DESCRIPTION

The inorganic mercury salts are typically solid compounds used in industrial processes.

FORMS AND USES

• Inorganic mercury compounds are of two types.
• Mercuric compounds include mercuric chloride, acetate, arsenate, bromide, chloride, cyanide, iodide, nitrate, oxide, oxycyanide, potassium cyanide, potassium iodide, and mercuric sulfide.
• Mercurous compounds include mercurous acetate bromide, chloride (calomel), iodide, nitrate, oxide, sulfate, and ammoniated mercury.

TOXIC DOSE

The potentially lethal dose of mercuric chloride is 10 to 50 mg/kg orally; mercuric salts are more toxic than mercurous salts.

PATHOPHYSIOLOGY

• Mercury acts by binding to enzyme and protein sulfhydryl groups, producing cell dysfunction and death.
• Inorganic mercury salts have corrosive gastrointestinal effects.

EPIDEMIOLOGY

• Poisoning is uncommon.
• Toxic effects following exposure are typically mild to moderate.
• Death is rare, usually due to large suicidal ingestion.
• Carcinogenesis. Inorganic mercury is characterized as IARC group 3: inadequate human evidence.

CAUSES

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

RISK FACTORS

Pediatric and geriatric patients are considered more sensitive to inorganic mercury exposure.

PREGNANCY AND LACTATION

• Inorganic mercury is a probable teratogen that easily passes placental and blood-brain barriers.
• Mercuric chloride has been associated with spontaneous abortions in humans.

WORKPLACE STANDARDS

• OSHA. TLV TWA: none given. PEL (ceiling) is 0.1 mg/m³ or 12 ppm.
• ACGIH. TLV TWA is 0.025 mg/m³.
• NIOSH. IDLH is 10 mg/m³.

Section Outline:

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

DIFFERENTIAL DIAGNOSIS

• Toxic causes of acute corrosive gastroenteritis include ingestion of acids or alkaline corrosives or another metal salt, such as arsenic or thallium.
• Other causes include any food poisoning or infectious gastroenteritis.

SIGNS AND SYMPTOMS

• Ingestion may cause severe corrosive damage to the gastrointestinal tract, which may be complicated by hemorrhage and shock; acute renal failure may develop within 24 hours.
• Inhalation causes acute respiratory distress.
• Chronic low-level inhalational exposure can produce tremor and neuropsychological changes.

HEENT

• Acute ingestion can cause oral burns.
• Chronic exposure may cause headache, metallic taste, gum swelling, salivation, visual disturbances, decreased visual acuity, and mercurialentis (discoloration of the lens and cornea, usually without visual impairment).

Dermatologic

• Chronic exposure may cause stomatitis and contact dermatitis.
• Acrodynia (pink disease) occurs rarely, primarily in children; leg cramps; painful and peeling skin; and pinkish color of fingers, hands, nose, and feet.

Cardiovascular

Ingestion may cause shock secondary to gastrointestinal hemorrhage.

Pulmonary

Inhalation may quickly produce dyspnea, cough, and chest tightness with edema of the trachea, bronchi, lungs, as well as pulmonary edema or adult respiratory distress syndrome in severe cases.

Gastrointestinal

• Ingestion may cause potentially massive gastrointestinal hemorrhage.
• Gingivitis, stomatitis, dysphagia, hematemesis, nausea, vomiting, abdominal pain, gastrointestinal mucosa necrosis, and diarrhea with melena can occur.

Genitourinary

• Acute exposure may cause proteinuria (albuminuria) and nephrotic syndrome.
• Hematuria, glycosuria, casts, oliguria, and aminoaciduria leading to renal failure may occur; onset is often within 24 hours of ingestion, but may be delayed.
• Chronic exposure may cause membranous glomerulonephropathy with nephrotic syndrome.

Fluids and Electrolytes

Recurrent vomiting or renal failure may cause electrolyte abnormality.

Hematologic

• Acute exposure may cause blood loss secondary to a gastrointestinal hemorrhage.
• Acute severe exposure may be complicated by disseminated intravascular coagulation.

Neurologic

• Acute inhalation exposure may cause tremor, irritability, loss of coordination, confusion, anxiety, and insomnia.
• Hyperreflexia, CNS excitation, and personality changes can occur.
• Irreversible brain damage may result.
• Acute exposure has been reported to cause a syndrome resembling amyotrophic lateral sclerosis; these symptoms may be associated with decreased mental function.
• Chronic exposure may cause personality changes, weakness, tremors, headache, short-term memory loss, decreased appetite, shyness, insomnia, emotional instability, paresthesia, and peripheral neuropathy.

PROCEDURES AND LABORATORY TESTS

Essential Tests

• Whole-blood mercury may be useful in confirming acute exposure if the level is elevated; normal level is below 5 µg/dl.
• Urinary mercury, 24-hour collection, is used for acute or chronic exposure
  • In chronic exposure, no clinical effect is expected with urine mercury levels below 20 µg/L, the normal level.
    • Decreased verbal skills, tremor, 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 inflammation, gingivitis, and marked tremor and CNS dysfunction occur at mercury levels from 500 to 1000 µg/L.
  • In acute exposure, urinary levels are performed serially to assess mercury excretion; they do not correlate well with clinical effects.

