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==Background==
==Background==
*Orthopedic hip prostheses contain cobalt and are a possible source of toxicity.
*Cobalt is essential for life as a catalytic center for vitamin B12. Toxicity is rare.
*Cobalt toxicity has been reported through the following exposures:<ref>Simonsen, L., 2012. Cobalt metabolism and toxicology—A brief update.</ref>
**Orthopedic hip prostheses containing cobalt
**Work-related cobalt exposure
**Excessive drinking of beer containing cobalt sulfate


==Clinical Features<ref>Devlin, J., 2021. Clinical Features, Testing, and Management of Patients with Suspected Prosthetic Hip-Associated Cobalt Toxicity: a Systematic Review of Cases.</ref>==
==Clinical Features<ref>Devlin, J., 2021. Clinical Features, Testing, and Management of Patients with Suspected Prosthetic Hip-Associated Cobalt Toxicity: a Systematic Review of Cases.</ref>==

Revisión del 18:47 28 jun 2021

Background

  • Cobalt is essential for life as a catalytic center for vitamin B12. Toxicity is rare.
  • Cobalt toxicity has been reported through the following exposures:[1]
    • Orthopedic hip prostheses containing cobalt
    • Work-related cobalt exposure
    • Excessive drinking of beer containing cobalt sulfate

Clinical Features[2]

  • Neurologic Dysfunction
    • Hearing impairment
    • Cognitive impairment
    • Parasthesias
  • Cardiovascular Dysfunction
  • Thyroid Dysfunction

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

Management

Disposition

See Also

External Links

References

  1. ↑ Simonsen, L., 2012. Cobalt metabolism and toxicology—A brief update.
  2. ↑ Devlin, J., 2021. Clinical Features, Testing, and Management of Patients with Suspected Prosthetic Hip-Associated Cobalt Toxicity: a Systematic Review of Cases.
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