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

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

Evaluation

  • History of exposure and respiratory / gastrointestinal complaints

Management

Inhalation

  • Supplemental oxygen
  • Monitor ABG, check CXR
  • Treat wheezing and pulmonary edema

Ingestion

Disposition

See Also

References

  1. Traub, S., & Elinder, C. (2017). Epidemiology and toxicity of cadmium. In G. Curhan (Ed.), UpToDate. UpToDate, Waltham, MA, (Accessed on February 22, 2018).
  2. 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.