Bismuth toxicity

Background

• Heavy Metal
• Available in two forms
  • Elemental
    • Nontoxic
  • Bismuth Salts
    • Uses
      • Oral preparations for traveler's diarrhea, nausea, and vomiting
      • Bismuth-impregnated surgical packing pastes for ileostomies and colostomies
      • Gastric ulcers
    • Cause toxicity

Toxicokinetics

• Poorly understood due to lack of data
• Low absorption in the GI tract, approximately 0.2% is systemically absorbed
• 90% excreted from kidneys
• Levels may be increased in those taking PPI
  • Ranitidine does not alter the absorption of bismuth

Clinical Features

Acute

• Abdominal pain
• Oliguria
• Acute tubular necrosis and renal failure

Chronic

• Diffuse progressive encephalopathy
• Neurobehavioral changes
  • Apathy
  • Irritability
  • Poor concentration
  • Worsened short term memory
  • Visual hallucinations
• Movement disorders
  • Myoclonus
  • Ataxia
  • Tremors
• Pigmentation of skin and oral mucosa
• Seizure
• Coma and death

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

Encephalopathy

• Viral encephalopathy
• Ethanol withdrawal
• Creutzfeld-Jacob disease
• Lithium toxicity
• Neurodegenerative leukoencephalopathies
• Nonketotic hyperosmolar coma
• Postanoxic encephalopathies
• Progressive multifocal ataxia

Evaluation

• Need to have high index of suspicion
• BMP
• CBC
• Urinalysis
• CT head for cases of encephalopathy
  • May show diffuse cortical hyperdensity of the grey matter
• Salicylate level
  • In the United States bismuth subsalicylate is the most common oral compound, and up to 90% of salicylate is absorbed
• EEG

Management

• Supportive care
• Consider whole bowel irrigation
• Chelation
  • Limited data to support its use
  • Exact timing and dosages are unknown
  • Dimercaprol (BAL)
    • Undergoes biliary elimination which is useful in those with renal insufficiency
    • Benefits shown in experimental models

Disposition

• Admission if evidence of renal failure or encephalopathy manifestations
• Consult Toxicology or poison control

See Also

• Toxicology (main)

References

Rao, R. Bismuth. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1233-1236