Silver toxicity

Background

• Silver exposure is typically seen in workplace environments, herbal supplements, and other products
• Exposure is usually topical, but can also include inhalation, and ingestion
• Common work place environments include
  • Silver nitrate manufacturing
    • Used in manufacturing mirrors, inks, dyes, germicides, antiseptics, and analytical reagents
• Other possible sources of exposure
  • Acupuncture needles
  • Silver jewelry
  • Herbal supplements
  • Silver sulfadiazine

Clinical Features

• Typically occur as chronic exposure
• Skin discoloration (Argyria)
  • Permanent bluish-gray discoloration thought to be due to increased melanin production

Significant Toxicity

• Rare
• 50 mg IV is considered fatal
• Thought to be related to blockade of Na-K-ATPase
• Pulmonary Edema
• Hemorrhage
• Necrosis of bone marrow, liver, and kidneys

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

• Usually a clinical diagnosis
• Serum and urine levels can be sent
  • Serum <1 µg/L (<9 nmol/L)
  • Urine (24 hour) <2 µg/L (<18 nmol/L)

Management

• Argyria
  • Topical hydroquinone 5%
  • Sunscreen to prevent further pigmentation
• Silver Ingestion
  • Supportive Care
• Silver salt ingestion
  • treat as caustic ingestion
• Burns from silver salt
  • treat as chemical burns

Disposition

• Discharge unless shows signs of systemic toxicity

References

Lai Becker M., Burns Ewald M. Silver. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1321-1325