Recommended Tests

• Complete blood count (CBC), serum electrolytes, BUN, and creatinine should be assayed to detect anemia or renal injury.
• Abdominal radiographs may help assess adequacy of gastrointestinal decontamination because mercury is radiopaque.
• Electromyography/NCV in symptomatic patients may demonstrate decreased motor and sensory conduction.

Section Outline:

• DIFFERENTIAL DIAGNOSIS
• SIGNS AND SYMPTOMS
  • HEENT
  • Dermatologic
  • Cardiovascular
  • Pulmonary
  • Gastrointestinal
  • Genitourinary
  • Fluids and Electrolytes
  • Hematologic
  • Neurologic
• PROCEDURES AND LABORATORY TESTS
  • Essential Tests
  • Recommended Tests

• Following acute exposure, treatment should focus on hemodynamic support and 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:

• Toxic effects develop.
• Coingestant, drug interaction, or underlying disease presents an unusual problem.

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

• History of inorganic mercury ingestion is obtained.
• Coingestant, drug interaction, or underlying disease presents an unusual problem.

Admission Considerations

Inpatient management is usually warranted if the patient exhibits any symptoms.

DECONTAMINATION

Out of Hospital

• Emesis should not be induced.
• Patient should be removed from source of inhalation exposure.

In Hospital

• Gastric lavage is generally not useful unless the patient presents before vomiting develops.
• One dose of activated charcoal (1-2 g/kg) should be administered without a cathartic if a substantial recent ingestion has occurred and recurrent vomiting has not developed.

ANTIDOTES

Succimer

Succimer is the preferred oral chelating agent.

Indications

Symptomatic acute mercury exposure or increased urinary excretion of mercury.

Contraindications

Known hypersensitivity to succimer.

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 need is indicated by continuing symptoms and elevated mercury levels.

Penicillamine

Indications

• A second line oral agent for symptomatic acute mercury exposure or documented increased urinary excretion of mercury.

Contraindications

Known hypersensitivity to penicillin or penicillamine.

Method of Administration

• Adult dose is 15 to 40 mg/kg per day, up to a maximum of 500 mg four times a day, orally before meals, for 5 to 10 days.
• Pediatric dose is 20 to 30 mg/kg per day, up to 250 to 500 mg/day, given orally once or twice daily before meals, for 5 to 10 days.
• Blood and urine mercury levels should be monitored to determine whether additional courses of chelation are required.

Adverse Effects

Nephrotic syndrome, hypersensitivity reactions, blood dyscrasia, aplastic anemia, agranulocytosis, and various autoimmune responses are possible.

British Anti-Lewisite (BAL)

Indications

• In acute mercury exposures when oral treatment is not possible (e.g., in the case of emesis or gastrointestinal burns), BAL should be considered.

Contraindications

Hypersensitivity to BAL or peanuts, glucose-6-phosphate dehydrogenase deficiency, or hepatic insufficiency contraindicate its use.

Method of Administration

Dose is 2.5 to 5 mg/kg intramuscularly every 4 hours tapering to every 6 to 12 hours over several days, until an oral chelator can be tolerated.

Adverse Effects

Headache, hypertension, pain at injection site, allergic reaction, and fever are possible.

ADJUNCTIVE TREATMENT

Hemodialysis may be needed as supportive therapy of renal failure.

Section Outline:

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

PATIENT MONITORING

• Continuous cardiac and respiratory monitoring should be performed in symptomatic patients following acute exposure.
• In patients with chronic or symptomatic acute exposure, blood and urine mercury levels should be monitored, along with CBC and tests of renal function such as electrolytes, BUN, and creatinine.

EXPECTED COURSE AND PROGNOSIS

• Toxic effects after acute exposure usually improve and may return to baseline.
• Chronic exposure is more likely to produce slow gradual improvement over months and may not improve to baseline.
• Permanent CNS or renal damage is possible in severe cases.

DISCHARGE CRITERIA/INSTRUCTIONS

• From the emergency department. Asymptomatic and reliable patients with acute ingestion may be discharged after 4 to 6 hours of observation and psychiatric evaluation (if needed).
• From the hospital. Patient may be discharged when CNS, pulmonary, and renal injury are stable or improving and management as an outpatient is possible.

Section Outline:

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

DIAGNOSIS

Clinical symptoms must be correlated with history and mercury levels; presence of mercury in blood or urine sample does not necessarily indicate mercury poisoning.

TREATMENT

Side effects from chelation therapy are common; consultation with medical toxicologist is recommended.

Section Outline:

• DIAGNOSIS
• TREATMENT

Toxic effect of other metals: mercury and its compounds.

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

RECOMMENDED READING

Clarkson TW, Hursh JB, Sager PR, Syversen TLM. Mercury. In: Biological monitoring of toxic metals. New York: Plenum, 1988:199-246.

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: Katherine M. Hurlbut