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Background
- Transition metal
- Essential nutrient
- Exposure from diet, medicinal uses, nutritional supplements, and occupational exposures
- Multiple case reports of zinc toxicity related to ingestion of United States pennies which contain 97.5% zinc
Toxicokinetics
- Absorbed primarily in the jejunum
- Excreted via the GI tract with minimal amounts excreted in the urine
- Accumulates in erythrocytes
- Whole blood concentrations are 6-7x higher than in the serum
- Inverse relationship with copper
- Excess zinc absorption will cause a counterregulatory response resulting in copper elimination
Clinical Features
Acute
Chronic
- Zinc induced copper deficiency
- Progressive myeloneuropathy
Differential Diagnosis
Evaluation
- BMP
- CBC
- Copper level
- Ceruloplasmin level
- Abdominal films to assess for foreign bodies
- MRI
- Will show increase T2 signal in the dorsal columns of the cervical cord
Management
- Oral toxicity
- Inhalation
- Chelation
- Limited data on use, and data present is based off of case reports and treatment for lead toxicity [1]
- Consider in patients with hemodynamic compromise
- CaNa2EDTA, British antilewisite, DTPA were all successfully used in case reports
- 1000mg/m2/d IV CaNa2EDTA every 6 hours
- Based on a successful case report, but should be given in conjunction with toxicology or poison control center
- Dermal Exposures
- Do not use water in metallic zinc exposures
- Concern metal will ignite
- Remove zinc with forceps and apply mineral oil to affected skin
- Copper replacement
- Oral copper alone shown to improve hematopoietic effects and prevent further neurological deterioration [2]
Disposition
References
- ↑ Majlesi, N. Zinc. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1342
- ↑ Rowin J, Lewis SL. Copper deficiency myeloneuropathy and pancytopenia secondary to overuse of zinc supplementation. J Neurol Neurosurg Psychiatry. 2005;76:750-751.