Fatal manganese intoxication due to an error in the elaboration of Epsom salts for a liver cleansing diet.

We describe the case of a 50-year-old man with a fatal intoxication after accidental massive oral ingestion of manganese. The patient presented with lethargy, diffuse abdominal pain, vomiting, and profuse diarrhea after ingesting Epsom salts (magnesium sulfate heptahydrate) during a liver cleansing diet. Despite intensive care management with intubation, prone position ventilation, continuous venovenous hemofiltration, and multiple transfusions, he progressed to refractory shock with multiple organ dysfunction resulting in death within 72 h. Similar patients arrived at several hospitals with identical epidemiology (all had ingested the same salt obtained in the same place). Clinical and forensic investigations (X-ray diffraction) discovered that the supplier had mistakenly prepared the salts with hydrated manganese sulfate instead of magnesium sulfate heptahydrate. The results enabled the other patients to be successfully treated for hydrated manganese sulfate intoxication with life support in the intensive care unit and chelation therapy (EDTA). We describe the clinical presentation of acute manganese poisoning and alert professionals to the risk of an increasingly popular diet. This case demonstrates the importance of collaboration between clinicians, pathologists, and forensic scientists to resolve a difficult-to-diagnose case.

Lithium overdose causing non-convulsive status epilepticus--the importance of lithium levels and the electroencephalography in diagnosis.

We report a case of lithium overdose in a patient who presented in non-convulsive status epilepticus. The lithium toxicity was probably due to interaction with Moduretic. The diagnosis was not suspected until electroencephalography was performed. This case underscores the importance of therapeutic drug level monitoring of lithium, especially where toxicity is suspected, and the indispensable role electroencephalography plays by allowing a correct diagnosis to be made promptly.

[Age characteristics of cadmium content in the organism of poisoned rats with experimental metabolic acidosis].

The paper demonstrates age peculiarities of cadmium content in the liver, kidneys and spleen of 3-month and 18-month rats poisoned by cadmium sulfate. It was registered that the content of cadmium is 266.7 times higher in 3-month old rats, and 141.8 times in 18 months rats in comparison with intact ones. A biological model of introducing 3-month and 18-month rats into the state of metabolic acidosis before and after poisoning with cadmium sulfate was developed. The result of the research showed that changes in acid-base equilibrium of poisoned rats towards metabolic acidosis may influence a decrease of cadmium content in their organisms. Thus, when modeling of metabolic acidosis before the poisoning with cadmium, the content of cadmium decreases in 3-month rats' liver by 21%, in kidneys by 53%; in metabolic acidosis modeling after cadmium poisoning its content decreases, accordingly, by 44% and by 56.5% in comparison with the just poisoned ones. In metabolic experimental acidosis modeling the content of cadmium in 3-month poisoned rats' spleen decreased by 36.5% before and after poisoning. Such changes were also registered in 18-month old rats but to lower extent. Thus, the results of the researches showed more effective correction of cadmium intoxication decrease in the organism of 3-month rats when using the model of acid-base equilibrium change in the organisms of poisoned animals.

Evaluating the health risk from secondary sulfates in eastern North American regional ambient air particulate matter.

Epidemiological studies of particulate matter (PM) using central area monitors have associated total PM mass, as well as certain individual components of PM, including sulfate, with adverse human health effects. However, some recent studies that used concentrated ambient particles (CAPs) or analyzed the effects of air pollution from different sources or geographic areas suggest that while some particles may be harmful, other particulate species including secondary sulfates may have negligible health effects. Toxicology studies to date also suggest that secondary sulfates pose little health risk. While studies using central-area monitors implicitly assume that all residents of the area are exposed to the same levels of pollution, newer studies find substantial health effects for those in close proximity to major roads. These latter studies recognize that although population exposure to widespread pollutants, such as total PM mass and sulfates, may be relatively uniform over a wide area, exposure to pollutants from local sources is not. While there is an emerging literature associating several adverse health effects with proximity to local pollution sources, the current database provides limited information that allows identification of specific particulate species that may cause little to no harm. In this article, we suggest that ambient secondary sulfates, and eastern North American regional air masses generally, appear to have little adverse impact on public health. This suggestion is based on evidence gleaned from eight avenues of investigation: (1) recent non-central-area monitor studies, including exposure gradient or proximity studies; (2) CAPs studies; (3) studies that examine effects related to different geographic areas or sources; (4) toxicology studies; (5) the limited number of studies that analyze existing central-area monitor data to explicitly examine the health impacts of sulfate and acidity versus PM mass; (6) "modern" area monitor studies with additional capabilities to distinguish among sources of pollution; (7) partial reinterpretation of two pivotal cohort studies; and (8) studies separating effects of secondary sulfates from those of primary metal sulfates. However, uncertainties remain regarding the role that secondary sulfates may play in ambient PM chemistry pathways leading to potentially harmful products, such as the possible effects of secondary organic aerosols that may be the product of acid catalysis of sulfur dioxide. Thus, more targeted study is needed, and some research suggestions are made in this regard.

