CaNa EDTA

Ethylenediaminetetraacetic acid (EDTA) is a polycarboxylic acid chelator its sodium salt (edetate disodium, Na EDTA), and a number of closely related compounds chelate many divalent and triva-lent metals. The cation used to make a water-soluble salt of EDTA has an important role in the toxicity of the chelator. Na EDTA causes hypocalcemic tetany. However, edetate calcium disodium (CaNa EDTA) can be used for treatment of poisoning by metals that have higher affinity for the chelating agent than does Ca +. 

Initial treatment of the acute phase of lead intoxication involves supportive measures. Prevention of further exposure is important. Seizures are treated with diazepam or phenytoin (see Chapter 19), fluid and electrolyte balances must be maintained, and cerebral edema is treated with mannitol and dexamethasone or controlled hyperventilation. The concentration of lead in blood should be determined or at least a blood sample obtained for analysis prior to initiation of chelation therapy. Chelation therapy is indicated in symptomatic patients or in patients with a blood lead concentration in excess of 50-60 pg/dL (about 2.5 pM). Four chelators are employed edetate calcium disodium (CaNa EDTA), dimercaprol, D-penicillamine, and succimer (2,3-dimercaptosuccinic acid [DMSA], chemet). CaNa EDTA and dimercaprol usually are used in combination for lead encephalopathy. 

CaNa EDTA is initiated at a dose of30—50 mg/kg/day in 2 divided doses either by deep intramuscular injection or slow intravenous infusion for up to 5 consecutive days. The first dose of CaNa EDTA should be delayed until 4 hours after the first dose of dimercaprol. An additional course of CaNa EDTA may be given after an interruption of 2 days. Each course of therapy with CaNa EDTA should not exceed a total dose of 500 mg/kg. Urine output must be monitored because the chelator—lead complex is believed to be nephrotoxic. Treatment with CaNa DTA can alleviate symptoms quickly. Colic may disappear within 2 hours paresthesia and tremor cease... 

Effective therapy for cadmium poisoning is difficult to achieve. Although there is no proven benefit, some clinicians recommend chelation therapy with CaNaffsDTA. The dose of CaNa DTA is 75 mg/kg/day in 3-6 divided doses for 5 days. After a rrunirrmm of 2 days without treatment, a second 5-day course is given. The total dose of CaNa EDTA per 5-day course should not exceed 500 mg/kg. Animal studies suggest that chelation therapy should be instituted as soon as possible after cadmium exposure because a rapid decrease in effectiveness of chelation therapy occurs in parallel with distribution to sites inaccessible to the chelators. The use of dimercaprol and substituted dithiocarbamates appears promising for individuals chronically exposed to cadmium. 

Reiders (R2) has found that the urinary lead excretion following intravenous administration of CaNa-.-EDTA is increased significantly more in persons with excessive lead burden than in unexposed individuals, and he has suggested this as a definite diagnostic test. Intoxicated patients or those with increased lead absorption excrete at least 1 mg of lead in the first 24 hours following treatment, while normal individuals excrete a maximum of 700 /xg. CaNaaEDTA is frequently used in the treatment of lead intoxication (E4). 

The successful use of CaNa2EDTA in the treatment of lead poisoning is due, in part, to the capacity of lead to displace calcium from the chelate. Enhanced mobilization and excretion of lead indicate that the metal is accessible to EDTA. Bone provides the primary source of lead that is chelated by CaNa DTA. After such chelation, lead is redistributed from soft tissues to the skeleton. 

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