Selenium toxicity

Background

• Essential trace element
• Deficiency found to be the cause of Keshan disease and Kashin-beck disease
• Recommended daily dose is 5 μg/d

Uses

• Gun bluing solution
• Dietary supplement
• Antidandruff shampoo
• Glass decolorizer and manufacturing
• Insecticide
• Vulcanization of rubber
• Used in copper refineries

Toxicokinetics

• Cofactor in glutathione peroxidase
• Varied GI absorption
• Minimal dermal absorption
• Bioavailability (Lowest - Highest)
  • Elemental selenium
  • Inorganic selenite and selenate salt
  • Selenious acid
• Limited data on toxicokinetics as it varies amongst compounds

Clinical Features

Acute

• Oral exposure
  • Triphasic course
  • Rapid and fulminant
    • Symptoms can occur within minutes and death can occur with 1-4 hours
  • GI
    • Abdominal pain
    • Diarrhea
    • Nausea and vomiting
    • Caustic esophageal and gastric burns
    • Some patients have a garlic odor
  • Myopathic
    • Weakness
    • Hyporeflexia
    • Myoclonus
    • Fasciculations
    • Elevated CPK
    • Renal insufficiency
    • Delirium and coma
  • Circulatory symptoms
    • Dyspnea
    • Chest pain
    • Tachycardia
    • Hypotension
      • Toxic cardiomyopathy
    • EKG abnormalities
      • ST elevation
      • Prolonged QT
      • T wave inversions
    • Pulmonary edema
    • Ventricular dysrhythmias
    • Myocardial infarction
    • Mesenteric infarction
    • Metabolic acidosis
• Inhalation
  • Hydrogen selenide
    • Throat and eye pain
    • Rhinorrhea
    • Wheezing
    • Pneumomediastinum
    • Restrictive and obstructive pulmonary disease
  • Selenium dioxide and selenium oxide
    • Forms selenius acid in presence of water in respiratory tract
    • Bronchospasm
    • Hypotension
    • Tachycardia
    • Tachypnea
    • Chemical pneumonitis
    • Fevers
    • Vomiting and diarrhea
• Dermal
  • Caustic burns
• Ophthalmic
  • Corneal injuries
  • Lacrimation
  • Conjunctival edema

Chronic or Selenosis

• No deaths from chronic exposures
• Seen in those taking nutritional supplements and in rural areas with farmland that has high selenium levels
• Alopecia with brittle hair
• Fatigue
• Nail deformities
• Pruritic scalp rash
• Blistered skin with persistent red color
• Neurologic
  • Hyperreflexia
  • Paresthesia
  • Anesthesia
  • Hemiplegia

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

• BMP
• LFTs
• CBC
• CPK
• EKG
• Thyroid function tests
• Whole blood = 0.1–0.34 mg/L (1.27–4.32 μmol/L)
• Serum = 0.04–0.6 mg/L (0.51–7.6 μmol/L)
• Urine < 0.03 mg/L (<0.38 μmol/L)
• Hair < 0.4 μg/g (0.01 μmol/L)

Management

• Decontamination
  • Irrigation for dermal exposures
  • Consider activated charcoal or oral gastric lavage in cases that could produce significant toxicity
  • Selenious acid
    • Judicious use of NG lavage (as will cause caustic burns) based on time of ingestion, amount and concentration due to potential for serious systemic poisoning
• Consult Toxicology or poison control
• Supportive care
  • Mainstay of treatment
  • Acute toxicities usually require multi system support
• Pain management
  • 10% sodium thiosulfate solution/ointment to skin, nail, and eyes
    • Relief of pain by reduction of selenium dioxide to elemental selenium
  • Selenium hexafluoride gas exposures
    • Calcium gluconate gel
      • Same treatment as hydrofluoric acid exposures
• Chelation
  • Dimercaprol, CaNa₂EDTA, or Succimer may form nephrotoxic complexes and worsen toxicity

Disposition

• Acute toxicities will likely require ICU level of care
• Chronic exposures are likely safe for discharge and outpatient follow up

See Also

• Toxicology (main)

References

Calellor, D. Selenium. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1316-1320