Case report: severe mercuric sulphate poisoning treated with 2,3-dimercaptopropane-1-sulphonate and haemodiafiltration.

INTRODUCTION: Inorganic mercury poisoning is uncommon, but when it occurs it can result in severe, life-threatening features and acute renal failure. Previous reports on the use of extracorporeal procedures such as haemodialysis and haemoperfusion have shown no significant removal of mercury. We report here the successful use of the chelating agent 2,3-dimercaptopropane-1-sulphonate (DMPS), together with continuous veno-venous haemodiafiltration (CVVHDF), in a patient with severe inorganic mercury poisoning. CASE REPORT: A 40-year-old man presented with haematemesis after ingestion of 1 g mercuric sulphate and rapidly deteriorated in the emergency department, requiring intubation and ventilation. His initial blood mercury was 15 580 microg/l. At 4.5 hours after ingestion he was started on DMPS. He rapidly developed acute renal failure and so he was started on CVVHDF for renal support and in an attempt to improve mercury clearance; CVVHDF was continued for 14 days. METHODS: Regular ultradialysate and pre- and post-filtrate blood samples were taken and in addition all ultradialysate generated was collected to determine its mercury content. RESULTS: The total amount of mercury in the ultrafiltrate was 127 mg (12.7% of the ingested dose). The sieving coefficient ranged from 0.13 at 30-hours to 0.02 at 210-hours after ingestion. He developed no neurological features and was discharged from hospital on day 50. Five months after discharge from hospital he remained asymptomatic, with normal creatinine clearance. DISCUSSION: We describe a patient with severe inorganic mercury poisoning in whom full recovery occurred with the early use of the chelating agent DMPS and CVVHDF. There was removal of a significant amount of mercury by CVVHDF. CONCLUSION: We feel that CVVHDF should be considered in patients with inorganic mercury poisoning, particularly those who develop acute renal failure, together with meticulous supportive care and adequate doses of chelation therapy with DMPS.

[Cellular mechanisms of postnatal growth of rat liver in during chronic exposure of cadmium sulfate and strontium chloride]. / Kletochnye mekhanizmy postnatal'nogo rosta pecheni krys pri khronicheskom vozdeistvii sul'fata kadmiia i khlorida strontsiia.

A cytophotometric investigation was performed to study the ploidy level and total protein content in hepatocytes of rats of different ages (1, 7, 14, 21, 30, 90, 180, 365 days), both intact and chronically treated with cadmium sulfate or strontium chloride. It was established that during the first month of postnatal ontogenesis, compositions of liver parenchyma cell population of intact and treated rats did not differ. Compared to control animals, the process of cell polyploidization in the liver of rats treated with heavy metal salts of 30-90 days proceeded slower, especially in Cd(2+)-treated rats. Within 180-365 days the cell polyploidization in the treated animals increased. The proportion of (4c x 2)-hepatocytes in 1 year old Cd(2+)- or Sr(2+)-treated rats increased, resp., by 2.7 and 1.5 times, and that of 8c hepatocytes was higher by 3.9 and 1.5 times than in the control, the average ploidy level rising by 20 and 5%. respectively. It was established that until 90 days the rate of protein accumulation in liver cells of intoxicated rats was slower than in intact animals. Thus, the average protein content per diploid hepatocyte in Cd(2+)- or Sr(2+)-treated 30 day old rats was lower by 20 and 16%, respectively, compared to control animals. The protein content increased in liver cells of Cd(2+)- or Sr(2+)-intoxicated rats following 90 and 180 days, respectively, and this process was exclusively associated with cell polyploidization. During the first 3 weeks after birth, no significant difference was observed in the extent of involvement of cell proliferation, polyploidization and hypertrophy in the growth of liver in intact and intoxicated animals. At this period the liver was growing due completely to cell proliferation and hypertrophy. During 21-30 days the contribution of cell proliferation to the liver growth of intact rats was not significant (29%), whereas it remained at higher level (50%) in the treated animals. In 30-90 days after birth, the involvement of proliferation process to the liver growth of intoxicated rats decreased to 25-28%, while in intact animals it increased up to 37%. At this period the cell polyploidization plays an essential role in the growth of liver in both intact and intoxicated animals to reach in average 37-46%. The contribution of polyploidization and hypertrophy to the liver growth of Cd(2+)-treated rats within 30-90 days was obviously higher than in Sr(2+)-treated animals. Both at the late (3-12 months) and at the early (1-21 days) stages of experiments, the pattern of correlation of different cell components in the growing liver of intact and intoxicated rats differed only a little.

