THALLIUM

Classification | Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

Specific Substances

1) Molecular Formula: Tl

1) CFS
2) C.F.S.
3) Sulfuric acid, dithallium(1+) salt
4) Thallium acetate, CAS 563-68-8
5) Thallium chloride
6) Thallium sulfate
7) Thallous acetate
8) Thallous chloride
9) Thallium(I) sulfate (2:1)

1.2.1) MOLECULAR FORMULA
1) Tl

Available Forms Sources

1) SUMMARY

a) Thallium salts were formerly used as active ingredients in rodenticides and insecticides until its sale was regulated due to its high toxicity. Thallium household formulations were banned in 1965.
b) It is still used in the manufacture of optical lenses and imitation jewelry and by government agencies as a pesticide.
c) Thallium is also used in some newer technologies such as high temperature ceramic superconductor materials.
d) Thallium acetate was formerly used as a depilatory.

2) ADULTERANTS

a) In Iran, several young adults with a history of chronic (greater than 10 years) heroin abuse, developed symptoms of thallium poisoning. Laboratory screening in the urine confirmed the presence of thallium; symptoms improved after heroin was discontinued (all were started on a treatment program). Although the exact source of thallium was unclear, a traditional depilatory powder may have been used to increased the weight of the heroin (Afshari et al, 2012).
b) A sample believed to be cocaine by a 34-year-old drug abuser turned out to be 99% thallium sulfate (Insley et al, 1986).
c) A Chinese herbal medication (Nutrien) was found to be contaminated with 3.05% thallium (Schaumburg & Berger, 1992).

Overview

Life Support

Clinical Effects

0.2.1)

A) USES: Thallium is a metal used in manufacturing. Previously, it had been used as a rodenticide and insecticide and in hair removal products. It has been used in homicides. Thallium 201 is still used as a radioisotope for nuclear medicine studies.
B) EPIDEMIOLOGY: Exposures are very rare but deaths have occurred.
C) PHARMACOLOGY: Thallium is distributed similar to potassium in the body. It is taken up by red blood cells and therefore can be used to track blood flow in diagnostic studies.
D) TOXICOLOGY: Thallium is a general cellular poison. It inhibits ATP formation and blocks sulfhydryl group crosslinking.
E) WITH POISONING/EXPOSURE

1) OVERDOSE: Symptoms are usually delayed 12 to 24 hours after exposure.
2) MILD TO MODERATE TOXICITY: Nausea, vomiting and diarrhea may occur.
3) SEVERE TOXICITY: Severe GI effects including hematemesis, massive diarrhea leading to severe hypovolemia. If the patient recovers, they will go on to develop a painful sensory peripheral neuropathy, generally beginning 1 to 5 days after exposure. This may be followed by a motor neuropathy which can progress to cranial nerve palsies, to paralysis, and respiratory failure. Seizures have been reported and in dysrhythmias and cardiovascular collapse may occur in severe cases. Alopecia generally develops 2 to 4 weeks after exposure.

0.2.3)

A) WITH POISONING/EXPOSURE

1) Fever may occur.

0.2.4)

A) WITH POISONING/EXPOSURE

1) Optic neuritis, decreased visual acuity and impaired color vision may occur.

0.2.7)

A) WITH POISONING/EXPOSURE

1) Early effects may include paresthesias, myalgias, peripheral burning sensation, headache, cranial nerve palsies, seizures, delirium, coma, peripheral neuropathy, severe pain, and muscle weakness/atrophy. Protracted cases may develop ataxia, choreiform movements, dementia, depression and psychosis. Neurological damage resolves slowly and may be permanent.

0.2.20)

A) Infants born to mothers with thallium poisoning had clinically significant manifestations of thallium toxicity in addition to quantitative evidence of thallium exposure.
B) Thallium may cross the placental barrier in humans and may be associated with fetal mortality particularly if exposure occurs during organogenesis.
C) Thallium is excreted into breast milk of nursing mothers.

Laboratory Monitoring

Treatment Overview

0.4.2)

A) MILD TO MODERATE TOXICITY

1) Replete fluids with normal saline. Initial episodes of vomiting may provide some decontamination, but persistent vomiting should be treated with antiemetics. Administer Prussian blue, if available.

B) SEVERE TOXICITY

1) Initiate resuscitation with isotonic saline. Treat persistent hypotension with adrenergic vasopressors. Treat seizures with benzodiazepines. Administer Prussian blue as soon as possible.

C) DECONTAMINATION

1) PREHOSPITAL: DERMAL: Wash affected areas with water. There is no clear role for prehospital gastrointestinal decontamination.
2) HOSPITAL: Ipecac contraindicated. Gastric lavage or aspiration (if a liquid form is ingested) should be considered if the patient presents soon after the ingestion. Activated charcoal binds thallium and activated charcoal should be administered, but vomiting may limit the utility of charcoal.

D) AIRWAY MANAGEMENT

1) Orotracheal intubation for airway protection should be performed early in cases where the patient has decreased consciousness or coma.

E) ANTIDOTE

1) Prussian blue increases the clearance of thallium. The recommended dose is 3 g orally 3 times a day for adults and 1 g 3 times daily for children. Administer with a laxative to avoid obstipation. The optimal duration of therapy is unknown. Continue therapy until urinary thallium excretion is less than 0.5 mg/day.

F) ENHANCED ELIMINATION

1) Multi-dose activated charcoal has increased clearance in rodent models, but has not been studied in humans. Hemodialysis and forced diuresis may increase the clearance of thallium.

G) PATIENT DISPOSITION

1) HOME CRITERIA: There is no data to support home management of thallium exposure.
2) OBSERVATION CRITERIA: All patients with thallium exposures should be referred to a healthcare facility and observed for a minimum of 24 hours.
3) ADMISSION CRITERIA: All patients with gastrointestinal or neurological effects should be admitted.
4) CONSULT CRITERIA: Contact a medical toxicologist or poison center for any exposure.

H) PITFALLS

1) Failure to recognize that symptoms may be delayed. Failure to consider occult (or malicious) poisoning in a patient with painful neuropathy and hair loss.

I) TOXICOKINETICS

1) Well absorbed. Volume of distribution is 1 to 5 L/kg, concentrates in red blood cells. Eliminated in urine and feces, after overdose elimination is primarily fecal. Half-life reported after poisoning ranges from 1 to 30 days. In a series of 34 patients, Prussian blue reduced mean thallium half-life to 3 from 8 days.

J) DIFFERENTIAL DIAGNOSIS

1) Arsenic toxicity, mercury toxicity, selenium toxicity, mushroom ingestion or gastroenteritis.

0.4.3)

A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
B) Monitor cardiac, renal and hepatic function.
C) Insoluble Prussian Blue: It is a nonabsorbable binding agent, used to treat patients with known or suspected internal contamination with radioactive or nonradioactive thallium, to increase their rates of elimination.
D) Contraindications: Diethylthiocarbamate has been reported to result in dangerous redistribution of thallium to the CNS and is contraindicated.
E) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
F) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).

1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.

0.4.4)

A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

0.4.5)

A) OVERVIEW

1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

Clinical Effects

Summary Of Exposure

Vital Signs

3.3.1)

A) WITH POISONING/EXPOSURE

1) Fever may occur.

3.3.3)

A) WITH POISONING/EXPOSURE

1) Fever may develop.

Heent

3.4.1)

A) WITH POISONING/EXPOSURE

1) Optic neuritis, decreased visual acuity and impaired color vision may occur.

3.4.3)

A) WITH POISONING/EXPOSURE

1) IMPAIRED VISION: Impaired color vision, decreased visual acuity, and optic atrophy have been described (Anon, 1978; Grant & Schuman, 1993; Tabandeh & Thompson, 1993; Tabandeh et al, 1994).

a) PATHOLOGY: Vision loss associated with thallium exposure may be attributed to optic neuritis, maculopapular bundle involvement, iridocylitis, and cataract (Kalita & Misra, 2006).
b) In patients with optic neuropathy the electroretinogram may be abnormal and visual evoked responses delayed (Tabandeh & Thompson, 1993; Moore et al, 1993).
c) INCIDENCE: Severe lesions of the optic nerve have been observed in approximately 25% of patients acutely exposed (one time exposure) to thallium; whereas 100% of patients developed optic nerve lesions following repeated small doses (Kalita & Misra, 2006).

