Thallium Toxicity 

Thallium Toxicity 

Summary

Key Points

  • Thallium toxicity results from its similarity to potassium
  • Thallium is odorless, colorless, and tasteless as well as extremely toxic
  • Exposure sources include rodenticides, as well as optical, electronic, and chemical research industries
  • The diagnosis of acute or chronic thallium poisoning is made primarily on the basis of history and clinical presentation in the setting of a possible exposure
  • Initial findings in acute toxicity may include nausea, vomiting, abdominal pain and diarrhea; subsequent symptoms include ascending sensorimotor neuropathy and intractable constipation
  • Confirm diagnosis by measurement of thallium in serum or urine
  • Procedures to aid in diagnosis include electroretinography, electromyography, and nerve biopsy
  • ECG may reveal flatted or inverted T waves
  • Aggressive supportive therapy to support circulation and respiration is imperative
  • Decontamination and enhanced elimination using activated charcoal (or Prussian blue if available) may be considered
  • Intermittent hemodialysis is advised to be initiated as soon as possible if thallium toxicity is suspected or measured thallium level is greater than 0.4 mg/L
  • Patients with exposure to heavy metals may have significant body burdens of these toxicants and repeat treatment may be necessary
  • Admit patients who are acutely symptomatic for supportive care and consideration of chelation therapy

Alarm Signs and Symptoms

  • Hemodynamic instability
  • Respiratory distress
  • Seizures, coma, altered mental status

Basic Information

Background Information

  • Thallium is an extremely toxic metal
  • Thallium compounds are odorless, colorless, and tasteless
  • Thallium toxicity results from its similarity to potassium1
    • Thallium depolarizes excitable membranes and disturbs the function of sodium-potassium ATP pump; mitochondria are particularly susceptible
  • Toxic ingestion produces a pathognomic clinical triad of gastroenteritis, polyneuropathy, and alopecia
  • Toxicokinetics2
    • Thallium is distributed extensively and has significant enterohepatic recycling
    • Elimination half-life ranges from 3 to 8 days, although half-lives as long as 15 days have been reported
    • About two-thirds of a thallium dose is excreted in the feces, and the remainder is excreted in the urine
    • Seventy percent of a single dose is excreted within 1 month
  • Severe thallium toxicity occurs with ingestions exceeding 200 mg, and the average lethal adult dose is 1 g3

Etiology and Risk Factors

Etiology

  • Sources of thallium exposure:
    • Historically widely used as rodenticides
    • Currently used in optical, electronic, and chemical research industries

Diagnosis

Approach to Diagnosis

  • The diagnosis of acute or chronic thallium poisoning is made primarily on the basis of history and clinical presentation in the setting of a possible exposure
  • Evaluate patient’s medical history to determine possible sources of exposure as well as symptom onset, duration, and evolution
    • Ingestion is the usual pathway of toxicity; however, significant toxicity can also be seen following inhalation or dermal exposure
    • Thallium poisoning produces a pathognomonic triad of gastroenteritis, polyneuropathy, and alopecia
  • Initial examination findings in acute toxicity may include abdominal pain and hematochezia
  • Confirm diagnosis by measurement of thallium in serum or urine
    • Serum levels greater than 50 mcg/dL suggest poisoning, but because 70% of thallium is bound to erythrocytes, whole-blood measurements are likely to be more accurate4
    • Urinary excretion of greater than 10 to 20 mg per 24 hours is considered excessive
  • Other potential methods for identifying thallium poisoning include electroretinography, electromyography, and sural nerve biopsy
  • ECG may reveal flat or inverted T-waves3

Workup

History

  • Assess patient’s current symptoms and possible sources of exposure
    • Evolution of symptoms associated with acute toxicity
      • Initial symptoms include nausea, vomiting, and diarrhea, which may appear within 3 to 4 hours
      • Subsequent symptoms (within 1 week of exposure) may include:
        • Palpitations and chest pain
        • Vision changes and pain with eye movements
        • Confusion, lethargy, hallucinations
        • Weakness and ataxia
        • Hyperesthesia of the soles of the feet that makes walking difficult
        • Shortness of breath
        • Hyperpigmentation of the hair and gingiva
        • Severe, intractable constipation
      • Late symptoms (2 to 4 weeks after exposure) may include:
        • Significant alopecia
        • Rash or palmar erythema
        • Painful perioral lesions

Physical Examination

  • Thallium toxicity is characterized by:
    • Central nervous system
      • Seizures, confusion, coma
    • Peripheral nervous system
      • Hyperesthesia of soles of the feet
      • Motor weakness of the extremities (rapidly ascending motor weakness may occur)
    • Cardiovascular
      • Hypertension, tachycardia
    • Gastrointestinal
      • Abdominal tenderness
      • Hematochezia
    • Pulmonary
      • Shallow respirations with decreased air movement (due to muscular weakness/paralysis)
    • Head, eyes, ears, nose, and throat
      • Ptosis may occur due to muscle weakness
      • Decreased visual acuity, visual field loss, afferent pupillary defect may be present due to optic neuritis
      • Gingival hyperpigmentation may occur
      • Perioral lesions
    • Dermatologic
      • Transverse lines across the fingernails
      • Transverse lines in hair
      • Alopecia
      • Palmar erythema
      • Nonspecific diffuse rash

Laboratory Tests

  • Confirm diagnosis by measurement of thallium in serum or urine4
    • Serum levels greater than 50 mcg/dL suggest poisoning, but because 70% of thallium is bound to erythrocytes, whole-blood measurements are likely to be more accurate
    • Urinary excretion of greater than 10 to 20 mg per 24 hours is considered elevated
  • General laboratory studies to evaluate for systemic toxicity3
    • Complete blood count
      • Abnormalities such as anemia and thrombocytopenia may occur
    • Chemistry panel to assess electrolyte derangements and renal function
    • Liver function tests
      • Increased levels of hepatic transaminases may be seen in toxicity
    • Complement levels
      • Decreased complement levels may be seen in toxicity

Diagnostic Procedures

  • Electroretinography
    • May reveal delayed visual evoked response
  • Electromyography
    • May demonstrate decreased motor units and membrane instability
  • Sural nerve biopsy
    • May show axonal destruction and demyelination3

Diagnostic Tools

  • ECG
    • May reveal flattened or inverted T waves

Differential Diagnosis

Table 1. Differential diagnosis: Thallium toxicity.

