Mercury Toxicity Treatment & Management
- Author: David A Olson, MD; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS more...
Notify state and local health officials to clarify the mechanism of exposure and to institute appropriate decontamination measures, should these be necessary.
Treatment of mercury toxicity consists of removal of the patient from the source of exposure, supportive care, and chelation therapy. Patients with cognitive and emotional sequelae may require psychotropic medications.
Although laboratory studies are important, acute treatment in critical situations should be based on the patient’s history and clinical presentation, without waiting for laboratory confirmation.
Little information is available about the treatment of mercury-induced tremulousness, but initiation of empiric treatment for patients who are functionally impaired with this complication would be reasonable.
Once the neurologic consequences of Minamata disease appear, they are, unfortunately, irreversible. The goal of medical management in Minamata disease is to reduce the total body burden of mercury and minimize further damage.
Prehospital management includes gathering information on the time, type, and mode of mercury exposure, as well as the following:
Initial assessment - Airway, breathing, and circulation (ABCs)
Intravenous (IV) access
Removal from the contaminated area
Surgery does not have a role in the treatment of Minamata disease; however, in other forms of mercury exposure, surgical intervention is sometimes warranted. Surgery occasionally has been employed to remove ingested mercury that has become lodged in the intestine or colon.
Surgical removal of subcutaneous deposits of self-injected elemental mercury has also been described. Early, definitive surgical excisions of the mercury deposits resulted in good outcomes with minimal toxicity.
All patients in unstable condition should be admitted to an intensive care unit (ICU). After the patient is admitted, supportive measures, decontamination, and careful monitoring should be continued. In cases of inorganic mercuric salt ingestion, carefully monitor the patient's renal function.
Serious clinical manifestations due to mercury exposure should be managed in a tertiary care facility by physicians experienced with toxicologic emergencies.
Employment and driving should be restricted if patients have significant emotional or cognitive problems.
Consult with the regional poison control center or a medical toxicologist (certified through the American Board of Medical Toxicology and/or the American Board of Emergency Medicine) for additional information and patient care recommendations.
Determine follow-up care on a case-by-case basis. Obtain laboratory measurements of toxicity in patients with possible continued sources of exposure.
Emergency Department Care
Supportive care begins with the ABCs, especially when managing the inhalation of elemental mercury and the ingestion of caustic inorganic mercury, both of which may cause the onset of airway obstruction and respiratory failure. The next step in supportive care is the removal of contaminated clothing and copious irrigation of exposed skin. Aggressive hydration may be required for acute inorganic mercury poisoning because of its caustic properties. Do not induce emesis if the compound ingested is of the caustic inorganic form.
Gastric lavage is recommended for organic ingestion, especially if the compound is observed on an abdominal radiograph series.
Activated charcoal is indicated for GI decontamination because it binds inorganic and organic mercury compounds to some extent.
Whole bowel irrigation may be used until rectal effluent is clear and void of any radiopaque material. However, its effectiveness in decreasing the GI transit time of elemental mercury is doubtful because of the high density of elemental mercury and the low density of the whole bowel irrigant solutions. Likewise, whole bowel irrigation has no adsorptive effect on any type of mercury within the GI tract.
Use chelating agents if the patient is symptomatic, if systemic absorption is anticipated, or if increased blood or urinary mercury levels are present. Chelating agents contain thiol groups, which compete with endogenous sulfhydryl groups.
Hemodialysis is used in severe cases of toxicity when renal function has declined. The ability of regular hemodialysis to filter out mercury is limited because of mercury's mode of distribution among erythrocytes and plasma. However, hemodialysis with L-cysteine compound as a chelator has been successful.
Older literature indicates that neostigmine may help motor function in methylmercury toxicity as this toxicity may lead to acetylcholine deficiency.
Because mercury binds to the body's ubiquitous cellular sulfhydryl groups, chelating agents should be administered early in treatment.
Chelating agents contain thiol groups, which bind to mercury. For acute, inorganic toxicity, dimercaprol (British antilewisite [BAL]) has traditionally been recommended, but oral agents are gaining prominence. Chelation with 2,3-dimercaptosuccinic acid (DMSA or succimer) has been shown to result in increased mercury excretion, compared with N -acetyl-D,L-penicillamine, in adults with acute mercury vapor exposure. DMSA is generally well tolerated and has also demonstrated efficacy in children exposed to mercury. Chelation treatment may be administered in the outpatient setting with an oral chelator, such as DMSA.
Polythiol is a nonabsorbable resin that can theoretically help in facilitating the removal of methylmercury (short chain alkyl organic mercury), which is then excreted in the bile after enterohepatic circulation.
Exchange transfusion has been used as a treatment of last resort. Because mercury-chelating agent complexes are large molecules, they may fail to be filtered out by standard hemodialysis membranes, rendering conventional hemodialysis ineffective.
Despite the increased excretion of mercury with chelating agents, chelation removes only a small portion of the body's mercury stores. Furthermore, the efficacy of chelating agents in treating neurologic complications has not been established; however, among patients with amalgam fillings, placebo responses to chelation treatment have been reported.
Finally, caution is warranted, however, as some physicians have documented initial clinical deterioration during chelation therapy.
Seafood rich in organic mercury should of course be avoided. Predators such as sharks and tuna typically have increased mercury concentrations compared with herbivorous fishes.
In some studies, the levels of mercury in shark, swordfish, and large tuna steaks exceeded the Food and Drug Administration (FDA) safety limit of 1 part per million. However, most other fish sold in the United States have clearly lower levels of approximately 0.3 part per million.
Because of the high morbidity and mortality rates associated with methyl mercury poisoning, especially in utero, pregnant women and nursing mothers should avoid consuming larger fish, because their mercury concentrations tend to be higher than those in smaller fish.
Deterrence and Prevention
Workplace hygiene and careful monitoring and disposal of industrial waste are equally important in the prevention of mercury poisoning.
Because of the high morbidity and mortality rates associated with methyl mercury poisoning, especially in utero, pregnant women and nursing mothers should avoid consuming larger fish because their mercury concentrations tend to be higher than those in smaller fish.
Minamata disease can be prevented by reducing or eliminating one's consumption of fish caught from bodies of water that are contaminated with high concentrations of mercury.
Other forms of mercury exposure, such as elemental mercury vapor inhalation, occur when people vacuum or sweep mercury spills in an enclosed space. The proper authorities must handle any spill with the appropriate mercury decontamination kits and procedures.
Significant oral ingestion of elemental mercury may lead to significant environmental contamination as the mercury is passed, essentially unabsorbed, through the GI tract and expelled in the feces.
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