Cadmium encephalopathy : a report with elemental analysis and pathological findings

We report a boy of East Indian origin, aged 2 years and 10 months, who died suddenly and unexpectedly. Autopsy findings showed marked cerebral swelling with herniation and histological evidence of marked cerebral edema with perivascular protein leakage, indicating blood-brain barrier disruption. Ene...

Full description

Saved in:
Bibliographic Details
Published in:Acta neuropathologica 1994-12, Vol.88 (6), p.583-586
Main Authors: PROVIAS, J. P, ACKERLEY, C. A, SMITH, C, BECKER, L. E
Format: Article
Language:English
Subjects:
Biological and medical sciences
Blood-Brain Barrier
Brain Diseases - chemically induced
Brain Diseases - pathology
Brain Edema - chemically induced
Brain Edema - pathology
Cadmium - adverse effects
Cadmium - analysis
Chemical and industrial products toxicology. Toxic occupational diseases
Child, Preschool
Humans
Kidney - metabolism
Male
Medical sciences
Metallothionein - metabolism
Metals and various inorganic compounds
Toxicology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:We report a boy of East Indian origin, aged 2 years and 10 months, who died suddenly and unexpectedly. Autopsy findings showed marked cerebral swelling with herniation and histological evidence of marked cerebral edema with perivascular protein leakage, indicating blood-brain barrier disruption. Energy dispersive X-ray microprobe analysis of the brain demonstrated the presence of cadmium and a marked increase in sulfur, predominantly intracellular, both within neuroglial, and to a lesser degree endothelial, cells. Localization was predominantly in the nucleus. Analysis of the kidney showed cadmium deposition in renal tubules and in the basal lamina of podocytes within the glomerulus. Although the environmental source of cadmium remains unknown, we speculate that acute cadmium toxicity led to brain intracellular accumulation with resultant cellular dysfunction, blood-brain barrier disruption, and lethal cerebral edema.
ISSN:0001-6322
1432-0533
DOI:10.1007/BF00296497