluation of the differential risk of different exposure profiles can reasonably be based on biochemical examinations of the "detoxifying" pathways. This points out the relevance of studies of the patterns of different metabolites of vinyl chloride in man under varying exposure profiles.
The metabolic elimination of vinyl chloride in Rhesus monkeys is a dose-dependent, satruable process, as in rats. Below 200-300 ppm of vinyl chloride (VC) in atmosphere, elimination obeys a first-order law; the clearance rate is much closer to that found in man than the values for rats, mice and gerbils. The maximal velocity of metabolic elimination of VC at high concentrations in Rhesus monkeys is only about half that of rats when related to kg body weight. It s suggested that Rhesus monkeys mimic the quantitative aspects of VC metabolism better than rats or mice.
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