ABSTRACT
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.
Subject(s)
Sulfates/poisoning , Accidents , Administration, Oral , Forensic Pathology , Forensic Toxicology , Hemorrhage/pathology , Humans , Liver/pathology , Male , Manganese Compounds/analysis , Manganese Compounds/pharmacokinetics , Middle Aged , Multiple Organ Failure/chemically induced , Necrosis , Pancreas/pathology , Shock/chemically induced , Spectrophotometry, Atomic , Sulfates/analysis , Sulfates/pharmacokinetics , Tissue Distribution , X-Ray DiffractionABSTRACT
Management of complex thyroid nodules (CTN) is a common dilemma due to their high prevalence and frequent nondiagnostic fine needle aspiration cytology (FNAC). In order to know the rate of malignancy, we reviewed our experience about histopathologic diagnosis of CTN with nondiagnostic FNAC, and we analyzed if cytological variants of nondiagnostic FNAC indicated different histopathologic outcomes. We conducted a review of 927 consecutive aspirations performed between 2003 and 2008. We selected patients without history of radiation, with echographic CTN, and nondiagnostic FNAC, who underwent surgery. We analyzed histopathologic results and compared patients with benign and malignant nodules, and searched for differences between patients with cystic changes in FNAC (C-FNAC), and patients with acellular or only bloody FNAC (A-FNAC). Thirty-six patients were included (mean age 45.7 ± 13 years; 30 females). Four patients had malignant nodules; all were papillary carcinomas. Patients with benign nodules had a similar profile to patients with malignant nodules. Patients with C-FNAC (n = 21) were younger (41.3 ± 12.6 vs. 51.8 ± 11.2 years; P < 0.02), had more lymphocytic thyroiditis (33.3 vs. 0%; P < 0.02), a slightly higher rate of carcinoma in the nodule (14.3 vs. 6.6%; P: ns), and also of papillary microcarcinoma outside the nodule (9.6 vs. 0%; P: ns) than patients with A-FNAC. In conclusion, we report an 11.1% malignancy rate in CTN with nondiagnostic FNAC. Nodules with C-FNAC variant had a slightly higher rate of malignancy than A-FNAC, which may be in relation with younger age and higher prevalence of lymphocytic thyroiditis in this group of patients.
