1/34. Successful donation and transplantation of multiple organs after fatal poisoning with brodifacoum, a long-acting anticoagulant rodenticide: case report.BACKGROUND: Successful organ donation has been reported after death from poisonings with cyanide, carbon monoxide, methanol, benzodiazepines, and tricyclic antidepressants. In this report, we describe a case of multiple organ donation from a previously healthy individual who died from poisoning with the long-acting anticoagulant rodenticide, brodifacoum. methods: Case report and review of the literature. RESULTS: All organs procured from the poisoned donor functioned adequately, and there were no hemorrhagic complications in any of the recipients. CONCLUSION: This case demonstrates that brodifacoum poisoning is not an absolute contraindication to organ donation from brain-dead patients who have sustained a fatal ingestion.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
2/34. organophosphate poisoning versus brainstem stroke.Two patients presented unconscious after deliberate organophosphate ingestion. Both were initially misdiagnosed as having brainstem stroke, and plans were made for withdrawing treatment within 24 hours. Once correctly diagnosed and appropriately treated, both recovered, illustrating the importance of considering a wide differential diagnosis before withdrawing support and of not relying on routine "drug screens" to detect organophosphates.- - - - - - - - - - ranking = 5keywords = brain (Clic here for more details about this article) |
3/34. A case of transient diabetes insipidus associated with poisoning by a herbicide containing glufosinate.BACKGROUND: The herbicide BASTA (AgrEvo, germany), containing glufosinate ammonium (20%) and an anionic surfactant, polyoxyethylene alkylether sulfate (33%), is widely used. In acute oral BASTA poisoning, patients develop a variety of clinical signs, including disturbed consciousness, convulsions, and apnea. These effects are suspected to be due to the effects of glufosinate on the central nervous system. CASE REPORT: A 60-year-old man ingested 500 mL of BASTA herbicide in a suicide attempt. He developed not only unconsciousness, respiratory distress, and convulsions but also an increase in urine output (7885 mL/d), elevated serum sodium (167 mEq/L), elevated plasma osmolality (332 mOsm/kg), and a decrease in both urine osmolality (200 mOsm/kg) and urine specific gravity (1.003), which suggested the development of diabetes insipidus. The plasma level of antidiuretic hormone remained within the normal range (1.3 pg/mL), despite high plasma osmolality. The administration of desmopressin was successful in normalizing urine volume, specific gravity, and osmolality. serum sodium corrected gradually within 48 hours. The possible mechanisms causing the diabetes insipidus are discussed.- - - - - - - - - - ranking = 5.5176773849457keywords = central nervous system, nervous system (Clic here for more details about this article) |
4/34. Ineffectiveness of hemodialysis in copper sulphate poisoning.A fatal case of severe copper sulphate poisoning is reported in whom hemodialysis was performed 13 h after ingestion. At autopsy a significant amount of copper was found in the brain, heart, liver, kidney, spleen and adrenals. This case indicates sopper is nondialysable and that hemodialysis is ineffective in the treatment of acute copper sulphate poisoning.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
5/34. Death following cupric sulfate emesis.Case history: A 25-year-old woman who had ingested about 20 tablets of diazepam 2.5 mg in a suicide attempt was given cupric sulfate 2.5 g in 1750 mL water as an emetic, but died 3 days later. On autopsy, death was attributed to acute hemolysis and acute renal failure due to copper poisoning. copper concentrations were 5.31 microg/mL in whole blood, 19.0 microg/g in the liver, 8.9 microg/g in the kidney, 1.1 microg/L in the brain, 1.1 microg/g in the gastric wall, 1.5 microg/g in the jejunal wall, 0.3 microg/g in the colon wall, 4.6 microg/g in the gastric contents, and 12.6 microg/g in the intestinal contents (fresh weight). This case and 10 others from the Chinese medical literature provide additional evidence that cupric sulfate is a corrosive poison and contraindicated as an emetic.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
6/34. Permanent brain damage following acute clonidine poisoning in Munchausen by proxy.A child presented with recurrent episodes of lethargia for which he underwent several hospital admissions and investigations. A further episode culminated in respiratory arrest and hypoxic ischemic encephalopathy with permanent mental regression. Eighteen months later the mother was discovered while providing clonidine pills to the child; the mother appears to feature a munchausen syndrome by proxy.- - - - - - - - - - ranking = 4keywords = brain (Clic here for more details about this article) |
