Antimony toxicity

Background

• Antimony is a metalloid and will react as a metal and nonmetal
  • Shares many similar properties with arsenic
• Used to treat leishmaniasis and schistosomiasis
  • Most reported cases are due to complication of treatment
• Most common forms used for treatment are trivalent and pentavalent compounds
• Additional exposure occur from industrial exposures as inhalation of antimony dusts or fumes during processing
• Antimony is thought to exert its toxic effects due to inactivation of various thiol-containing proteins and enzymes

Stibine

• Most toxic form of antimony
• Colorless gas that is formed when antimony reacts with hydrogen
  • Can result when mixing drain cleaners containing sodium hydroxide in areas with antimony ore
• Can result in massive hemolysis

Toxicokinetics

• Absorption
  • Inhalation
  • Ingestion
  • Transcutaneous
  • Bioavailability is 15-50%
• Distribution
  • Predominately in highly vascular organs
  • Trivalent form seen in red blood cells
  • Pentavalent form accumulates in the liver
• Metabolism
  • Pentavalent form is converted to trivalent form in the liver
• Excretion
  • Trivalent form undergoes enterohepatic recirculation
  • Renal
    • Trivalent has a slow elimination with approximately 10% cleared within the first 24 hours
    • Pentavalent will have approximately 50-60% cleared within the first 24 hours

Clinical Features

Clinical features can range from mild local irritation to organ dysfunction

• GI
  • Anorexia
  • Nausea/vomiting
    • Leading to profound volume depletion
  • Abdominal pain
  • Diarrhea
  • Hemorrhagic gastritis
  • Pancreatitis
  • Can react with water in salvia, producing sufficient hydrochloric acid to cause GI burns
• CV
  • Decreases myocardial contraction
  • Decreased systolic pressure through decreased coronary vasomotor tone
  • Bradycardia
  • EKG changes
    • More common in pentavalent preparations
    • Prolonged QT
    • Inversion or flattening of T waves
    • Torsades de pointes
• Pulmonary
  • Local irritation
    • Laryngitis and Tracheitis
  • Antimony pneumoconiosis
    • Chronic exposure
    • Cough, wheezing, and exertional dyspnea
    • CXR showing diffuse, dense, punctate non-confluent opacities in the middle and lower lobes
• Renal
  • Proteinuria
  • Increased BUN
  • ATN
  • Renal failure
• Hepatic
  • Elevated aminotransferase
  • Hepatic necrosis
• Hematologic
  • Thrombocytopenia
  • Leukopenia
  • Severe anemia seen in HIV patients being treated for leishmaniasis
• Dermatologic
  • Antimony Spots
    • Papules and pustules around sweat glands
    • Can resemble varicella
  • Eczema
  • Lichenification
• Musculoskeletal
  • Myalgias
  • Arthralgias
• Reproductive
  • Increased risk of spontaneous abortion and premature labor
• Ocular
  • Local irritation
  • Conjunctivitis
  • Photophobia
  • Corneal burn

Background

Heavy metal toxicity results from exposure to metals like lead, mercury, arsenic, or cadmium, which interfere with cellular function. Exposure may occur occupationally, environmentally, through ingestion, or from alternative medicines. Chronic toxicity can present insidiously, while acute toxicity may mimic sepsis or encephalopathy. Diagnosis is often delayed due to nonspecific symptoms.