[Effect of cadmium sulfate and strontium chloride on the glycogen content in hepatocytes of rats of various ages]. / Vliianie sul'fata kadmiia i khlorida strontsiia na soderzhanie glikogena v gepatotsitakh krys raznogo vozrasta.

Cytophotometry and image analysis being used, hepatocyte glycogen contents were measured in periportal and pericentral zones of liver lobules at different stages (1, 7, 14, 21, 30, 90, 180 and 365 days) of postnatal development of both intact rats and rats exposed to chronic CdSO4 (1 mg/kg body weight) and SrSO4 (6.5 mg/kg body weight) intoxication. The glycogen content in hepatocytes of intact rats increased continuously in the course of development being most highest at the initial stage of development. The glycogen content ratio in cells of portal and central zones of liver lobules varied during ontogenesis. The maximum value of this ratio is reached on the 21st day after the rat birth, dropping sharply at later age to reach its minimum in adults. Intoxication of rats by Cd2+ and Sr2+ within 1-90 days interval reduced hepatocyte glycogen levels, compared to normal liver. The prolongation of rat treatment with heavy metals for 90-365 days led to glycogen accumulation in hepatocytes. Rat intoxication with heavy metals for 1 year brought about the increase in both glycogen content per cell and glycogen concentration. Cd2+ treatment for 30-90 days resulted in glycogen accumulation inhibition in both the investigated zones of liver lobules. Thereafter an increased glycogen accumulation took place in hepatocytes of the portal and central liver lobules. Following Cd2+ treatment, the value of the ratios of glycogen levels in the portal and central liver lobules was lower than in the normal liver on all stages of the postnatal rat development. The lowest value (< 1.0) of this ratio was reached in the cirrhotic liver. Distinct from Cd2+ treatment of rats, the treatment with Sr2+ does not lead to significant changes in glycogen levels in cells of different zones of liver lobules. Nevertheless certain destructive changes in glycogen-forming function of hepatocytes after Sr2+ treatment are apparent. This is suggested from the lower glycogen levels in the portal and central zones of liver lobules on 30-180 days interval compared to the normal liver. Besides, the values of ratios in glycogen levels in the portal and central zones of liver lobules in 14 and 21 days old rats was noticeably lower than in the intact rats of the same age.

Chronic intoxication with lead- and sulfur compounds may produce Parkinson's disease.

Parkinson's disease was found in three post office workers who were in close contact with lead-sulfate batteries over a period between 1947 and 1983. The workers had been working in a charging station for lead storage batteries used for the battery-traction of post wagons. Parkinson's disease was diagnosed by the characteristic features of rigidity, tremor and elements of hypo-, brady- and akinesia. Additional symptoms were: bradyphrenia (n = 3), memory deficits (n = 3), depressive symptoms (n = 2) and peripheral neuropathy (n = 2). We hypothesize that the parkinsonian symptoms of these post office workers are primarily caused by lead or lead compounds. However a possible toxicity of sulfur containing compounds cannot be ruled out.

Death by tanning--a case of fatal basic chromium sulphate poisoning.

A woman ingested 400 ml of leather tanning solution containing 48 g of basic chromium sulphate (CrOHSO4). This substance forms hydrogen ions and trivalent chromium when it reacts with tissue proteins. The patient died of cardiogenic shock, complicated by pancreatitis and gut mucosal necrosis and haemorrhage. There are no reported cases of toxicity due to oral ingestion of trivalent chromium. Toxicity of hexavalent and trivalent chromium is discussed and suggestions made for management of future cases.

[Acute zincteral oral poisoning]. / Ostre zatrucia zincteralem droga doustna.

Zinc vapour poisoning by inhalation in the form of zinc fever is more frequent than oral zinc product poisoning, the product used in therapy. The main aim of the study was the evaluation of clinical manifestation present after Zincteral ingestion as well as attempt to find the relationship between the presence and aggravation of the clinical manifestation and zinc level in the blood. The course of acute clinical suicidal poisoning by ingestion of Zincteral 50 tablets (10.0 g) and 100 tablets (20.0 g) is presented. The clinical picture revealed the following symptoms and signs: tachycardia, changes of arterial BP, vascular shock; dyspeptic nausea, vomiting cramps in abdominal region, diarrhoea. Damage of the parenchymatous organs, mainly liver was evident. In pregnant woman (9-week-pregnancy) on the 12-th day of her stay in the Clinic complete miscarriage took place accompanied by haemorrhage from reproductive organs. The kind and exacerbation of the clinical manifestations in relation to the zinc level in body fluid were analysed.

Whole-bowel irrigation as treatment for zinc sulfate overdose.