7/34. neuroimaging supports the clinical diagnosis of methanol poisoning.In addition to visual loss, methanol intoxication can cause brain damage that is revealed by neuroimaging. We report on a 34-year-old man whose visual acuity deteriorated dramatically during his journey round the world, shortly after an evening with excessive alcohol consumption. Two months after the start of visual disturbances he returned to finland. At examination, poor visual acuity and glaucomatously cupped pale optic discs were detected. The history and clinical findings indicated possible methanol intoxication, which was supported by both CT and MRI. The MRI findings are discussed in the light of the MRI appearance of the pallidum nuclei among patients of different age groups.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
8/34. Fatal rodenticide poisoning with brodifacoum.The increased prevalence of rodents resistant to warfarin led to the development of the hydroxycoumarin anticoagulant brodifacoum. A 25-year-old man attempted suicide by consuming four boxes of d-CON Mouse-Prufe II; each box contains 42 g of bait that is 0.005% brodifacoum. He presented to a hospital nine days later with syncope, hematochezia, gross hematuria, epistaxis, anemia, and a severe coagulopathy. Radiographic studies were consistent with pleural, pericardial, and mediastinal hemorrhages. vitamin k and fresh frozen plasma were given, and he was later discharged on oral phytonadione (vitamin K1). The patient's coagulopathy recurred, necessitating multiple plasma transfusions and prolonged treatment with oral phytonadione. Fifteen weeks after hospital discharge, he presented again with a history of additional brodifacoum ingestion. Neurologic status was initially normal, but in the emergency department he suddenly became comatose soon after emesis was induced with syrup of ipecac. Computed tomography of the brain revealed a subarachnoid hemorrhage that led to brain death less than 24 hours later. This case demonstrates the severe and prolonged coagulopathy that can result from ingestion of brodifacoum, a compound that has a toxic potency about 200-fold that of warfarin and a half-life as much as 60 times longer.- - - - - - - - - - ranking = 2keywords = brain (Clic here for more details about this article) |
9/34. Fatal paraquat poisoning: a light microscopic study in eight autopsy cases.Eight autopsy cases of paraquat poisoning from 1980 to 1990 were studied by light microscopy. An attempt was made to correlate the severity of poisoning, as assessed by the blood paraquat concentrations and the time between ingestion and treatment, with the survival periods and pathological changes. Six of the patients were male. The mean age was 21 years (range 12-33 years). The blood paraquat concentrations on admission ranged from 0.04 to 4.27 micrograms/ml. The survival periods were between 26 hours and 59 days. The main causes of death included circulatory collapse in one patient with 26 hours survival, and acute alveolar injury of the lungs and acute tubular necrosis or diffuse cortical necrosis of the kidneys in 4 patients who survived less than 7 days. Pulmonary proliferative changes leading to respiratory failure were detected in the remaining patients, who survived 11, 17, and 59 days. The liver revealed bile duct injury in the portal areas, centrolobular cholestasis, fatty metamorphosis, and inconspicuous centrolobular hepatic necrosis. The adrenal glands showed diffuse cortical necrosis in 3 severe cases. Mild acute pancreatitis was evident in one case. The brain was edematous with or without focal minimal hemorrhages. Toxic myocarditis, myositis, and aplasia of erythropoiesis, as previously described, were not present in this study. The severity of poisoning seems to correlate reversely with the survival periods and directly with degrees of pulmonary damage and adrenal cortical necrosis.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
10/34. Diffuse white matter lesions in carbon disulfide intoxication: microangiopathy or demyelination.Long-term exposure to carbon disulfide (CS(2)) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS(2). The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T(2)-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS(2) encephalopathy using brain MRI. In addition, the (99m)Tc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS(2), possibly through microangiopathy. In addition, CS(2) poisoning can be considered as one of the causes of chronic leukoencephalopathy.- - - - - - - - - - ranking = 4keywords = brain (Clic here for more details about this article) |
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