Severe lead toxicity is defined as a venous blood lead level ≥70 μg/dL, or having symptoms of encephalopathy. It is a medical emergency even if the child is asymptomatic. Parenteral chelating agents are the mainstay of therapy for these children and can be lifesaving. In 1950, calcium disodium ethylene diamine tetraacetate (CaNa2EDTA) was found to be clinically useful as a chelating agent in the treatment of lead poisoning. Similar to dimercaprol, also known as British Anti-Lewisite or BAL, CaNa2EDTA increases the urinary excretion of lead through the formation of nonionizing soluble chelate. CaNa2EDTA has very low bioavailability orally and treatment necessitates hospitalization and parenteral administration.

The appropriate protocol for administration of CaNa2EDTA is controversial. Its use may cause increased lead concentration in the central nervous system and subsequent increased intracranial pressure. Therefore, CaNa2EDTA is recommended only after administered of dimercaprol. CaNa2 EDTA can be administered 4 hours after the first dose of dimercaprol and once urine output is established. CaNa2EDTA can be administered intravenously or intramuscularly. The intravenous route is usually preferred because it is less painful than the intramuscular route and it permits continuous chelation. However, the intramuscular route should be used in patients with acute encephalopathy. In addition to the possible elevation in intracranial pressure, the major side effects of CaNa2EDTA include local reactions at the injection site, fever, hypercalcemia, the excretion of other essential minerals, and renal dysfunction. The renal dysfunction can manifest as rising blood urea nitrogen, proteinuria, or hematuria. There has been a case report describing the effectiveness of intraperitoneal CaNa2EDTA therapy in patients with renal failure requiring chelation therapy. The use of disodium salt alone (Na2EDTA), as opposed to calcium disodium salt (CaNa2EDTA), is crucial because it may result in severe hypocalcemia and possible death.