2) OPTIC NEURITIS: Severe bilateral optic neuritis was reported to occur in 25% of acute thallium poisonings and in virtually all chronic poisonings (p 1092).

a) CASE REPORT: Following thallium exposure a 42-year-old man developed immediate ptosis and vision loss (vision 6/60 bilaterally). At 3 year follow-up, persistent visual impairment was observed with no improvement noted, despite complete recovery from peripheral neuropathy. The authors suggested that vision loss was due to severe irreversible toxic optic neuropathy (Kalita & Misra, 2006).

3) OPHTHALMOPLEGIA may develop in patients with severe motor neuropathy (Anon, 1978; Grant & Schuman, 1993).
4) NYSTAGMUS: Horizontal jerky nystagmus developed in a 44-year-old man with neuropathy involving peripheral and cranial nerves after thallium poisoning (Tabandeh et al, 1994). Multidirectional gazing nystagmus was also reported in a 48-year-old woman following thallium poisoning (Tsai et al, 2006). Gaze evoked nystagmus persisted in a 42-year-old man up to 3 years after thallium poisoning along with decreased visual acuity (vision 6/60 bilaterally) (Kalita & Misra, 2006).
5) VISUAL FIELD testing may reveal the presence of scotomata (Moore et al, 1993; Tabandeh et al, 1994).

3.4.6)

A) WITH POISONING/EXPOSURE

1) GUM LINES: A bluish line in the gums may appear 3 to 4 weeks after ingestion.
2) DENTAL CARIES may become evident several months after exposure to thallium (Moeschlin, 1980).
3) PAROTITIS: Bilateral parotid enlargement developed in a 38-year-old man with thallium poisoning (Moore et al, 1993).

Cardiovascular

3.5.2)

A) HYPERTENSIVE EPISODE

1) WITH POISONING/EXPOSURE

a) Hypertension is common (Wainwright et al, 1988; Herrero et al, 1995; Feldman & Levisohn, 1993; Desenclos et al, 1992).
b) Hypertension may develop as early as 4 to 8 days after exposure (Meggs et al, 1994).

B) SINUS TACHYCARDIA

1) WITH POISONING/EXPOSURE

a) Tachycardia is frequently present (Tsai et al, 2006; Kuo et al, 2005; Cavanagh et al, 1974; Wainwright et al, 1988; Moore et al, 1993; Meggs et al, 1994; Herrero et al, 1995).
b) Gradual development of tachycardia may be due to direct vagal nerve and myocardial damage (Saddique & Peterson, 1983).

C) VENTRICULAR ARRHYTHMIA

1) WITH POISONING/EXPOSURE

a) Bradycardia as well as ventricular and atrial dysrhythmias and myocardial dysfunction have been reported (Roby et al, 1984).

D) ELECTROCARDIOGRAM ABNORMAL

1) WITH POISONING/EXPOSURE

a) T wave abnormalities may develop on ECG (Meggs et al, 1994; Niehues et al, 1995).
b) ECG changes similar to hypokalemia may develop (Saddique & Peterson, 1983).

E) HYPOTENSIVE EPISODE

1) WITH POISONING/EXPOSURE

a) Severe cases of acute poisoning may result in refractory cardiogenic shock. Two adults died 10 days after exposure following a period of refractory cardiogenic shock (Herve et al, 2000).

Respiratory

3.6.2)

A) APNEA

1) WITH POISONING/EXPOSURE

a) Respiratory failure may develop in patients with severe motor neuropathy (Desenclos et al, 1992; Herve et al, 2000). Prolonged ventilatory support may be required.

B) ACUTE LUNG INJURY

1) WITH POISONING/EXPOSURE

a) Adult respiratory distress syndrome (ARDS) has been observed (Roby et al, 1984).

C) CHEST PAIN

1) WITH POISONING/EXPOSURE

a) CASE SERIES: Pleuritic chest pain developed within 2 days of exposure in 3 of 4 patients poisoned with thallium in one case series (Meggs et al, 1994).
b) CASE REPORT: Chest tightness developed in a 42-year-old man about 10 minutes after drinking thallium contaminated tea (Moore et al, 1993).

Neurologic

3.7.1)

A) WITH POISONING/EXPOSURE

3.7.2)

A) SECONDARY PERIPHERAL NEUROPATHY

1) WITH POISONING/EXPOSURE

a) Painful peripheral neuropathy and paresthesia, primarily of the legs and feet, are among the first symptoms noted following thallium poisoning (Li et al, 2014; Sun et al, 2012; Al Hammouri et al, 2011; Wang et al, 2007; Aasly, 2007; Grunfeld & Hinostroza, 1964; Desenclos et al, 1992; Tabandeh et al, 1994; Niehues et al, 1995; Malbrain et al, 1997).

1) Pain may be described as aching, stabbing tingling or burning and may be so severe as to prohibit walking (Wang et al, 2007; Desenclos et al, 1992; Meggs et al, 1994; Schaumburg & Berger, 1992). Pain may also be aggravated by touching the lower extremities (Sun et al, 2012).
2) INCIDENCE: In a series of 14 patients with thallium toxicity secondary to intentional poisoning, all patients developed painful peripheral neuropathy. Symptoms included excruciating bilateral leg and foot pain (Sun et al, 2012).
3) ONSET: Symptoms may be noted within a few days of exposure (Sun et al, 2012). It may develop within 2 to 6 days in severe poisoning (Meggs et al, 1994; Herve et al, 2000).
4) Loss of pain, temperature, vibratory and position sense may all occur and an unsteady gait may develop (Schaumburg & Berger, 1992; Tabandeh et al, 1994).
5) Tingling and numbness were reported in 38.5% of patients (n=26) following consumption of wheat contaminated with thallium (Saha et al, 2004).
6) CASE SERIES: Lower limb pain and weakness were the first symptoms observed in 5 adults and 2 children that developed thallium poisoning after ingesting a cake contaminated with thallium (the source was unknown) from a local bakery. The median onset of symptoms was 6 hours (range: 4 to 48 hours). Neuropathic pain was treated with a combination of opioids, anticonvulsants (ie, gabapentin) and antidepressants. A total of 10 individuals (5 adults and 5 children) were exposed and were member of 2 families (Al Hammouri et al, 2011).
7) CASE SERIES: In a series of 9 cases of intentional thallium poisoning, every patient presented with peripheral neuropathy. Of the 9 patients, 3 patients could not walk and 2 patients had difficulty walking (Wang et al, 2007).
8) CASE REPORT: A 16-year-old teenager with a history of anxiety and depression, intentionally ingested a rodent poison containing 1.3 g of thallium sulphate, and was hospitalized within 3 days with severe lower limb pain, abdominal cramps and difficulty breathing. Three weeks after exposure, a neurologic exam showed severe and widespread hyperalgesia, distal tremor of the upper limbs, diffuse muscle weakness and atrophy, with absent tendon reflexes and sensory deficit mainly involving the lower limbs; cranial nerves were not involved. After 3 months, the patient was still unable to walk. Following 3 years of follow-up, walking became possible with the assistance of ankle-foot orthoses. Electroencephalography was normal and electrodiagnostic findings were consistent with persistent sensorimotor polyneuropathy. At 6 years, the patient was able to walk without ankle-foot orthoses (Ammendola et al, 2007).
9) CASE REPORT: A 50-year-old woman presented with an extremely painful ascending polyneuropathy (Vergauwe et al, 1990).
10) CASE REPORT: A 35-year-old woman presented 6 weeks after exposure to a thallium rodenticide with severe dysesthesias in her hands and feet, with difficulty walking. Physical examination revealed a symmetrical (4/5) decrease in muscle strength of all 4 extremities (Benavides et al, 1997).

b) Peripheral motor neuropathy may also develop, and is manifested as extremity weakness that is usually more severe in the lower extremities (Desenclos et al, 1992; Moore et al, 1993).

