Cadmium toxicity: Difference between revisions
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===Ingestion=== | ===Ingestion=== | ||
*[[Activated charcoal]] or lavage | *[[Activated charcoal]] or [[gastric lavage]] | ||
*Volume resuscitation to counter fluid losses | *[[IVF|Volume resuscitation]] to counter fluid losses | ||
*No role for hemodialysis | *No role for [[hemodialysis]] | ||
==Disposition== | ==Disposition== | ||
Revision as of 00:09, 9 March 2021
Background
- Used in electroplating, soldering, pigments, and plastics
- Once absorbed, cadmium distributes to most major organs, however it has a predilection for the liver and kidneys
Routes of exposure
- Inahlation (up to 25%)
- Cigarette smoking, occupational exposure
- Particle size influences the amount absorbed
- Smaller particles are more likely to penetrate the alveolar-capillary membrane
- Gastrointestinal (1-10%)
- Cadmium is ubiquitous in food systems
- Total daily amount ingested is influenced by a variety of factors
- Reduced total body iron stores leads to upregulation of the gene that encodes for DMT1, a heavy metal transporter located on the luminal side of enterocytes. Consequently, more cadmium is absorbed from the gastrointestinal tract. [1]
- In certain parts of Japan, consumption of cadmium ranges from 59 to 113 mcg per day, which is more than twice the daily average of individuals in Europe. This is in large part due to rice irrigated with cadmium-contaminated water. [2]
- Dermal (less than 1%)
Mechanism of Toxicity
- Inhaled form is 60 times more toxic than ingested form
- Chemical pneumonitis
- Pulmonary edema/hemorrhage
- GI irritation
- Renal tubule damage
Clinical Features
- Local skin and eye irritation
- Cough, wheezing, pulmonary edema
- Nausea, vomiting, diarrhea
- Chronic exposure can lead to bone deposition and "itai-itai" disease
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
Evaluation
- History of exposure and respiratory / gastrointestinal complaints
Management
Inhalation
Ingestion
- Activated charcoal or gastric lavage
- Volume resuscitation to counter fluid losses
- No role for hemodialysis
Disposition
See Also
References
- ↑ Traub, S., & Elinder, C. (2017). Epidemiology and toxicity of cadmium. In G. Curhan (Ed.), UpToDate. UpToDate, Waltham, MA, (Accessed on February 22, 2018).
- ↑ Traub, S., & Elinder, C. (2017). Epidemiology and toxicity of cadmium. In G. Curhan (Ed.), UpToDate. UpToDate, Waltham, MA, (Accessed on February 22, 2018).
- Olson, K. Poisoning and Drug Overdose, 1999.
