Manganese toxicity

Background

  • An essential element in the diet
    • Used in various enzymatic processes
    • Mn2+ can take the place of Mg2+, Ca2+, and Fe2+ in various proteins and enzymes, and has been seen to replace Fe2+ in Hgb
    • Low enteral absorption
    • Cleared by the liver and excreted in the bile
  • Typical routes of exposure
    • Inhalation of dusts/fumes
      • Seen in industrial areas as manganese is used to make steel
    • Parenteral nutrition (TPN)
    • IV Methcathinone
  • Readily crosses the blood brain barrier and can be seen concentrated in the basal ganglia, particularly the globus pallidus

Clinical Features

Differential Diagnosis

Heavy metal toxicity

Evaluation

  • Lab
    • Whole blood 4-15 μg/L (73-273 nmol/L)
    • Serum 0.9-2.9 μg/L (16-52 nmol/L)
    • Urine (24h) <10 μg/L (182 nmol/L)
    • No definite toxic level
    • Elevated levels are typically seen in acute toxicity, as manganese is quickly cleared from the blood
  • MRI
    • Will show abnormal T1- weighted signal hyperintensity in the basal ganglia, particularly in the globus pallidus, with normal T2-weighted images

Management

  • Supportive care
  • Remove source of exposure
  • Chelation therapy with CaNa2EDTA or DTPA
    • Can improve urinary excretion of manganese without affecting the neurologic manifestations

Disposition

  • Will depend on severity, most cases are likely seen in patients receiving TPN, and will likely need changes to their TPN orders and a consultation from nutrition
  • Consult Toxicology or poison control

References

Soghoian, S. Manganese. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1294-1298