Dimercaprol is an intramuscularly administered chelating agent approved for the treatment of arsenic, gold, mercury, and acute lead poisoning (when given in combination with edetate calcium disodium). The drug contains 2 sulfhydryl, or thiol, groups which bind heavy metals; thereby rendering the metals inert until they are excreted. For poisonings due to antimony or bismuth, the efficacy of dimercaprol is questionable. Additionally, dimercaprol should not be used in iron, cadmium, or selenium poisoning because the resulting dimercaprol-metal complexes are more toxic than the metals alone, especially to the kidneys.
General Administration Information
For storage information, see the specific product information within the How Supplied section.
Route-Specific Administration
Injectable Administration
-Administer only by deep intramuscular injection.
-Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit. Dimercaprol is a colorless or slightly yellowish viscous oily liquid. The drug is formulated with peanut oil and has a disagreeable, mercaptan-like odor.
Intramuscular Administration
-Inject deeply into a large muscle. Avoid injection into a blood vessel.
-If given with edetate calcium disodium (calcium EDTA), administer at separate injection sites.
-Inform patients that the injection may cause painful sterile abscesses.
Administration of dimercaprol is associated with the development of hypertension. This effect is dose-related and usually accompanied by sinus tachycardia.
An injection site reaction (i.e., a painful, sterile abscess) may occur following administration of dimercaprol. Administer dimercaprol only by deep intramuscular injection.
Adverse effects reported during dimercaprol therapy include abdominal pain, nausea, vomiting, headache, paresthesias or tingling of the hands, and a feeling of constriction or pain in the hands, throat, or chest [chest pain (unspecified)]. Many of the above symptoms are often accompanied by anxiety, weakness, and unrest and may be relieved by administration of antihistamines.
Dimercaprol also causes a burning sensation of the lips, mouth, throat (throat irritation), and penis (i.e., penile irritation). Lacrimation, hypersalivation, rhinorrhea, diaphoresis (specifically, sweating of the forehead, hands, and other areas), conjunctivitis, and blepharal spasm also have been reported.
Patients receiving dimercaprol doses exceeding 5 mg/kg may experience seizures, vomiting, and stupor beginning within 30 minutes and subsiding within 6 hours after the injection.
Approximately 30% of children who receive dimercaprol develop a fever that persists throughout treatment. Transient decreases in polymorphonuclear leukocytes (neutropenia) also can occur.
There was a case report of dimercaprol causing hemolysis, that can be severe, in children with glucose 6-phosphate dehydrogenase deficiency.
Dimercaprol is indicated for the treatment of poisoning due to arsenic, gold, lead (with edetate calcium disodium), and mercury. The efficacy in treating poisoning due to other heavy metals such as antimony and bismuth is questionable. Do not use dimercaprol in iron, cadmium, or selenium poisoning because the resulting dimercaprol-metal complexes are more toxic than the metal alone, especially to the kidneys.
Dimercaprol injection is formulated with peanut oil. Caution is advised when using dimercaprol in patients who have a history of peanut hypersensitivity or hypersensitivity to related foods. Administer only by deep intramuscular injection; never administer via intravenous administration.
Dimercaprol-metal complexes can dissociate, especially in an acidic environment or as the concentration of dimercaprol decreases, thereby releasing the metal and increasing the drug's potential nephrotoxicity. This nephrotoxicity can be prevented by alkalizing the urine. Dosages of the drug should be decreased in patients with oliguria, and the drug should be discontinued or only used with extreme caution in patients who develop acute renal impairment or renal failure because the drug can accumulate, possibly leading to serum toxicity. Because the dimercaprol-metal complex is eliminated renally, this drug should be used cautiously in patients with preexisting renal disease. Medicinal iron therapy should not be given to patients receiving dimercaprol. The resulting dimercaprol-iron complex may be more toxic to the kidneys than iron alone.
Use dimercaprol with caution in patients with preexisting hypertension. Administration of the drug has been associated with a rise in blood pressure accompanied by tachycardia. This effect is roughly proportional to the dose administered.