1) CASE REPORT: An electrophysiologic examination revealed moderate to severe sensorimotor axonal polyneuropathy of the lower extremities in a 38-year-old woman 16 days after ingesting about 9 g of thallium sulfate (Malbrain et al, 1997).
2) CASE REPORT: A 48-year-old man presented with severe pain in his hands and feet. Prior to presentation, the patient developed gastrointestinal upset and weight loss. Forty-eight hours after hospital admission, the patient developed slurred speech, decreased consciousness, ptosis, weakness, and loss of deep tendon reflexes. A random urine sample revealed a thallium level of 50,000 microns/liter (normal is less than 5 microns/liter). During analysis of the urine sample, a fatal cardiac arrest occurred. It is believed that the patient's girlfriend was intentionally poisoning him with thallium and the forensic autopsy confirmed that the cause of death was acute and chronic thallium poisoning (Sharma et al, 2004).
3) In severe cases respiratory failure or cranial nerve palsies may develop (Desenclos et al, 1992; Tabandeh et al, 1994).
4) Pseudobulbar paralysis with paralysis of ocular muscles, ptosis, amblyopia, and facial paralysis occurred in severe intoxications (Moeschlin, 1980).

c) CASE REPORT: A 42-year-old man developed grade 3 quadriplegia with sensory loss after thallium poisoning. Neurologic function gradually improved and he was able to walk independently by 6 months. At 3 year follow-up, initial peripheral neuropathy and cognitive impairment were completely resolved. However, some mild residual deficits including extrapyramidal signs (ie, masking, positive Mearson's sign, broken saccades and pursuit eye movements, and loss of associated movement during walking), cerebellar signs (ie, gaze evoked nystagmus, defective tandem walking) and mild abnormalities in autonomic function were still present (Kalita & Misra, 2006).
d) CASE REPORTS: Two patients experienced severe painful dysesthesias in the lower extremities after drinking water that contained thallium (3,124 mg/L). Both patients also experienced perioral numbness, diarrhea, dry mouth, and acne-like skin lesions in the cheeks and perioral areas. Two to three weeks following exposure, alopecia, hyperkeratosis, and leg weakness were also noted. The urinary concentrations of thallium ranged from 11,325 to 14,520 mcg/L. Nerve conduction studies, performed 2 months following exposure, showed axonal degeneration. A cutaneous nerve biopsy, performed on one of the patients, showed a loss of epidermal nerves and fragmented dermal nerve fibers in the subepidermal regions, indicating the involvement of small sensory nerves as well as motor nerve fibers and large sensory fibers (Tsai et al, 2006; Kuo et al, 2005).

B) PARKINSON'S DISEASE

1) WITH POISONING/EXPOSURE

a) CASE SERIES: Parkinsonian tremors were reported in 6 (46%) of 13 patients exposed to thallium from ingesting contaminated food (edible fungi) or water. All patients were initially misdiagnosed. However, Prussian blue was given to each patient except one who died of leukemia. Upon follow-up (median time 7 years; range, 1 to 12 years), 2 (18%) out of 11 patients continued to complain of Parkinsonian tremor (Li et al, 2014).

C) CRANIAL NERVE DISORDER

1) WITH POISONING/EXPOSURE

a) Cranial nerve injury is less common than peripheral nerve damage, but has been reported. In a series of 9 patients with acute thallium poisoning, one developed decreased visual acuity, hoarseness and difficulty swallowing, another developed ptosis and restriction of downward movement of the eyes, and a third developed facial diplegia (Wang et al, 2007).

D) SEIZURE

1) WITH POISONING/EXPOSURE

a) Seizures have occurred rarely with thallium poisoning (Moeschlin & Condrau, 1950; Smith & Doherty, 1964; Rambar, 1932; Feldman & Levisohn, 1993). However, children may be more likely to develop seizures following exposure (Al Hammouri et al, 2011).
b) CASE SERIES: Ten cases of thallium poisoning occurred in 2 families after ingesting a cake contaminated with thallium (the source was unknown) from a local bakery. Of the 10 cases, 5 patients (all children; ranging in age from 2 to 14 years) developed seizures. In 2 cases, the youngest children (a 2 year-old boy and a 5-year-old girl) developed sudden cardiorespiratory arrest and died (Al Hammouri et al, 2011).

E) COMA

1) WITH POISONING/EXPOSURE

a) CNS depression and coma may occur in severe cases (Desenclos et al, 1992).
b) CASE SERIES: Loss of consciousness was reported in 5 cases (n=10) of thallium poisoning that occurred in 2 families after ingesting a cake contaminated with thallium (the source was unknown) from a local bakery. All patients were managed initially by peritoneal dialysis and then hemodialysis in 9 cases, until Prussian blue was available. Of the 10 cases, 5 patients (4 children and 1 adult) were admitted to the ICU. Mechanical ventilation was needed in 3 cases due to the sudden loss of consciousness and coma. Three patients admitted to ICU died (2 children (cardiorespiratory arrest) and 1 adult (multiorgan failure)) (Al Hammouri et al, 2011).

F) SEQUELA

1) WITH POISONING/EXPOSURE

a) In the more protracted cases, ataxia (Augenstein et al, 1988), choreiform movements, dementia, depression and psychosis may be prominent.
b) Sequelae, including mental retardation, psychosis, abnormal reflexes, ataxia, and tremor were noted in 26 of 48 children who survived thallium sulfate poisoning (Reed et al, 1963). There are other isolated reports of neurological sequelae lasting more than 30 years (Barnes et al, 1984).
c) Sequelae one year after a large acute ingestion included flaccid paraparesis, cerebellar ataxia, and mental impairment (Wainwright et al, 1988).
d) CASE REPORT: Electrophysiologic findings in a 45-year-old victim of acute thallium toxicity included profound axonal loss of the plantar nerves and a primarily distal axonopathy that was significantly worse in the lower extremities. Repeat examinations over the next 2 years demonstrated axonal loss in the sural and peroneal nerves also. Final examination 2 years after initial admission revealed recovery of sural and peroneal nerve function but continued absence of plantar nerve function (Dumitru & Kalantri, 1990).

G) HEADACHE

1) WITH POISONING/EXPOSURE

a) Headache is also occasionally reported (Moeschlin & Condrau, 1950; Smith & Doherty, 1964).
b) Headaches were reported in 92.3% of patients (n=26) following consumption of wheat contaminated with thallium (Saha et al, 2004).

H) PERSONALITY DISORDER

1) WITH POISONING/EXPOSURE

a) Acute psychosis, with agitation and hysteria, has been described after thallium poisoning (Li et al, 2014; Al Hammouri et al, 2011; Moeschlin, 1980; Desenclos et al, 1992; Niehues et al, 1995).
b) CASE SERIES: Psychotic symptoms that manifested as agitation and irritability were reported in 5 (38%) of 13 patients exposed to thallium from ingesting contaminated food (edible fungi) or water (Li et al, 2014).
c) CASE SERIES: Psychotic symptoms were reported in 5 patients (n=10) exposed to thallium after ingesting a cake contaminated with thallium (the source was unknown) from a local bakery (Al Hammouri et al, 2011).
d) Anxiety is a common symptom (Cavanagh et al, 1974).
e) Irritability and restlessness have been reported (Feldman & Levisohn, 1993; Herrero et al, 1995);

I) IMPAIRED COGNITION

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Significantly lower scores on several psychologic function and intelligence tests were seen in a 20-year-old victim of thallium poisoning when compared with his twin bother who had equivalent background and education. The patient also experienced uncharacteristic aggression and hostility. Repeated tests 13 months after ingestion showed little improvement (Thompson et al, 1988).
b) Confusion, disorientation to time, place and person, lack of attention, delusions, and incoherent speech occurred in two patients who drank 500 to 750 mL of water containing thallium (3,124 mg/L). The initial EEG of the first patient, a 48-year-old woman, revealed mild diffuse cortical dysfunction. An MRI, performed one month after presentation of symptoms, showed lesions in the corpus striatum and neuropsychological tests revealed impairments in digital span (backward), memory recall, memory recognition, verbal fluency, and proverb reasoning. The second patient, a 52-year-old man (the spouse of the first patient), initially had normal brain MRI studies; however, neuropsychological studies showed similar impairment. Both patients showed significant cognitive improvement following aggressive decontamination measures and therapy with Prussian blue (Tsai et al, 2006).

J) INSOMNIA

1) WITH POISONING/EXPOSURE

a) Insomnia is a common complaint (Meggs et al, 1994; Herrero et al, 1995).

K) HALLUCINATIONS

1) WITH POISONING/EXPOSURE

a) SUMMARY: Auditory and visual hallucinations have been described following thallium poisoning (Li et al, 2014).
b) CASE SERIES: Auditory and visual hallucinations occurred in 2 (13%) of 13 patients exposed to thallium from ingesting contaminated food (edible fungi) or water (Li et al, 2014).
c) CASE REPORT: Visual hallucinations were reported in a 48-year-old woman who drank approximately 750 mL of water containing thallium (3,124 mg/L). She also experienced confusion, disorientation, incoherent speech, and delusions. An initial brain MRI showed lesions in the corpus striatum and an EEG revealed mild diffuse cortical dysfunction. The patient gradually improved following Prussian blue therapy (Tsai et al, 2006).

L) HYPERREFLEXIA

1) WITH POISONING/EXPOSURE

a) Generalized hyperreflexia was reported in two patients who drank 500 to 750 mL of water containing thallium (3,124 mg/L) (Tsai et al, 2006).

