What is Bismuth Toxicity?
Bismuth is a heavy metal found in a variety of everyday products, including cosmetics, fire sprinklers, and perhaps most famously, over-the-counter stomach-soothing medications like bismuth subsalicylate [1.5.8, 1.3.6]. While elemental bismuth is considered nontoxic, certain bismuth salts can cause toxicity if they accumulate in the body [1.5.2]. Toxicity is rare because less than 1% of ingested bismuth is typically absorbed, with the rest being excreted [1.3.5, 1.5.2]. However, prolonged use of high doses can lead to a dangerous buildup of the metal, primarily affecting the brain and kidneys [1.6.5, 1.4.1]. Chronic exposure is more often linked to neurotoxicity, while acute overdose is more likely to cause nephrotoxicity (kidney damage) [1.6.5].
Common Sources of Bismuth Exposure
- Medications: Long-term, high-dose use of oral medications containing bismuth subsalicylate or other bismuth salts for issues like traveler's diarrhea, nausea, or gastric ulcers is a primary cause [1.5.2, 1.3.4].
- Occupational Exposure: While rare, individuals working in industries that use bismuth for alloys, solders, or ceramics could be at risk [1.3.9, 1.5.2].
- Surgical Pastes: Bismuth-impregnated pastes used in surgical dressings have been reported to cause toxicity [1.5.2, 1.5.9].
- Cosmetics: Some cosmetics like lipsticks and eyeshadows use bismuth compounds for their pearlescent quality [1.3.9, 1.5.6].
Symptoms of Bismuth Toxicity
The clinical presentation of bismuth toxicity can be divided into acute and chronic symptoms [1.3.1]. A hallmark of chronic toxicity is a progressive encephalopathy (brain disease) that can develop over weeks or months [1.3.5].
Acute Symptoms
- Abdominal pain and nausea [1.4.9, 1.3.1]
- Acute kidney injury, potentially leading to renal failure [1.3.1, 1.3.8]
- Oliguria (low urine output) [1.3.1]
Chronic Symptoms (Bismuth Encephalopathy)
- Neurological Changes: The most prominent feature is a subacute, progressive encephalopathy [1.6.7]. This often starts with a prodromal phase of mood changes, anxiety, irritability, and poor concentration [1.3.5, 1.3.1].
- Movement Disorders: This can rapidly escalate to include ataxia (unsteady gait), tremors, and myoclonus (sudden, involuntary muscle jerks) [1.3.1, 1.3.4].
- Cognitive Decline: Severe confusion, memory difficulty, and disorientation are common [1.3.4, 1.3.1]. In severe cases, it can progress to coma [1.3.1].
- Other Signs: A blue-black line on the gums (bismuth line) and darkening of the tongue are classic, though less common, signs [1.5.3, 1.3.2].
Diagnosing Bismuth Toxicity
Diagnosis requires a high index of suspicion, especially when a patient presents with rapidly progressive encephalopathy and myoclonus [1.3.4]. A careful medication history is critical, as patients may not consider over-the-counter products to be medically relevant [1.6.7].
- Blood and Urine Tests: Elevated levels of bismuth in the blood and urine confirm the diagnosis [1.4.4]. Toxicity is generally associated with blood levels above 50 µg/L [1.3.2].
- Imaging: While often normal, a CT scan of the head may show diffuse hyperdensity (brightness) of the grey matter due to bismuth accumulation [1.4.1, 1.6.7]. Brain MRIs can sometimes show atrophy in later stages [1.6.7].
- Electroencephalogram (EEG): An EEG typically shows generalized slowing, which is indicative of a diffuse encephalopathy but is not specific to bismuth toxicity [1.3.4, 1.6.7].
How to Treat Bismuth Toxicity: Primary Strategies
The cornerstone of treatment is immediate cessation of exposure to the bismuth-containing product [1.4.4, 1.5.1].
1. Removal of Bismuth Source and Supportive Care
The most critical step is to identify and eliminate the source of bismuth exposure [1.2.1]. For most patients, particularly those with encephalopathy, this discontinuation combined with supportive care is the primary treatment [1.6.3, 1.4.7]. Supportive measures include:
- Intravenous (IV) fluids to maintain hydration and support kidney function [1.2.1, 1.4.6].
- Management of symptoms, such as using medications to control seizures or agitation [1.2.1, 1.6.1].
- Hemodialysis in cases of severe acute renal failure to help filter the blood [1.4.6, 1.2.2].
- Gastrointestinal decontamination (e.g., gastric lavage or activated charcoal) may be considered in cases of recent, large, acute ingestion [1.4.2, 1.5.3].
2. Chelation Therapy
Chelation therapy involves administering agents that bind to heavy metals in the bloodstream, forming a compound that can be more easily excreted from the body [1.2.6]. The role of chelation in bismuth toxicity is not well-established, and its use is controversial and typically reserved for severe cases in consultation with a toxicologist [1.2.1, 1.4.7]. Some evidence suggests certain chelators might worsen neurotoxicity by redistributing bismuth into the brain [1.2.2]. Therefore, it should only be considered in life-threatening situations [1.2.2].
| Chelating Agent | Administration | Notes on Use in Bismuth Toxicity |
|---|---|---|
| Dimercaprol (BAL) | Intramuscular Injection [1.2.3] | Has been used for bismuth poisoning and undergoes biliary elimination, which is useful in patients with renal failure [1.4.8, 1.4.1]. However, its effectiveness is not definitively proven and it can be toxic itself [1.6.3, 1.4.5]. |
| Succimer (DMSA) | Oral [1.2.3] | DMSA is a dithiol compound shown to be effective in animal studies [1.2.5]. However, some case reports describe clinical deterioration with its use, possibly due to bismuth redistribution to the brain [1.2.2]. |
| DMPS | Oral or IV | Similar to DMSA, DMPS is a dithiol compound that may be effective but also carries a risk of worsening neurological symptoms [1.4.5, 1.2.2]. |
| Penicillamine | Oral [1.2.3] | Sometimes used for bismuth toxicity, but its efficacy in humans has not been clearly demonstrated [1.2.3, 1.6.3]. |
Prognosis and Recovery
For most patients, simply stopping the bismuth exposure leads to a gradual but full recovery over weeks to months [1.6.7, 1.4.7]. Neurological symptoms like confusion and myoclonus typically resolve as blood bismuth levels fall [1.3.2, 1.6.8]. However, in very severe cases, some residual neurological deficits may remain, and death has been reported [1.3.2, 1.6.4]. Early recognition and treatment are key to preventing long-term complications or death [1.6.2].
Conclusion
Treating bismuth toxicity begins with the fundamental step of removing the source of exposure. For the vast majority of cases, this action, supplemented by supportive medical care to manage symptoms like kidney dysfunction and seizures, is sufficient to ensure a full recovery over several months [1.6.7]. While chelation therapy exists as an option, its use is debated and reserved for the most severe poisonings due to the potential risk of exacerbating neurological symptoms [1.2.2, 1.4.7]. Awareness of the risks associated with long-term use of bismuth-containing products is the most effective tool for prevention [1.5.1].
For more information from an authoritative source, you can visit Bismuth Toxicity on WikEM. [1.2.1]