Dimercaprol is contraindicated for use in patients with hepatic disease, except for cases of post-arsenical jaundice.
It is not known if administration of dimercaprol during pregnancy can cause fetal harm or adversely affect reproductive capacity. Therefore, in making the decision to administer this drug during pregnancy, the potential risks to the fetus must be weighed against the potential benefits to the mother. Administer dimercaprol to a pregnant patient only if clearly needed.
According to the manufacturer, it is not known whether dimercaprol is excreted in human milk. The indications necessitating the use of dimercaprol (e.g., heavy metal poisoning) lead to a cessation of breast-feeding during maternal treatment of those toxicities. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally administered drug, healthcare providers are encouraged to report the adverse effect to the FDA.
Dimercaprol may cause hemolysis in patients with G6PD deficiency. Use cautiously in these patients, especially during stressful situations (i.e., infection).
For the treatment of arsenic toxicity or gold toxicity:
-for the treatment of mild arsenic toxicity or gold toxicity:
Intramuscular dosage:
Adults: 2.5 mg/kg deep IM injection every 6 hours for 2 days, then every 12 hours on the third day, and then once daily for 10 days.
Children and Adolescents: 2.5 mg/kg deep IM injection every 6 hours for 2 days, then every 12 hours on the third day, and then once daily for 10 days.
-for the treatment of severe arsenic toxicity or gold toxicity:
Intramuscular dosage:
Adults: 3 mg/kg deep IM injection every 4 hours for 2 days, then every 6 hours on the third day, and then every 12 hours for 10 days.
Children and Adolescents: 3 mg/kg deep IM injection every 4 hours for 2 days, then every 6 hours on the third day, and then every 12 hours for 10 days.
For the treatment of acute mercury toxicity:
NOTE: Effective for acute toxicity if started within 1 to 2 hours after ingestion of mercury salts. Treatment is not very effective for chronic mercury poisoning.
Intramuscular dosage:
Adults: 5 mg/kg deep IM injection given within 1 to 2 hours of mercury ingestion. Then, 2.5 mg/kg deep IM injection once or twice daily for 10 days.
Children and Adolescents: 5 mg/kg deep IM injection given within 1 to 2 hours of mercury ingestion. Then, 2.5 mg/kg deep IM injection once or twice daily for 10 days.
For the treatment of severe lead toxicity (i.e., acute lead encephalopathy or blood lead concentrations greater than 70 mcg/dL) in combination with edetate calcium disodium (calcium EDTA):
Intramuscular dosage:
Adults: 4 mg/kg by deep IM injection given alone as the first dose. Thereafter, 4 mg/kg by deep IM injection given every 4 hours in combination with edetate calcium disodium (calcium EDTA) via separate injection sites. NOTE: Ensure urine flow has been established prior to starting calcium EDTA. For less severe toxicity, the maintenance dose can be reduced to 3 mg/kg after the first dose. Duration of therapy is 2 to 7 days depending on clinical response. Treatment success depends on rapid initiation of therapy and use of adequate doses given at frequent intervals.
Children and Adolescents: 4 mg/kg by deep IM injection given alone as the first dose. Thereafter, 4 mg/kg by deep IM injection given every 4 hours in combination with edetate calcium disodium (calcium EDTA) via separate injection sites. NOTE: Ensure urine flow has been established prior to starting calcium EDTA. For less severe toxicity, the maintenance dose can be reduced to 3 mg/kg after the first dose. Duration of therapy is 2 to 7 days depending on clinical response. Treatment success depends on rapid initiation of therapy and use of adequate doses given at frequent intervals.
Maximum Dosage Limits:
-Adults
5 mg/kg per dose IM for loading dose; 4 mg/kg per dose IM for maintenance.
-Geriatric
5 mg/kg per dose IM for loading dose; 4 mg/kg per dose IM for maintenance.
-Adolescents
5 mg/kg per dose IM for loading dose; 4 mg/kg per dose IM for maintenance.
