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.

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.

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.

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)