3.7.3)

A) ANIMAL STUDIES

1) NEUROPATHY

a) RATS: In rats thallium distributes more readily to the brain in younger animals (Galvan-Arzate & Rios, 1994). This suggests that young children may develop thallium neurotoxicity more readily because of an immature blood brain barrier.

Gastrointestinal

3.8.2)

A) CONSTIPATION

1) WITH POISONING/EXPOSURE

a) Gastrointestinal manifestations include initial constipation unresponsive to laxatives and abdominal pain (Saddique & Peterson, 1983; Moeschlin, 1980; Wainwright et al, 1988; Malbrain et al, 1997).
b) INCIDENCE: In a series of 9 cases, constipation and abdominal distension were reported in 3 patients intentionally poisoned with contaminated drinking water containing thallium. Abdominal tenderness also occurred in 2 patients (Wang et al, 2007). Constipation was reported in 11.5% of patients (n=26) following consumption of wheat contaminated with thallium (Saha et al, 2004).
c) In a series of 10 patients (2 families, a total of 4 adults and 6 children, 9 poisoned by eating a contaminated cake and one child poisoned via ingestion of contaminated breast milk), 8 patients developed constipation (Al Hammouri et al, 2011).

B) NAUSEA AND VOMITING

1) WITH POISONING/EXPOSURE

a) Nausea, vomiting and severe paroxysmal abdominal pain may occur (Al Hammouri et al, 2011; Wang et al, 2007; Feldman & Levisohn, 1993; Schaumburg & Berger, 1992; Moore et al, 1993; Tabandeh et al, 1994; Benavides et al, 1997; Saha et al, 2004; Tsai et al, 2006).
b) CASE SERIES: Vomiting was the first symptom observed in 3 children that developed thallium poisoning after ingesting a cake contaminated with thallium (the source was unknown). The children were members of 2 families (a total of 10 cases) that became exposed after eating a cake from a local bakery; one case was a child that became ill after being breastfed by their mother who ate the contaminated cake. Of the 10 cases, nausea, vomiting and abdominal pain were reported in 8 cases (Al Hammouri et al, 2011).

C) DIARRHEA

1) WITH POISONING/EXPOSURE

a) Diarrhea and melena have also been reported (Tsai et al, 2006; Kuo et al, 2005; Saha et al, 2004; Desenclos et al, 1992).
b) CASE SERIES: Diarrhea was reported in 2 patients (n=10) that developed thallium poisoning after ingesting a cake contaminated with thallium (the source was unknown) from a local bakery (Al Hammouri et al, 2011).

D) DYSPHAGIA

1) WITH POISONING/EXPOSURE

a) CASE SERIES: Dysphagia was reported in 9 patients (n=10) exposed to thallium after ingesting a cake contaminated with thallium (the source was unknown) from a local bakery (Al Hammouri et al, 2011).

E) LOSS OF APPETITE

1) WITH POISONING/EXPOSURE

a) Severe anorexia may occur (Feldman & Levisohn, 1993; Moore et al, 1993).

F) EXCESSIVE SALIVATION

1) WITH POISONING/EXPOSURE

a) Excessive salivation may occur.

G) GASTROINTESTINAL HEMORRHAGE

1) WITH POISONING/EXPOSURE

a) Gastrointestinal hemorrhage has been reported but is not common (Saddique & Peterson, 1983; Meggs et al, 1994).

Hepatic

3.9.2)

A) TOXIC HEPATITIS

1) WITH POISONING/EXPOSURE

a) Liver damage occurs but is not prominent clinically. Mild elevation in SGOT was reported in 2 patients who snorted thallium sulfate (Insley et al, 1986).
b) CASE REPORT: Liver enzymes were elevated in a 16-year-old girl who ingested a thallium-containing rat poison. Her liver function normalized after 10 days (Niehues et al, 1995).
c) In a series of 10 patients (2 families, a total of 4 adults and 6 children, 9 poisoned by eating a contaminated cake and one child poisoned via ingestion of contaminated breast milk), 7 patients had elevations in LDH, 6 had elevations in ALT, 7 had elevations in AST (Al Hammouri et al, 2011).

Genitourinary

3.10.2)

A) ABNORMAL URINE

1) WITH POISONING/EXPOSURE

a) Shortly after thallium ingestion, the urine may have a green discoloration common to thallium poisoning (Malbrain et al, 1997).

B) RETENTION OF URINE

1) WITH POISONING/EXPOSURE

a) Urinary retention was reported in two patients who drank water contaminated with thallium (3,124 mg/L) (Tsai et al, 2006; Kuo et al, 2005). Dysuria was reported in one patient poisoned with thallium (Wang et al, 2007).

C) INCONTINENCE

1) WITH POISONING/EXPOSURE

a) In a series of 9 cases, urinary incontinence was reported in 1 patient intentionally poisoned with contaminated drinking water containing thallium (Wang et al, 2007).

D) OLIGURIA

1) WITH POISONING/EXPOSURE

a) Kidney damage is manifested by proteinuria, decreased creatine clearance, increased BUN, cylindruria and sometimes oliguria and hematuria. With the continued administration of smaller doses, symptoms may first be apparent in a week with progression for several more weeks.

E) ALBUMINURIA

1) WITH POISONING/EXPOSURE

a) CASE SERIES: Albuminuria was present in the first week after ingestion in 8 of 70 cases in one series (Moeschlin, 1980).
b) CASE SERIES: Proteinuria developed in 2 of 4 patients in another series (Meggs et al, 1994).

3.10.3)

A) ANIMAL STUDIES

1) ALBUMINURIA

a) RATS: In rats, thallium administration induced proteinuria and decreased glomerular filtration rates (Appenroth et al, 1995).

1) Doses of 5 or 10 mg/kg thallium IP induced polyuria while 20 mg/kg induced oliguria (Appenroth et al, 1995).

Acid-Base

3.11.2)

A) ACIDOSIS

1) WITH POISONING/EXPOSURE

a) Mild hypochloremic metabolic acidosis has been reported (Saddique & Peterson, 1983).

Hematologic

3.13.2)

A) ANEMIA

1) WITH POISONING/EXPOSURE

a) Hemolytic changes (unrelated to hemolysis) have been reported following acute ingestions, and anemia has been reported following chronic ingestions (Saddique & Peterson, 1983).

B) THROMBOCYTOPENIC DISORDER

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Thrombocytopenia was reported in a case of fatal acute poisoning (Luckit et al, 1990).
b) CASE REPORT: Thrombocyte levels of 65,000/microL and megakaryocytosis was evident in bone marrow cytology in a 16-year-old girl following an intentional overdose of a thallium-containing compound (Niehues et al, 1995).
c) In a series of 10 patients (2 families, a total of 4 adults and 6 children, 9 poisoned by eating a contaminated cake and one child poisoned via ingestion of contaminated breast milk), 3 patients developed thrombocytopenia (Al Hammouri et al, 2011).

Dermatologic

3.14.2)

A) DISORDER OF SKIN

1) WITH POISONING/EXPOSURE

a) Anhydrosis, diaphoresis and dry and scaly skin may be noted. Severe acne and hyperkeratosis may result (Tsai et al, 2006; Kuo et al, 2005; Moeschlin, 1980).
b) In a series of 10 patients (2 families, a total of 4 adults and 6 children, 9 poisoned by eating a contaminated cake and one child poisoned via ingestion of contaminated breast milk), 7 patients developed scaling of the skin on the palms and soles (Al Hammouri et al, 2011).

B) DISCOLORATION OF SKIN

1) WITH POISONING/EXPOSURE

a) Eczematous metallic skin discoloration or lesions may occur as a result of thallium poisoning (Aasly, 2007).

C) HAIR DISCOLORATION

1) WITH POISONING/EXPOSURE

a) Black pigmentation of hair roots may be seen within 4 days (Moeschlin, 1980; Burnett, 1990; Niehues et al, 1995).
b) In a series of 10 patients (2 families, a total of 4 adults and 6 children, 9 poisoned by eating a contaminated cake and one child poisoned via ingestion of contaminated breast milk), 4 patients developed a change in hair color (Al Hammouri et al, 2011).