Clinical Features

Symptoms depend on the metal and exposure duration but may include:

Neurologic: Peripheral neuropathy, confusion, tremor, encephalopathy

GI: Abdominal pain, nausea, vomiting, diarrhea, anorexia

Heme: Anemia (especially microcytic or hemolytic), basophilic stippling (lead)

Renal: Tubular dysfunction, proteinuria, Fanconi syndrome

Dermatologic: Mees’ lines (arsenic), hyperpigmentation, hair loss

Others: Fatigue, weight loss, hypertension (cadmium), immunosuppression

Differential Diagnosis

Sepsis or systemic inflammatory response

Drug toxicity or overdose

Metabolic disorders (e.g., porphyria, uremia)

Psychiatric illness (if symptoms are vague or bizarre)

Neurologic diseases (e.g., Guillain-Barré, MS, Parkinson’s)

Vitamin deficiencies (e.g., B12, thiamine)

Evaluation

Workup

History: Occupational exposures, home remedies, hobbies (e.g., jewelry making, battery recycling), diet, water source, imported goods

Labs:

• CBC, CMP, urinalysis
• Blood lead level, serum/urine arsenic, mercury, or cadmium (based on suspicion)
• Urine heavy metal screen (note: spot testing may require creatinine correction)

Imaging: Abdominal X-ray (radiopaque material in GI tract, especially with lead)

EKG: Evaluate for QT prolongation or arrhythmias in severe cases

Diagnosis

Confirmed by elevated blood or urine levels of the specific metal in the context of clinical findings. Hair and nail testing are unreliable for acute toxicity. Interpret results with toxicologist input if possible.

Management

Remove the source of exposure (e.g., occupational control, GI decontamination if recent ingestion)

Supportive care: IV fluids, seizure control, electrolyte repletion

Chelation therapy (in consultation with toxicology or Poison Control):

Lead: EDTA, dimercaprol (BAL), succimer

Mercury/arsenic: Dimercaprol or DMSA

Cadmium: No effective chelation—focus on supportive care

Notify local public health authorities if exposure source is environmental or occupational

Disposition

Admit if symptomatic, unstable, or requiring chelation

Discharge may be appropriate for asymptomatic patients with low-level exposure and outpatient follow-up

Arrange toxicology or environmental medicine follow-up for source control and serial testing

See Also

• Aluminum toxicity
• Antimony toxicity
• Arsenic toxicity
• Barium toxicity
• Bismuth toxicity
• Cadmium toxicity
• Chromium toxicity
• Cobalt toxicity
• Copper toxicity
• Gold toxicity
• Iron toxicity
• Lead toxicity
• Lithium toxicity
• Manganese toxicity
• Mercury toxicity
• Nickel toxicity
• Phosphorus toxicity
• Platinum toxicity
• Selenium toxicity
• Silver toxicity
• Thallium toxicity
• Tin toxicity
• Zinc toxicity

Evaluation

• BMP
• CBC
• Urinalysis
• EKG to look for cardiac affects of antimony
• Cardiac monitor to assess for arrhythmia
• CXR
• Cases of stibine
  • Add type and cross, and coagulation factors as transfusions are likely required
• Serum level 0.8 - 3 μg/L (6.6-24.6 nmol/L)
• Urine level (24 hr) 0.5-6.2 μg/L (4.1-50.1 nmol/L)

Management

• Consult Toxicology or poison control
• Decontamination
  • Gastric lavage may be of benefit
  • Activated charcoal
    • Additionally may use multi-dose activated charcoal due to enterohepatic circulation
  • Dermal exposure
    • Irrigation with soap and water
• Supportive Care
  • Fluid resuscitation
  • Electrolyte repletion
  • Monitor I/Os
  • Antiemetics
  • Blood transfusions based on institutional criteria
• Chelation
  • Dimercaprol
    • 200-600mg/d IM shown in a case series to increase urinary excretion of antimony₁
  • Succimer
  • Dimercaptopropane-sulfonic acid (DMPS)
  • All have shown improved survival in animal models

Stibine

• Place on high flow oxygen
• Consider need for exchange transfusion to remove stibine-hemoglobin complexes

Disposition

• Will require admission to a monitored bed, likely ICU.

See also

• Toxicology (main)

References

Tarabar, A. Antimony. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1207-1213

1. 1. Lauwers LF, Roelants A, Rosseel PM, et al. Oral antimony intoxications in man. Crit Care Med. 1990;18:324-326.