A 16-year-old boy ingested approximately 50 zinc sulfate tablets (ZnSO4; 500-mg tablets). After spontaneous emesis, ipecac-induced emesis, and orogastric lavage, an abdominal radiograph performed four hours after ingestion still demonstrated approximately 50 ZnSO4 tablets within the stomach and three pills within the colon. Whole-bowel irrigation was begun with a polyethylene glycol lavage solution (PEG; Golytely) that was administered through a nasogastric tube; within one hour, the patient began producing a rectal effluent that contained pills. The patient remained asymptomatic throughout whole-bowel irrigation. Stool guaiac tests were negative. The serum chloride, however, increased from 105 to 127 mEq/L. Follow-up kidney, ureter, and bladder studies demonstrated the clearance of the zinc tablets from the gastrointestinal tract during the next 24 hours.

Self-induced abortion and an elevated anion gap.

PIP: A 19-year old woman who developed rapid nausea, vomiting, tachypnea, and alkalosis within 90 min of taking 3.25 g quinine S04 to induce abortion, was found to have an elevated anion gap and other electrolyte abnormalities. She was normovolemic, and had benign findings on drug screen except for quinine. Her abnormal laboratory values were high serum anion gap of 20 (normal 8-14), high urine anion gap of 171, low HC03- of 29 mEq/L, high Pa)@ of 130 mm Hg, alkalotic pH of 7.5, and hypokalemia of 2.6 mEq/L. Her hypokalemia was judged due to diuresis and vomiting. She was successfully treated with intravenous fluids and supportive care and was discharged on the third day. Quinine intoxication can also cause cinchonism, which is marked by tinnitus, vertigo, blurred vision and scotomata, and possible optic atrophy or death. The toxic dose is 2 g, and the lethal dose 8 g.^ieng

[Experimental study of the effect of rubidium on the cardiovascular system]. / Eksperimental'noe issledovanie deistviia na serdechnososudistuiu sistemu.

The experimental data on the chronic inhalation effects of rubidium on the myocardium and the rate of natural organism aging are presented. No cardiotoxic effect of rubidium sulfate has been established. Hypotensive effect is associated with neurohormonal shifts at the level of an integral organism. Its impact does not result it potassium displacement in cells. Rubidium standardization should be carried out without taking account of gerontogenic effect.

An epidemiologic study of mortality in veal calves subsequent to an episode of zinc toxicosis on a California veal calf operation using zinc sulfate-supplemented milk replacer.

Ninety-five 3- to 6-month old male Holstein veal calves were evaluated after an episode of zinc toxicosis, to describe clinical signs and to identify management and/or host-related factors that may have contributed to death. Clinical signs appeared 23 days after feeding of milk replacer commenced. Of 85 calves examined, 64 had pneumonia (75.5%), 62 had ocular signs (72.9%), 46 had diarrhea (54.1%), 34 were anorectic (40.0%), 15 were bloated (17.6%), 8 had cardiac arrhythmias (9.4%), 3 had convulsions (3.5%), and 3 were polydipsic/polyphagic (3.5%). Clinical signs began to appear when calves each were being fed approximately 1.5 to 2.0 g of zinc/day and exposed to a cumulative zinc intake of 42 to 70 g, from a milk replacer containing 706 micrograms of elemental zinc/g of milk replacer. Of 95 calves studied, 1 died before zinc was supplemented, 16 died during the episode, 12 were euthanatized, 1 was lost to follow-up evaluation, 1 was culled, and 64 were slaughtered. Deaths attributable to zinc toxicosis were observed between 25 and 53 days after the milk replacer was supplemented with zinc. Calves died while being exposed cumulatively to 30 to 66 g of zinc. The factors of previous pneumonia severity, age, cumulative daily exposure to zinc, and calf location within a bay were examined for possible associations with mortality, using stepwise logistic regression. Though younger calves tended to have a higher mortality than older calves, neither age category nor severity of pneumonia, before zinc supplementation, accounted for a significant mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Mortality of waterfowl on a hypersaline wetland as a result of salt encrustation.

Approximately 300 geese, primarily lesser Canada geese (Branta canadensis parvipes) were found unable to fly or dead on a small hypersaline lake (conductivity 77,000-90,000 mumhos/cm) in western Saskatchewan in September 1985. The birds were heavily encrusted with sodium sulfate crystals. Dead birds that were necropsied had aspirated lake water and had evidence of acute muscle degeneration. The live geese (155) were captured and moved to nearby freshwater wetlands where most apparently survived. Some birds died of severe myopathy after translocation. Five northern shovelers (Anas clypeata) were found encrusted with salt and unable to fly on the lake approximately 10 days later. Salt encrustation apparently occurred when rapid cooling of the lake resulted in supersaturation and crystallization of the dissolved salt. A local resident recalled similar events occurring on the lake in autumn on at least two other occasions during the past 50 yr.