D) MEE'S LINE

1) WITH POISONING/EXPOSURE

a) Transverse lines on the finger and toe nails may appear after 2 to 8 weeks (Saddique & Peterson, 1983; Grunfeld & Hinostroza, 1964; Pai, 1987; Moore et al, 1993; Herrero et al, 1995; Tsai et al, 2006).
b) Mee's lines and erosion of the proximal parts of the fingernails occurred in 11.5% and 73.1% of patients (n=26), respectively, following consumption of wheat contaminated with thallium (Saha et al, 2004).
c) CASE REPORT: Whitish spots on the proximal part of the nails with subsequent nail erosion occurred in a 26-year-old woman following continuous consumption, for 15 days, of wheat contaminated with thallium. The proximal part of the nails completely eroded during a 3-week period. Laboratory analysis of the patient's blood, hair, and urine showed thallium levels of 0.1206 ppm, 0.0459 ppm, and 30 ppb, respectively. The recommended normal thallium levels are less than 2 ppb, 5 to 10 ppb, and less than 5 ppb, respectively (Saha et al, 2004).

E) ALOPECIA

1) WITH POISONING/EXPOSURE

a) Hair loss may be seen in 2 to 4 weeks after exposure and is considered a classic finding of thallium poisoning (Aasly, 2007; Wang et al, 2007; Kalita & Misra, 2006; Tsai et al, 2006; Kuo et al, 2005; Herrero et al, 1995; Feldman & Levisohn, 1993; Desenclos et al, 1992; Moore et al, 1993; Niehues et al, 1995; Malbrain et al, 1997; Herve et al, 2000).
b) Alopecia may involve the eyelashes and brows as well as scalp hair (Saha et al, 2004; Schaumburg & Berger, 1992).
c) Alopecia is generally reversible once serum thallium levels have decreased (Malbrain et al, 1997).
d) INCIDENCE: In a series of 14 patients with thallium toxicity secondary to intentional poisoning, all patients developed hair loss. ONSET: Hair loss occurred a few days after the onset of limb and abdominal pain (Sun et al, 2012).
e) INCIDENCE: In a series of 9 case reports, alopecia was reported in 3 patients intentionally poisoned with contaminated drinking water containing thallium (Wang et al, 2007). Alopecia was also reported in 57.7% of patients (n=26) following consumption of wheat contaminated with thallium (Saha et al, 2004).
f) In a series of 10 patients (2 families, a total of 4 adults and 6 children, 9 poisoned by eating a contaminated cake and one child poisoned via ingestion of contaminated breast milk), 7 patients developed alopecia (Al Hammouri et al, 2011).

F) MACULOPAPULAR ERUPTION

1) WITH POISONING/EXPOSURE

a) Maculopapular rash which progressed to scabbing has been reported (Tabandeh et al, 1994).

G) PHOTOSENSITIVITY

1) WITH POISONING/EXPOSURE

a) Sunlight hypersensitivity was reported in 11.5% of patients (n=26) following consumption of wheat contaminated with thallium (Saha et al, 2004).

Musculoskeletal

3.15.2)

A) JOINT PAIN

1) WITH POISONING/EXPOSURE

a) Alarcon-Segovia et al (1989) reported features of connective tissue disease (arthralgia, polyarthritis) associated with thallium intoxication (Alarcon-Segovia et al, 1989).

B) MUSCLE PAIN

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Generalized myalgia was reported in a 48-year-old woman after drinking water contaminated with thallium (3,124 mg/L). The patient also experienced severe dysesthesia of her legs and feet, dry mouth, diarrhea, urinary retention, tachycardia, skin lesions in her cheek and perioral regions, alopecia, hyperkeratosis, leg weakness and hyporeflexia. Urinary thallium concentration was 14,520 mcg/L (Tsai et al, 2006; Kuo et al, 2005).

Immunologic

3.19.2)

A) ANTI-NUCLEAR FACTOR POSITIVE

1) WITH POISONING/EXPOSURE

a) Alarcon-Segovia et al (1989) reported features of connective tissue disease (systemic lupus erythematosus with positive antinuclear antibodies) associated with thallium intoxication (Alarcon-Segovia et al, 1989).
b) CASE REPORT: Positive antinuclear antibodies (1:160 with a homogenous pattern) were reported in a 20-year-old man with thallium intoxication (Herrero et al, 1995).

Reproductive

3.20.1)

3.20.2)

A) ACUTE TOXICITY

1) In a retrospective literature review, Hoffman (2000) reported that many infants born to mothers with thallium poisoning had clinically significant manifestations of thallium toxicity in addition to quantitative evidence of thallium exposure. It is inconclusive with regard to the risk of congenital abnormalities from thallium poisoning due to the small number of human cases. Prognostic markers of fetal outcome are lacking due to insufficient data (Hoffman, 2000).

3.20.3)

A) ABORTION

1) A female exposed to a thallium rodenticide during her 13th week of pregnancy had a 24 hour urine thallium level of 3400 mcg/L (normal less than 5 mcg/L) 6 weeks after the exposure. Chelation with Prussian blue improved her clinical status and she was discharged from the hospital. Approximately 11 to 12 weeks after the thallium exposure she spontaneously aborted a child with normal external morphology for its estimated gestational age (Hoffman, 2000; Benavides et al, 1997).

B) ALOPECIA

1) Maternal ingestion of thallous sulfate 0.75 mg 60 days before delivery resulted in a neonate with alopecia (Moeschlin, 1980).

C) PLACENTAL BARRIER

1) Thallium may cross the placental barrier in humans and may be associated with fetal mortality particularly if exposure occurs during organogenesis (Hoffman, 2000; Benavides et al, 1997). Thallium has been shown to be present in both colostrum and in umbilical cord blood of some samples in exposed pregnant women (Hoffman, 2000).

D) BIRTH PREMATURE

1) There appears to be a trend toward prematurity and low birth weight, particularly in neonates exposed during early gestation (Hoffman, 2000). In some instances, normal infants have been delivered from mothers with clinically severe thallium poisoning.

3.20.4)

A) BREAST MILK

1) Thallium is excreted into breast milk of nursing mothers (Hoffman, 2000).
2) CASE SERIES: Ten cases of acute thallium poisoning occurred in 2 families that consumed a cake from a local bakery that was contaminated with thallium (the source was unknown); one case was a toddler that became ill and eventually died of thallium poisoning after being breastfed by a mother who consumed the cake (Al Hammouri et al, 2011).

Carcinogenicity

3.21.1)

A) IARC Carcinogenicity Ratings for CAS7440-28-0 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):

1) Not Listed

B) IARC Carcinogenicity Ratings for CAS563-68-8 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):

1) Not Listed

3.21.3)

A) LACK OF EFFECT

1) Thallium appears to have little if any carcinogenic potential (Hoffman, 2000).

Genotoxicity

Laboratory Monitoring

Monitoring Parameters Levels

4.1.1)

A) Monitor vital signs, mental status and neurologic exam. Monitor serum electrolytes, renal function and liver enzymes. Obtain 24 hour urine collection for thallium.
B) Urinary excretion of thallium in excess of 10 to 20 mg in 24 hours is considered diagnostic. Although less reliable for diagnosis than 24 hour urinary thallium excretion, whole blood thallium exceeding 100 mcg/dL indicates potential poisoning.
C) Thallium is radiopaque, an abdominal radiograph may help assess the adequacy of GI decontamination after acute ingestion.
D) Nerve conduction studies may be useful to evaluate peripheral neuropathy.

4.1.2)

A) BLOOD/SERUM CHEMISTRY

1) Monitor liver and renal function tests.
2) Normal thallium concentrations ranged from 0 to 0.08 mg/L in 320 young urban children (Singh et al, 1975).

4.1.3)

A) URINARY LEVELS

1) Thallium is excreted in the urine for many weeks following ingestion or dermal absorption. In severe intoxications, urinary excretions have been greater than 5 to 10 mg/24 hours (Grunfeld & Hinostroza, 1964) (Van der Merwe et al, 1972) (Pederson et al, 1978) (Koshy & Lovejoy, 1981).
2) THALLIUM MOBILIZATION TEST: One reported method of diagnosis involves administration of 45 mEq of oral potassium and measuring a 24-hour urine collection (Insley et al, 1986). The value of this test is debatable, since urinary excretion has been reported to be identical before and after potassium administration (Anon, 1978).

4.1.4)

A) OTHER

1) HAIR

a) Black pigmentation of the hair roots when examined under a microscope will be seen 4 days after ingestion of thallium (Saddique & Peterson, 1983).

2) ELECTROPHYSIOLOGY STUDIES

a) Electromyography (EMG) and nerve conduction studies have been used to evaluate peripheral neuropathy symptoms (ie, paraesthesia) that are commonly reported following thallium poisoning. Diffuse axonal damage and demyelination has been observed in patients exposed to thallium (Li et al, 2014).

Radiographic Studies

1) Thallium is radiopaque (Grunfeld & Hinostroza, 1964). Abdominal x-ray may be useful in documenting adequate gastric decontamination following acute ingestion.

