DESCRIPTION

Elemental mercury (Hg) exists as a silver-colored liquid. Inorganic and organic mercury are covered in following chapters.

FORMS AND USES

• Other names for elemental mercury include colloidal mercury, hydrargyrum, liquid silver, metallic mercury, and quicksilver.
• It is used in dental amalgams, thermometers, calibration of instruments, ceramics, electrical apparatus, fluorescent light bulbs, and silver and gold extraction, among others.

TOXIC DOSE

• Death has occurred after inhalation of fumes, usually in a closed space.
• The lethal concentration is unknown.

PATHOPHYSIOLOGY

• Elemental mercury is volatile at room temperature and easily inhaled, with 80% of the inhaled dose absorbed.
• Toxicity is caused by binding to enzyme and protein sulfhydryl groups.
• Toxicity to the respiratory system is the major acute life threat; a spectrum ranging from pneumonitis to necrotizing bronchiolitis to pulmonary edema occurs, depending on severity of exposure.
• Elemental mercury is very poorly absorbed by ingestion or across intact skin; however, inflammatory bowel disease or gastrointestinal obstruction may allow clinically significant absorption to occur.

EPIDEMIOLOGY

• Poisoning is common.
• Toxic effects following exposure are typically mild to moderate.
• Death is rare.

CAUSES

• Toxicity is usually the result of an accidental incident.
• Child abuse or neglect must be considered if the patient is less than 1 year of age; suicide attempt if the child is over 6 years of age.

RISK FACTORS

• Pediatric patients are considered more sensitive to elemental mercury exposure.
• Geriatric patients are considered more sensitive to elemental mercury exposure due to possible reduced functioning of renal, pulmonary, and CNS systems.

PREGNANCY AND LACTATION

Mercury is a probable teratogen that easily passes placental and blood-brain barriers.

WORKPLACE STANDARDS

• ACGIH. TLV TWA is 0.025 mg/m³.
• OSHA. Not listed.
• NIOSH. REL TWA is 0.05 mg/m³; IDLH is 10 mg/m³.
• NIOSH. REL is 0.05 mg/m³; IDLH 10 mg/m³.

Section Outline:

• DESCRIPTION
• FORMS AND USES
• TOXIC DOSE
• PATHOPHYSIOLOGY
• EPIDEMIOLOGY
• CAUSES
• RISK FACTORS
• PREGNANCY AND LACTATION
• WORKPLACE STANDARDS

A thorough history of exposure generally reveals the source of toxicity.

DIFFERENTIAL DIAGNOSIS

Toxic causes of acute pulmonary injury and altered mental status include smoke inhalation and other respiratory irritants (e.g., chlorine, nitrogen dioxide).

SIGNS AND SYMPTOMS

• Acute inhalation is most common and may produce pulmonary edema within hours of exposure.
• Chronic respiratory exposure primarily produces CNS effects.
• Intravenous, intramuscular, or subcutaneous injection allows prolonged absorption and may lead to chronic poisoning.

HEENT

Headache, metallic taste, visual disturbances, weakness, and chills may occur after acute exposure.

Dermatologic

• Stomatitis and contact dermatitis may develop following acute exposure or during chronic exposure.
• Acrodynia (pink disease) is a rare effect of chronic exposure featuring pink discoloration and desquamation of fingers, nose, and toes; irritability; sweating; and miliary-type diffuse rash.

Pulmonary

Dyspnea, cough and chest tightness may be seen acutely after inhalation, followed by bronchitis, pneumonitis, necrotizing bronchiolitis, and pulmonary edema in more serious cases.

Gastrointestinal

Gingivitis, stomatitis, nausea, vomiting, abdominal pain, and diarrhea may develop with chronic exposure.

Hepatic

Liver enzyme abnormalities may occur.

Genitourinary

• Proteinuria and nephrotic syndrome have been reported.
• Acute tubular necrosis and renal failure may occur.

Neurologic

Acute inhalation may cause tremor, confusion, and excitability.

• Early symptoms may be nonspecific: malaise, blurred vision, or hearing loss.
• Irreversible brain damage may result after massive exposure.
• Chronic exposure may produce personality changes, weakness, tremor, headache, short-term memory loss, decreased appetite, insomnia, emotional instability, paresthesia, and sensory and motor nerve conduction delays.
• Chronic intoxication from inhalation may produce erethism, the classic triad of gingivostomatitis, tremor, and neuropsychiatric effects (excitability, agitation, and withdrawal).

PROCEDURES AND LABORATORY TESTS

Essential Tests

No tests may be needed in asymptomatic patients or following ingestion.

Recommended Tests

• Whole blood mercury may be useful in confirming acute exposure if level is elevated; normal level is below 1.5 µg/dl.
• Urinary mercury, 24-hour collection, is used for chronic exposure.
  • Recent ingestion of seafood may temporarily increase urinary mercury level. This form of mercury is not toxic.
  • There is no clinical effect from urine mercury levels below 20 µg/L.
  • Decreased verbal skills and decreased nerve conduction may be evident at mercury levels from 20 to 100 µg/L.
  • Irritability, depression, memory loss, tremor, CNS dysfunction, and kidney damage occur at mercury levels ranging from 100 to 500 µg/L.
  • Kidney damage, swollen gums, and marked tremor and CNS dysfunction occur at mercury levels from 500 to 1,000 µg/L.
• Serum electrolytes, BUN, and creatinine should be assayed to evaluate renal injury.
• Elemental mercury is radio-opaque and is often apparent on radiographs.