ConditionDescriptionDifferentiated by
Guillain-Barré syndromeAutoimmune disorder causing ascending flaccid paralysisNot associated with gastrointestinal symptomsElevated cerebrospinal fluid protein found in GBS
SelenosisToxic syndrome caused by exposure to excessive levels of seleniumElevated levels of selenium
Arsenic poisoningToxicity caused by exposure to arsenicElevated levels of arsenic
Acute porphyriaMetabolic disorder associated with severe abdominal pain, nausea, vomiting, and possible muscle pain and weaknessUrine studies reveal porphyrin precursors and porphobilinogen in the urine during attacks
Treatment
Approach to Treatment
Thallium toxicity can be life threatening; aggressive supportive therapy is imperativeAssess respiration and support circulation
Early GI decontamination and enhanced elimination may be used to decrease toxicity
Consider intermittent hemodialysis3567
Dithiocarb chelation and forced potassium diuresis are not recommended89101112
Nondrug and Supportive Care
Thallium toxicity may cause cardiovascular instability and respiratory distressSupport cardiovascular system with fluids, vasopressors, and inotropes as needed
Closely monitor respiratory status and provide escalating respiratory support as needed to maintain ventilation and perfusion
Drug Therapy
Prussian blue may be used to enhance fecal elimination (however, this is not readily available in the United States)6
Activated charcoal may be used as an alternative to decrease absorption and enhance elimination of the toxic burden
Treatment Procedures
Extracorporeal Treatments in Poisoning workgroup recommends intermittent hemodialysis be initiated as soon as possible and ideally within 24 to 48 hours of thallium exposure in the following scenarios:7
If thallium exposure is highly suspected on the basis of history or clinical features
Assuming thallium concentrations are readily available, if thallium concentration is greater than 0.4 mg/L
It is suggested that therapy be continued until thallium serum concentrations are less than 0.1 mg/L for a minimum of 72 hours7
Persistent or Recurrent Disease
Patients with exposure to heavy metals may have significant body burdens of these toxicants
Long-term reassessment and repeat treatment may be necessary
Admission Criteria
Admit patients who are acutely symptomatic for supportive care and consideration of chelation therapy
Admit patients with respiratory or hemodynamic instability to an ICU
Special Considerations
Pregnancy
Thallium poisoning during pregnancy has resulted in a wide range of fetal effects from severe toxicity and residual sequelae to apparently normal development13
There is a trend toward low birth weight and prematurity13
Thallium crosses the placental barrier and is excreted in the breast milk14


References

1.Mulkey JP, Oehme FW: A review of thallium toxicity. Vet Human Toxicol 1993;35:445-453.

Reference

2.Pai V: Acute thallium poisoning. West Indian Med J 1987;36:256-258.

Reference

3.Schwartz JG, Stuckey JH, Kunkel SP, et al: Poisoning from thallium. Tex Med 1988;84:46-48.

Reference

4.Insley BM, Grufferman S, Ayliffe HE: Thallium poisoning in cocaine abusers. Am J Emerg Med 1986;24:545-548.

Reference

5.Desenclos J-CA, Wilder MH, Coppenger GW, et al: Thallium poisoning: an outbreak in Florida, 1988. South Med J 1992;85:1203-1206.

Reference

6.Rusyniak DE, Furbee RB, Kirk MA: Thallium and arsenic poisoning in a small Midwestern town. Ann Emerg Med 2002;39:307-311.

Reference

7.Ghannoum M, Nolin TD, Goldfarb DS, et al. Extracorporeal treatment for thallium poisoning: recommendations from the EXTRIP Workgroup. Clin J Am Soc Nephrol 2012;7(10):1682-1690.

Reference

8.Meggs WJ, Hoffman RS, Shih RD, et al: Thallium poisoning from maliciously contaminated food. Clin Toxicol 1994;32:723.

Reference

9.Gastel B: Clinical conferences at Johns Hopkins Hospital. Thallium poisoning. Johns Hopkins Med J 1978;142:27.

10.Papp JP, Gay PC, Dodson VN, et al: Potassium chloride treatment in thallotoxicosis. Ann Intern Med 1969;71:119.

Reference

11.Bank WJ, Pleasure DE, Suzuki K, Nigro M, Katz R. Thallium poisoning. Arch Neurol 1972;26(5):456-464.

Reference

12.Roby DS, Fein AM, Bennet RH, et al: Cardiopulmonary effects of acute thallium poisoning. Chest 1984;84:236.

Reference

13.Hoffman RS: Thallium poisoning during pregnancy: a case report and comprehensive literature review. J Toxicol Clin Toxicol 2000;38:767-775. Reference

14.Michael T, Kohn E, Daniel S, et al. Prenatal exposure to heavy metal mixtures and anthropometric birth outcomes: a cross-sectional study. Environ Health 2022;21(1):139 Reference

15585

Sign up to receive the trending updates and tons of Health Tips

Join SeekhealthZ and never miss the latest health information

15856