Methods

1) The most reliable result is from a 24 hour urine quantitative assay. Normal values are 0 to 5 ng/mL (CDC, 1987).

1) Thallium is measured most accurately by atomic absorption spectrophotometry (Wakid & Cortas, 1984).

Treatment

Life Support

Patient Disposition

6.3.1)

6.3.1.1) ADMISSION CRITERIA/ORAL

A) All patient with gastrointestinal or neurological effects should be admitted.

6.3.1.2) HOME CRITERIA/ORAL

A) There is no data to support home management of thallium exposure.

6.3.1.3) CONSULT CRITERIA/ORAL

A) Contact a medical toxicologist or poison center for any exposure.

6.3.1.5) OBSERVATION CRITERIA/ORAL

A) All patients with thallium exposures should be referred to a healthcare facility and observed for a minimum of 24 hours.

Monitoring

Oral Exposure

6.5.1)

A) ACTIVATED CHARCOAL

1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION

a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).

1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).

2) CHARCOAL DOSE

a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).

1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).

b) ADVERSE EFFECTS/CONTRAINDICATIONS

1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).

6.5.2)

A) ACTIVATED CHARCOAL

1) Activated charcoal has been reported to be effective in vitro in adsorbing thallium (Kamerbeck et al, 1971) (Lehmann & Favare, 1984; Hoffman et al, 1999).
2) ANIMAL STUDY: Activated charcoal was superior to Prussian blue in one study in rats; 93% of the dose was eliminated in 8 days after activated charcoal 500 mg/kg/day given twice daily compared to 82% after Prussian blue (Lehmann & Favare, 1984).
3) IN VITRO STUDY: At a physiologic potassium concentration, the maximal adsorptive capacities of Prussian blue and activated charcoal with thallium were very similar. In contrast, adsorption of thallium to sodium polystyrene sulfonate was relatively ineffective and would be expected to be even lower in vivo (Hoffman et al, 1999).
4) CHARCOAL ADMINISTRATION

a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.

5) CHARCOAL DOSE

b) ADVERSE EFFECTS/CONTRAINDICATIONS

B) GASTRIC LAVAGE

1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).

a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.

2) PRECAUTIONS:

a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.

3) LAVAGE FLUID:

a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.

4) COMPLICATIONS:

a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).

5) CONTRAINDICATIONS:

a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.

C) MULTIPLE DOSE ACTIVATED CHARCOAL

1) Thallium is thought to undergo enterohepatic recirculation, and multiple dose activated charcoal may enhance its elimination (Meggs et al, 1994). Multiple dose activated charcoal has not been proved to be of benefit, but is often used as therapy, particularly in areas where Prussian blue is not readily available (Meggs et al, 1994). It may be considered in patients with potentially serious or life threatening ingestions.
2) MULTIPLE DOSE ACTIVATED CHARCOAL

a) ADULT DOSE: Optimal dose not established. After an initial dose of 50 to 100 grams of activated charcoal, subsequent doses may be administered every 1, 2 or 4 hours at a dose equivalent to 12.5 grams/hour (Vale et al, 1999), do not exceed: 0.5 g/kg charcoal every 2 hours (Ghannoum & Gosselin, 2013; Mauro et al, 1994). There is some evidence that smaller more frequent doses are more effective at enhancing drug elimination than larger less frequent doses (Park et al, 1983; Ilkhanipour et al, 1992). PEDIATRIC DOSE: Optimal dose not established. After an initial dose of 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) (Chyka & Seger, 1997), subsequent doses may be administered every 1, 2 or 4 hours (Vale et al, 1999) in a dose equivalent to 6.25 grams/hour in children 1 to 12 years old.
b) Activated charcoal should be continued until the patient's clinical and laboratory parameters, including drug concentrations if available, are improving (Vale et al, 1999). The patient should be frequently assessed for the ability to protect the airway and evidence of decreased peristalsis or intestinal obstruction.
c) Use of cathartics has not been shown to increase drug elimination and may increase the likelihood of vomiting. Routine coadministration of a cathartic is NOT recommended (Vale et al, 1999).
d) AGENTS AMENABLE TO MDAC THERAPY: The following properties of a drug that are likely to allow MDAC therapy to be effective include: small volume of distribution, low protein binding, prolonged half-life, low intrinsic clearance, and a nonionized state at physiologic pH (Chyka, 1995; Ghannoum & Gosselin, 2013).
e) Vomiting is a common adverse effect; antiemetics may be necessary.
f) CONTRAINDICATIONS: Absolute contraindications include an unprotected airway, intestinal obstruction, a gastrointestinal tract that is not intact and agents that may increase the risk of aspiration (eg, hydrocarbons). Relative contraindications include decreased peristalsis (eg, decreased bowel sounds, abdominal distention, ileus, severe constipation) (Vale et al, 1999; Mauro et al, 1994).
g) COMPLICATIONS: Include constipation, intestinal bleeding, bowel obstruction, appendicitis, charcoal bezoars, and aspiration which may be complicated by acute respiratory failure, adult respiratory distress syndrome or bronchiolitis obliterans (Ghannoum & Gosselin, 2013; Ray et al, 1988; Atkinson et al, 1992; Gomez et al, 1994; Mizutani et al, 1991; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Mina et al, 2002; Harsch, 1986; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002).

6.5.3)

A) MONITORING OF PATIENT

1) Monitor vital signs, mental status and neurologic exam. Monitor serum electrolytes, renal function and liver enzymes. Obtain 24 hour urine collection for thallium.
2) Urinary excretion of thallium in excess of 10 to 20 mg in 24 hours is considered diagnostic. Although less reliable for diagnosis than 24 hour urinary thallium excretion, whole blood thallium exceeding 100 mcg/dL indicates potential poisoning.
3) Thallium is radiopaque, an abdominal radiograph may help assess the adequacy of GI decontamination after acute ingestion. Nerve conduction studies may be useful to evaluate peripheral neuropathy.

B) PRUSSIAN BLUE

1) Insoluble Prussian blue, a nonabsorbable lattice of potassium ferric ferrocyanide, is used to treat patients with known or suspected internal contamination with radioactive or nonradioactive thallium, to increase their rates of elimination (Prod Info Radiogardase(TM), 2003; Stevens et al, 1974; Schwartz et al, 1988).
2) AVAILABLE FORMS: Insoluble Prussian blue is available as 0.5 g blue powder in gelatin capsules for oral administration (Prod Info Radiogardase(TM), 2003).
3) DOSING

a) RADIOACTIVE THALLIUM: ADULTS AND ADOLESCENTS 13 YEARS OF AGE OR OLDER: 3 g orally 3 times a day; treatment should be initiated as soon as possible after contamination is suspected, and should be continued for a minimum of 30 days, and continued thereafter based on the level of contamination and the judgment of the clinician. When internal radioactivity has decreased substantially, the dose may be reduced to 1 or 2 grams 3 times a day to improve gastrointestinal tolerance. If swallowing large numbers of capsules is not tolerated, capsules may be opened and mixed with bland food or liquids. May be taken with food to stimulate excretion of thallium (Prod Info Radiogardase(TM), 2003).

1) Lactulose, sorbitol, or mannitol may be added to insoluble Prussian blue to prevent obstipation (Thompson & Church, 2001; Malbrain et al, 1997a).

b) THALLIUM POISONING: ADULTS AND ADOLESCENTS 13 YEARS OF AGE OR OLDER: 3 g orally 3 times a day. Optimal duration of therapy is not established. Monitor urinary thallium concentration to determine the need for continued therapy; some authors recommend continuing therapy until urinary thallium elimination is below 0.5 mg/day (Hoffman, 2003). The dose may be reduced to 1 or 2 grams 3 times a day to improve gastrointestinal tolerance in patients requiring prolonged treatment (Prod Info Radiogardase(TM), 2003). If swallowing large numbers of capsules is not tolerated, capsules may be opened and mixed with bland food or liquids. May be taken with food to stimulate excretion of thallium (Prod Info Radiogardase(TM), 2003).
c) In one case, a young adult was given Prussian blue 4 g every 6 hours for 2 weeks and received hemodialysis during one week and was discharged 2 weeks later. Most symptoms were resolved, but the patient had ongoing mild limitations in mobility and superficial paresthesias (ie, the toes) (Nocen et al, 2008).