-Children
5 mg/kg per dose IM for loading dose; 4 mg/kg per dose IM for maintenance.
Patients with Hepatic Impairment Dosing
Specific dosage guidelines have not been established; however, except for post-arsenical jaundice, dimercaprol is contraindicated for use in patients with hepatic impairment.
Patients with Renal Impairment Dosing
Specific dosage guidelines have not been established; however, dimercaprol should be discontinued or used only with extreme caution in patients who develop acute renal impairment during therapy.
*non-FDA-approved indication
Auranofin: (Major) Avoid concomitant use of therapeutic gold and dimercaprol. Concomitant use reduces the concentrations of both compounds and diminishes efficacy.
Ferric carboxymaltose: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Ferric Derisomaltose: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Ferric Maltol: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Ferumoxytol: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Gold: (Major) Avoid concomitant use of therapeutic gold and dimercaprol. Concomitant use reduces the concentrations of both compounds and diminishes efficacy.
Iron - Injectable Only: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Iron Dextran: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Iron Salts: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Iron Sucrose, Sucroferric Oxyhydroxide: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Iron: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Levonorgestrel; Ethinyl Estradiol; Ferrous Bisglycinate: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Levonorgestrel; Ethinyl Estradiol; Ferrous Fumarate: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Norethindrone Acetate; Ethinyl Estradiol; Ferrous fumarate: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Norethindrone; Ethinyl Estradiol; Ferrous fumarate: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Polysaccharide-Iron Complex: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Selenium: (Major) Avoid concomitant use of dimercaprol and products containing selenium. Dimercaprol forms toxic-chelates with selenium which increases the risk for nephrotoxicity and other adverse effects.
Sodium Ferric Gluconate Complex; ferric pyrophosphate citrate: (Major) Avoid concomitant use of dimercaprol and products containing iron. Dimercaprol forms toxic-chelates with iron which increases the risk for nephrotoxicity and other adverse effects.
Dimercaprol is an intramuscularly administered chelating agent that binds certain heavy metals in the body. The 2 sulfhydryl groups of dimercaprol form heterocyclic ring complexes with heavy metals, preventing them from reacting with or removing them from binding sites on sulfhydryl-containing enzymes. Once bound to dimercaprol, the metals are rendered inert and excreted by the kidneys. However, the dimercaprol-metal complexes can dissociate, especially in an acidic environment or as the concentration of dimercaprol decreases, thereby releasing the metal and increasing toxicity. To assure maximal excretion of the heavy metal, it is crucial to administer dosages of the drug that are in excess of the amounts of metal present.
Dimercaprol is indicated for arsenic, gold, and mercury poisoning and can be used in combination with edetate calcium disodium, calcium EDTA in the treatment of acute lead toxicity. Dimercaprol is of questionable value in treating antimony or bismuth toxicity. Dimercaprol should not be used in the treatment of iron, cadmium, or selenium toxicity because the dimercaprol-metal complexes are more toxic than the metals alone.
Dimercaprol is administered via deep intramuscular injection. Once absorbed, this lipophilic drug rapidly penetrates intracellular spaces, and is distributed in the highest concentrations in the liver, kidney, brain, and small intestines. After chelation occurs, the dimercaprol-metal complexes are eliminated from the body within 4 hours. However, these complexes can rapidly dissociate and result in toxicity, especially in an acidic environment; alkalization of the urine can help prevent the release of the metal and protect the kidneys. Drug that does not chelate with metal to form a dimercaprol-metal complex undergoes rapid hepatic metabolism and is excreted in the urine as an inactive product. Although most of the administered dose is eliminated in the urine, some is partly excreted in the feces via bile.
Affected cytochrome P450 isoenzymes and drug transporters: none
-Route-Specific Pharmacokinetics
Intramuscular Route
Dimercaprol has a time to peak plasma concentration (Tmax) of 30 to 60 minutes after intramuscular administration.
Topical Route
Dimercaprol is readily absorbed through the skin after topical application.