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

• Toxicity typically presents as cognitive issues
• Neuropsychiatric
  • Acute
    • “Manganese madness”
    • Visual [[hallucinations
    • Behavioral changes
    • Anxiety
    • Impotence
  • Late Manifestations
    • Tremor
    • Impaired speech
    • Loss of facial expressions
    • Gait disturbances
    • Low volume speech
    • Can mimic parkinson’s disease
• Pulmonary
  • Acute / Metal Fume Fever
    • Fever
    • Nausea
    • Headache
    • Myalgia
    • Arthralgia
  • Chronic
    • Persistent dry cough
    • Bronchitis
    • Chemical pneumonitis
• GI
  • Anorexia
• Musculoskeletal
  • Arthralgia
  • Muscle rigidity
• Constitutional
  • Lethargy
  • Asthenia

Differential Diagnosis

Heavy metal toxicity

• Aluminum toxicity
• Antimony toxicity
• Arsenic toxicity
• Barium toxicity
• Bismuth toxicity
• Cadmium toxicity
• Chromium toxicity
• Cobalt toxicity
• Copper toxicity
• Gold toxicity
• Iron toxicity
• Lead toxicity
• Lithium toxicity
• Manganese toxicity
• Mercury toxicity
• Nickel toxicity
• Phosphorus toxicity
• Platinum toxicity
• Selenium toxicity
• Silver toxicity
• Thallium toxicity
• Tin toxicity
• Zinc 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