Section Outline:

• DIFFERENTIAL DIAGNOSIS
• SIGNS AND SYMPTOMS
  • HEENT
  • Dermatologic
  • Pulmonary
  • Gastrointestinal
  • Hepatic
  • Genitourinary
  • Neurologic
• PROCEDURES AND LABORATORY TESTS
  • Essential Tests
  • Recommended Tests

• Treatment should focus on supportive respiratory care after inhalation exposure and on initiating early chelation.
• Dose and time of exposure should be determined for all substances involved.

DIRECTING PATIENT COURSE

The health-care provider should call the poison control center when:

• Respiratory symptoms, altered mental status, or other severe effects are present.
• Toxic effects are not consistent with elemental mercury poisoning.
• Coingestant, drug interaction, or underlying disease presents an unusual problem.

The patient should be referred to a health-care facility when:

• Attempted suicide or homicide is possible.
• Patient or caregiver seems unreliable.
• Toxic effects develop.
• Coingestant, drug interaction, or underlying disease presents an unusual problem.

Admission Considerations

Inpatient management is warranted if the patient exhibits any symptoms after mercury inhalation or injection.

DECONTAMINATION

Out of Hospital

• Emesis should not be induced due to low toxicity of ingestion.
• Patient must be removed from source of mercury fumes.
• Clean-up of large elemental mercury spills should not be attempted except by the local fire department; elemental mercury should not be vacuumed because of mercury aerosol production.

In Hospital

Emesis, gastric lavage, and activated charcoal are not needed, unless coingestant is suspected.

ANTIDOTES

Specific chelators are available for mercury poisoning (see individual chelator chapters in SECTION III for further details).

Succimer

Succimer is the preferred chelating agent.

• Indications. Succimer should be considered for symptomatic acute mercury exposure or increased urinary excretion of mercury.
• Contraindications. Known hypersensitivity to succimer contraindicates its use.
• Method of administration
  • Adult dose is 10 mg/kg (350 mg/m² for a child) orally three times a day for 5 days, followed by 10 mg/kg twice a day for 14 days; a repeat course may be given if the need is indicated by continuing symptoms and elevated urinary mercury levels.

Penicillamine

• Indications. Penicillamine also may be considered for symptomatic acute mercury exposure or increased urinary excretion of mercury.
• Contraindications. Known hypersensitivity to penicillin or penicillamine contraindicates its use.
• Method of administration
  • Adult dose is 15 to 40 mg/kg/day, up to a maximum of 250 to 500 mg orally four times a day, before meals.
  • Pediatric dose is 20 to 30 mg/kg per day, given orally once or twice daily before meals, for 5 to 10 days.
  • Urinary excretion of mercury should be monitored; if urine mercury falls rapidly, body burden is probably small.
  • After 10 days, baseline urine mercury should be repeated; if it is still elevated, another course of chelation may be required.
• Adverse effects. Nephrotic syndrome, hypersensitivity reactions, transient blood dyscrasia, aplastic anemia, agranulocytosis, and various autoimmune responses are possible.

British Anti-Lewisite

In the rare case in which oral treatment is not possible, parenteral therapy with British anti-Lewisite should be considered.

ADJUNCTIVE TREATMENT

Pulmonary edema occurs rarely and is managed as noncardiogenic pulmonary edema (see SECTION II, Pulmonary Edema chapter).

Section Outline:

• DIRECTING PATIENT COURSE
  • Admission Considerations
• DECONTAMINATION
  • Out of Hospital
  • In Hospital
• ANTIDOTES
  • Succimer
  • Penicillamine
  • British Anti-Lewisite
• ADJUNCTIVE TREATMENT

PATIENT MONITORING

• Clinical symptoms should be monitored closely.
• Serial urine mercury levels are used to guide therapy.

EXPECTED COURSE AND PROGNOSIS

• Ingestion. Unless a preexisting gastrointestinal obstruction or perforation is present, ingestion causes no effects.
• Inhalation
  • High-concentration exposure rapidly produces pulmonary symptoms; prognosis depends on the degree of pulmonary injury.
  • Permanent CNS, pulmonary, or renal system damage may occur in severe cases.
  • Less severe exposure may produce systemic mercury poisoning, which will take weeks or months to resolve.
• Chronic exposure is possible; symptoms of CNS, respiratory tract, and renal damage may be reversible if exposure is stopped before severe damage develops.

DISCHARGE CRITERIA/INSTRUCTIONS

From emergency department or hospital. After inhalation exposure, patient may be discharged when asymptomatic and when major organ involvement has been assessed and does not require hospitalization.

Section Outline:

• PATIENT MONITORING
• EXPECTED COURSE AND PROGNOSIS
• DISCHARGE CRITERIA/INSTRUCTIONS

A single elevated mercury level does not prove toxicity in an asymptomatic patient.

FOLLOW-UP

In patients with inflammatory bowel disease, fistula formation may absorb elemental mercury if mercury remains in the gastrointestinal tract due to obstruction.

Toxic effect of other metals: mercury and its compounds.

See Also: SECTION II, Pulmonary Edema chapter; SECTION III, British Anti-Lewisite, Penicillamine, Succimer; and SECTION IV, Mercury—Inorganic chapters.

RECOMMENDED READING

Goyer RA. Toxic effect of metals. In: Klaassen CD, Amdur MO, Doull J, eds. Casarett and Doull's toxicology: the basic science of poisons, 5th ed. New York: McGraw-Hill, 1996:712.

US Department of Health and Human Services. ATSDR case studies in environmental medicine: mercury toxicity, monograph 17, March 1992.

Author: Alvin C. Bronstein

Reviewer: Luke Yip