1) Lactulose, sorbitol, or mannitol may be added to insoluble Prussian blue to prevent obstipation (Thompson & Church, 2001; Malbrain et al, 1997a).

d) RADIOACTIVE THALLIUM

1) CHILDREN (2 TO 12 YEARS): 1 g orally 3 times a day; treatment should be initiated as soon as possible after contamination is suspected, and should be continued for a minimum of 30 days, and continued thereafter based on the level of contamination and the judgment of the clinician. Administration of a laxative may be required to prevent obstipation. Safety and efficacy of insoluble Prussian blue in infants and neonates have not been established. If swallowing large numbers of capsules is not tolerated, capsules may be opened and mixed with bland food or liquids. May be taken with food to stimulate excretion of thallium (Prod Info Radiogardase(TM), 2003).

e) THALLIUM POISONING

1) CHILDREN (2 TO 12 YEARS): 1 g orally 3 times a day. Optimal duration of therapy is not established. Monitor urinary thallium concentration to determine the need for continued therapy; some authors recommend continuing therapy until urinary thallium elimination is below 0.5 mg/day (Hoffman, 2003). Administration of a laxative may be required to prevent obstipation. Safety and efficacy of insoluble Prussian blue in infants and neonates patients have not been established (Prod Info Radiogardase(TM), 2003).
2) If swallowing large numbers of capsules is not tolerated, capsules may be opened and mixed with bland food or liquids. May be taken with food to stimulate excretion of thallium (Prod Info Radiogardase(TM), 2003).

4) MECHANISM

a) Insoluble Prussian blue acts via ion-exchange, adsorption, and mechanical trapping within its crystal structure, and has a very high affinity for radioactive and nonradioactive thallium. After oral administration, it is not absorbed by the gastrointestinal tract. It binds with thallium isotopes after ingestion or excretion in bile, thereby reducing GI absorption, as well as reducing reabsorption via enterohepatic circulation. This changes the primary route of elimination from the kidney to the feces, and increases the rate of elimination of these isotopes (Prod Info Radiogardase(TM), 2003).
b) There are 2 different forms of Prussian blue, soluble (colloidal) and insoluble (noncolloidal). In studies evaluating the binding characteristics, insoluble Prussian blue was slightly more effective in vivo; however, soluble and insoluble Prussian blue were about equally effective in vivo (Thompson & Church, 2001).
c) ADVERSE EFFECTS

1) Constipation, gastric distress, and asymptomatic hypokalemia have been reported in patients taking insoluble Prussian blue (Prod Info Radiogardase(TM), 2003; Hoffman, 2003; Thompson & Church, 2001).

d) EFFICACY

1) In data provided by the manufacturer, 34 patients with nonradioactive thallium poisoning treated with insoluble Prussian blue were reported in the literature. In these cases, the drug reduced the mean serum biologic half-life of thallium from 8 days to 3 days (Prod Info Radiogardase(TM), 2003).
2) In a small case series, 11 patients with thallium intoxication were successfully treated with Prussian blue after ingesting various amount of thallium. Patients presented from 1 to 151 days after thallium exposure, and all had classic symptoms of thallium poisoning to varying degrees. After 3 to 20 days of Prussian blue therapy, resolution of symptoms was observed, and elimination of thallium excretion in urine, feces, and blood was noted (Stevens et al, 1974a). Other similar cases of the use of Prussian blue following thallium exposure have been reported (Sun et al, 2012; Pau, 2000; Atsmon et al, 2000; Malbrain et al, 1997a; Pai, 1987a; Ghezzi & Bozza Marrubini, 1979).

e) Nine people poisoned with thallium tainted food received Prussian blue (Pai, 1987). Two grams of Prussian blue were administered orally three times a day for a total duration of six weeks. Symptoms improved and all patients were discharged from the hospital within six weeks. Total body thallium removal was not calculated nor were pretreatment serum or urine thallium levels given. Thus, efficacy in removal could not be documented.
f) Following a massive ingestion (about 9 grams), with serum Tl of 5240 mcg/L and urine Tl of 69,600 mcg/L, a 38-year-old woman was administered 3 g Prussian blue through a gastric tube, followed by 500 mg suspended in mannitol 6 times daily for 21 days in conjunction with hemodialysis (first session 14 hours followed by 10 days of 6 hours/day for a total of 74 hours). These treatments were stopped when serum Tl was 49 mcg/L and the urine Tl was 164 mcg/L (Malbrain et al, 1997). The authors attribute the success of these measures to early and aggressive treatment.
g) Prussian blue was reported to result in increased fecal excretion of thallium, with approximately 2,000 mg eliminated over 20 days by this route, compared to 820 mg over 46 days in the urine, and 225 mg over 25 days in dialysate. Because of other concomitant therapies, including diethyldithiocarbamate, potassium, hemodialysis, and hemofiltration, the effects of Prussian blue are difficult to assess. Fecal excretion while not receiving therapy was not reported (Wainwright et al, 1988).
h) In rodent models, Prussian blue has been shown to increase survival after thallium intoxication and decrease tissue thallium concentrations without redistributing thallium to brain (Meggs et al, 1994; Rios & Monroy-Noyola, 1992; Barroso-Moguel et al, 1994; Meggs et al, 1995).
i) In rat models, Prussian blue was superior to 2,3-dimercapto-1-propanesulfonic acid (DMPS) in decreasing tissue concentrations (in 4 target organs) of thallium in acutely poisoned animals. DMPS failed to significantly affect thallium in target organs, although it lowered thallium whole blood concentrations. Prussian blue limited incorporation of thallium in all tissues studied (Mulkey & Oehme, 2000).

5) END-POINT: Some authors advocate continuing Prussian blue until urine thallium excretion is in the normal range (0 to 10 mcg/24 hours) (Schwartz et al, 1988).

a) Normal urine thallium excretion is 0 to 10 mcg/24 hours (Feldman & Levisohn, 1993).

C) POTASSIUM

1) Potassium chloride therapy has been reported to enhance excretion of thallium. However, it may produce transient worsening of acute neurological symptoms (Roby et al, 1984; Bank, 1972; Anon, 1978). Furthermore, there are conflicting reports as to its efficacy in enhancing elimination (Koshy & Lovejoy, 1981).
2) CASE REPORT: Two to 3-fold increases in urinary excretion of thallium (20 to 30 mg/day) were documented in a 64-year-old man who ingested an unknown amount of thallium after treatment with 500 mg potassium chloride orally every 4 hours for 6 days (Bank, 1972; (Papp, 1969).
3) ANIMAL STUDY: In a murine model of severe thallium toxicity potassium chloride treated mice showed a trend towards decreased survival (1 of 10) compared with controls (6 of 20) (Meggs et al, 1995). The combination of potassium chloride and Prussian blue conferred no survival advantage over Prussian blue alone (3 of 10 vs 14 of 20 respectively).

D) PENICILLAMINE

1) In a rodent model penicillamine alone redistributed thallium from other tissues to the brain (Rios & Monroy-Noyola, 1992).

a) In the same study the combination of Prussian blue and penicillamine was more effective than Prussian blue alone in increasing the LD50 of thallium and removed thallium from tissues without redistribution to brain (Rios & Monroy-Noyola, 1992). Animals treated with penicillamine and Prussian blue had significantly lower renal thallium levels than those treated with Prussian blue alone.

2) In another rat study penicillamine alone increased mortality from thallium poisoning (100%) compared with controls (87%) while Prussian blue decreased mortality (56%) (Barroso-Moguel et al, 1994). The combination of penicillamine and Prussian blue was most effective in decreasing mortality (25%).

a) Histologic evaluation of cerebellar Purkinje cells revealed that the combination of Prussian blue and penicillamine was most effective in protecting against thallium induced neurotoxicity (Barroso-Moguel et al, 1994). Prussian blue alone was less effective in reducing neurotoxicity while penicillamine alone increased the number of altered Purkinje cells.

E) CONTRAINDICATED TREATMENT

1) Therapy with diethyldithiocarbamate has been reported to result in dangerous redistribution of thallium to the CNS and is CONTRAINDICATED (Kamerbeek et al, 1971a).
2) Administration of diethyldithiocarbamate was associated with an increase in serum thallium from 800 to 1,350 micrograms/liter in one case. This was accompanied by clinical deterioration (stupor). After the second dose ventilatory failure occurred, and artificial ventilation was required for 3 weeks (Wainwright et al, 1988).

F) ACUTE LUNG INJURY

1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

Inhalation Exposure

6.7.1)

A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Dermal Exposure

6.9.1)

A) DERMAL DECONTAMINATION

1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

1) SUMMARY

a) Hemodialysis is indicated in the presence of renal failure (Saddique & Peterson, 1983). Thallium is primarily eliminated in the kidneys (Sun et al, 2012).

