Bismuth toxicity: Difference between revisions
(Created page with "==Background== *Heavy Metal *Available in two forms **Elemental ***Nontoxic **Bismuth Salts ***Uses ****Oral preparations for traveler's diarrhea, nausea, and vomiting ***...") |
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****Gastric ulcers | ****Gastric ulcers | ||
***Cause toxicity | ***Cause toxicity | ||
==Toxicokinetics== | |||
===Toxicokinetics=== | |||
*Poorly understood due to lack of data | *Poorly understood due to lack of data | ||
*Low absorption in the GI tract, approximately 0.2% is systemically absorbed <ref>Hundal O, Bergseth M, Gharehnia B, et al. Absorption of bismuth from two bismuth compounds before and after healing of peptic ulcers. Hepatogastroenterology. 1999;46:2882-2886.</ref> | *Low absorption in the GI tract, approximately 0.2% is systemically absorbed <ref>Hundal O, Bergseth M, Gharehnia B, et al. Absorption of bismuth from two bismuth compounds before and after healing of peptic ulcers. Hepatogastroenterology. 1999;46:2882-2886.</ref> | ||
| Line 16: | Line 17: | ||
*Levels may be increased in those taking PPI | *Levels may be increased in those taking PPI | ||
**Ranitidine does not alter the absorption of bismuth | **Ranitidine does not alter the absorption of bismuth | ||
==Clinical Features== | ==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]] | |||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
{{Heavy metals list}} | |||
===[[Encephalopathy]]=== | ===[[Encephalopathy]]=== | ||
*[[Viral encephalopathy]] | *[[Viral encephalopathy]] | ||
| Line 71: | Line 52: | ||
*[[Postanoxic encephalopathies]] | *[[Postanoxic encephalopathies]] | ||
*[[Progressive multifocal ataxia]] | *[[Progressive multifocal ataxia]] | ||
==Evaluation== | ==Evaluation== | ||
*Need to have high index of suspicion | *Need to have high index of suspicion | ||
*BMP | *BMP | ||
*CBC | *CBC | ||
* | *[[Urinalysis]] | ||
*CT head for cases of encephalopathy | *CT head for cases of encephalopathy | ||
**May show diffuse cortical hyperdensity of the grey matter | **May show diffuse cortical hyperdensity of the grey matter | ||
*Salicylate level | *[[Salicylate]] level | ||
**In the United States bismuth subsalicylate is the most common oral compound, and up to 90% of salicylate is absorbed <ref>Pickering LK, Feldman S, Ericsson CD, Cleary TG. Absorption of salicylate and bismuth from a bismuth subsalicylate containing compound (Pepto- Bismol). J Pediatr. 1981;99:654-656.</ref> | **In the United States [[bismuth subsalicylate]] is the most common oral compound, and up to 90% of salicylate is absorbed <ref>Pickering LK, Feldman S, Ericsson CD, Cleary TG. Absorption of salicylate and bismuth from a bismuth subsalicylate containing compound (Pepto- Bismol). J Pediatr. 1981;99:654-656.</ref> | ||
*EEG | *EEG | ||
==Management== | ==Management== | ||
*Supportive care | *Supportive care | ||
| Line 87: | Line 70: | ||
**Limited data to support its use | **Limited data to support its use | ||
**Exact timing and dosages are unknown | **Exact timing and dosages are unknown | ||
** | **[[Dimercaprol]] (BAL) | ||
***Undergoes biliary elimination which is useful in those with renal insufficiency | ***Undergoes biliary elimination which is useful in those with renal insufficiency | ||
***Benefits shown in experimental models | ***Benefits shown in experimental models | ||
| Line 93: | Line 76: | ||
==Disposition== | ==Disposition== | ||
*Admission if evidence of renal failure or encephalopathy manifestations | *Admission if evidence of renal failure or encephalopathy manifestations | ||
*Consult Toxicology or | *Consult Toxicology or [[poison control]] | ||
==See Also== | |||
*[[Toxicology (main)]] | |||
==References== | ==References== | ||
<references/> | <references/> | ||
Rao, R. Bismuth. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1233-1236 | Rao, R. Bismuth. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1233-1236 | ||
[[Category:Toxicology]] | |||
Latest revision as of 21:51, 8 March 2021
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
- Uses
- Elemental
Toxicokinetics
- Poorly understood due to lack of data
- Low absorption in the GI tract, approximately 0.2% is systemically absorbed [1]
- 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
Differential Diagnosis
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 [2]
- 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
References
- ↑ Hundal O, Bergseth M, Gharehnia B, et al. Absorption of bismuth from two bismuth compounds before and after healing of peptic ulcers. Hepatogastroenterology. 1999;46:2882-2886.
- ↑ Pickering LK, Feldman S, Ericsson CD, Cleary TG. Absorption of salicylate and bismuth from a bismuth subsalicylate containing compound (Pepto- Bismol). J Pediatr. 1981;99:654-656.
Rao, R. Bismuth. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1233-1236
