Musculoskeletal Imaging

Aluminium poisoning

a toxic state due to excess amounts of aluminium from any of a number of causes. Patients with chronic renal disease may develop aluminium toxicity with a resulting low-turnover osteomalacia, termed dialysis osteomalacia or aluminium osteomalacia. Children may develop rickets. Significant morbidity and even death may ensue. In uraemic patients, aluminium toxicity initially occurred as a complication of excess amounts of aluminium in the dialysate. The main source of toxicity now is aluminium from oral phosphate binders, such as aluminium hydroxide, which lower serum phosphate levels by binding with phosphate in the intestine.

The mechanism for the production of bone disease is unknown. However, accumulation of aluminum at the site of calcification (the bone - osteoid junction) appears to inhibit mineralization through blocking of skeletal uptake of calcium. Early symptoms and signs of aluminium toxicity include bone pain, muscle weakness, dementia, microcytic anaemia and hypercalcaemia. Later complications may include pathologic fractures, seizures, encephalopathy, and death.

Radiographs may be helpful in predicting aluminium toxicity without resorting to biopsy. Diagnostic findings include an increased frequency of fractures, a lack of osteosclerosis, a relative decrease in subperiosteal resorption compared with patients without aluminium toxicity, and a significant increase in osteonecrosis after transplantation (Fig.1).

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Fig.1

a. Lateral radiograph of the knee demonstrates marked osteopenia and an insufficiency fracture through the distal femoral metaphysis. This encephalopathic patient had profound osteomalacia secondary to aluminium deposition from longstanding haemodialysis. b. AP radiograph of the hand in the same patient again demonstrates marked osteomalacia of the hands with profound osteopenia and cortical thinning.
Aluminium poisoning, Fig.1 (a)
Aluminium poisoning, Fig.1 (b)