2) CASE REPORT/CASE SERIES

a) CASE SERIES: In a series of 14 patients with thallium poisoning, 12 patients required hemodialysis. All patients were also treated with oral Prussian blue. Sessions (4 to 6 hours/day) were continued until symptoms resolved and blood and urine thallium concentrations were less than 50 and 300 mcg/L, respectively (Sun et al, 2012).
b) CASE REPORT: Hemodialysis instituted 12 hours postingestion and performed repeatedly for 200 hours over 10 days removed 143 mg of thallium in 120 hours in a patient who had ingested 2 g of thallium sulfate (1.6 g thallium); 110 mg was excreted in the urine during this time. Although the amount removed was more than the endogenous clearance, the total amount removed is small and is unlikely to affect clinical outcome (Pedersen et al, 1978).
c) CASE REPORT: Hemodialysis was initiated within hours of a massive Tl ingestion in conjunction aggressive potassium replacement (to maintain serum potassium between 4.5 and 5 mmol/L). The patient also received Prussian blue through a gastric tube. Initial serum Tl level was 5240 mcg/L. After the first hemodialysis session (14 hours) serum Tl levels decreased to 2490 mcg/L. Clearance rates were estimated to range from 96 to 150 mL/min. Hemodialysis was discontinued when serum Tl was 49 mcg/L (approximately 6 hours/day following initial session for 10 days for a total dialysis time of 74 hours) (Malbrain et al, 1997).
d) High-flux hemodialysis, with a blood and countercurrent dialysate flow of 300 mL/min, along with forced diuresis and administration of Prussian blue, was initiated in a 49-year-old man who intentionally ingested 50 g of rat poison containing thallium sulfate. It was determined, using a volume of distribution of 30 L/kg, that the total amount of thallium present in the body was 990 mg. His initial serum thallium level was 440 mcg/L. After 4 hours of high-flux hemodialysis, continuous hemodialysis was initiated, with a blood flow of 110 mL/min for 4 days and the dialysate and dialyzer changed every 12 hours.

1) After 5 days of continuous hemodialysis, the patient's serum thallium level decreased to less than 100 mcg/L. Regular measurements of the patient's blood, urine, and dialysate thallium concentrations indicated that he excreted approximately 130 mg of thallium via forced diuresis, and 480 mg of thallium was removed by hemodialysis. Approximately 4 weeks postingestion, the patient was discharged without sequelae. His blood thallium concentration at the time of discharge was 10 mcg/L (Kielstein et al, 2004).

1) Hemoperfusion has been reported to enhance excretion of thallium sulfate (De Backer et al, 1982).

a) CASE REPORT: A 32-year-old woman who ingested 100 mg of thallium sulfate by history was treated with a combination of hemoperfusion-hemodialysis following classical therapy including Prussian Blue. The clearance rates of the hemoperfusion and hemodialysis were calculated to be 139 and 47 mL/min, respectively.
b) A 4 hour hemoperfusion-hemodialysis treatment resulted in 12 mg and 1.2 mg thallium eliminated by hemoperfusion and hemodialysis, respectively. Hemoperfusion appeared to enhance excretion of thallium since only 2.3 mg was excreted in the urine over a 16 hour collection period (De Backer et al, 1982).
c) CASE REPORTS: Three young adults (ages 24 to 37 years) were intentionally poisoned with thallium and developed clinical and laboratory evidence of significant thallium toxicity. Hemoperfusion and hemodialysis were performed (between 5 and 8 cycles were completed) on each patient once the symptoms of thallium toxicity were confirmed (3 weeks after exposure). The patients clinically improved in regards to skin findings, neurological symptoms and liver function parameters; however, paresthesia persisted. A decrease in serum and urine thallium concentrations was also observed in each patient during the course of therapy (Zhao et al, 2008).

2) However, other investigators have concluded that hemoperfusion does not affect the time course of thallium intoxications.

a) CASE REPORT: Twelve hours of hemoperfusion removed 63 mg, compared to 300 mg eliminated in the urine during forced diuresis in one patient (Heath et al, 1983).
b) CASE REPORT: In another patient who ingested 8 g of thallium, 149 mg was removed after 4 hours of hemoperfusion-hemodialysis (Aoyama et al, 1986).
c) CASE SERIES: The amount of thallium removed during a 4 hour period of hemoperfusion ranged from 15 to 84 mg in 3 patients (DeGroot et al, 1985a).

1) CASE REPORT: A 40-year-old man was intentionally poisoned with thallium and about 10 hours after exposure he developed numbness in all 4 extremities with no pain or gastrointestinal symptoms. Upon admission on day 2, he was initially diagnosed with Guillain-Barre syndrome but his girlfriend admitted to poisoning his food with thallium nitrate (amount unknown). An initial blood thallium level was 3764 ng/mL (reference value, less than 0.1 ng/mL); other laboratory studies and diagnostic studies were within normal limits. Once admitted, the patient developed numbness and pain in the distal arms and legs that spread proximally. Initial treatment included the following: Prussian blue (250 mg/kg/day orally), potassium replacement (to maintain blood potassium at 4.0 to 4.5 mmol/L), DMPS (250 mg/day IM) and other supportive measures as needed. In addition, hemoperfusion (HP) was begun at 2 hours and 24 hours after admission and performed for 5 hours. After 47 hours, HP was repeated for 2.5 hours. This was followed by 5 rounds of continuous veno-venous hemodiafiltration (CVVH) on days 3, 7, 11, 14 and 21 for a total of 213.5 hours of therapy. Blood levels declined by 20.2%, 34.8% and 32.2%, respectively, following the 3 HP treatments and by 63.5%, 64.2%, 42.1%, 18.6% and 22.6%, respectively, following each of the 5 CVVH treatments. Side effects of CVVH therapy included bleeding at access sites and thrombocytopenia. By day 6, symptoms gradually began to improve with limb pain significantly improved by day 15. On day 23, his blood thallium level decreased to 24 ng/mL and he refused further CVVH therapy. On day 33, blood thallium was 9 ng/mL (Huang et al, 2014).

1) Forced diuresis may enhance both early and late excretion.
2) CASE REPORT: Forced diuresis in conjunction with Prussian blue was used to treat a 26-year-old woman who ingested 600 mg thallium. Increased thallium excretion was noted after treatment with 12 liters/hour 5 percent dextrose and normal saline (Van Hees, 1975).
3) CASE REPORT: Forced diuresis with furosemide and potassium replacement, in conjunction with continuous hemodialysis and oral Prussian blue 3 g followed by 0.5 g/hour, was used to treat a suicidal ingestion of thallium. Elimination of 95% of the target amount (41% of the ingested dose) was achieved within 100 hours using this methodology (Brodersen et al, 1995).
4) This procedure is not recommended where impaired renal and cardiac function complicate the clinical picture.
5) CASE REPORT: Forced diuresis in combination with Prussian blue administration and hemodialysis was used to treat a 49-year-old man who intentionally ingested 50 g of rat poison containing thallium sulfate. The patient's initial serum thallium level was 440 mcg/L. It was determined that the total amount of thallium present in the body, using a volume of distribution of 30 L/kg, was 990 mg. Measurement of the patient's urine showed that he excreted approximately 130 mg of thallium via forced diuresis (Kielstein et al, 2004).

1) CASE REPORT: A 48-year-old woman presented with acute peripheral neuritis and progressive alopecia. Laboratory studies revealed a blood thallium concentration of 97 mcg/L (normal 0.9 mcg/L), indicating acute thallotoxicosis. The patient refused administration of Prussian blue due to the possibility of constipation, therefore double-filtration plasmapheresis (DFPP) was performed. In one DFPP session, 460 mL of plasma was replaced with 10.3% of albumin and returned to the body with purified plasma and blood cells, with the duration of one session lasting 4 hours. The patient underwent a total of 5 treatments (one treatment every 2 days). Following the five DFPP sessions, the patient's blood thallium concentration decreased to 13 mcg/L and her peripheral neuritis gradually resolved (Tian et al, 2005).

Abstracts

Case Reports

1) A 26-year-old man who ingested 10 g of thallous malonate (8 g thallium or 114 mg/kg) developed immediate nausea and vomiting. On presentation 6 hours postingestion he was anuric, dehydrated, and had diarrhea and abdominal pain. Seven hours after admission, paresthesias began. Ventricular extrasystoles were noted 18 hours after admission; heart dilatation and bilateral pleural effusions were present. Blood pressure decreased progressively and the patient died of cardiac failure 40 hours postingestion. Postmortem evaluation revealed the highest concentration of thallium in the heart (142 mcg/g) (Aoyama et al, 1986).

1) A 20-year-old chemistry student presented approximately 2 to 6 days after presumed acute thallium ingestion. He reported polyuria, paresthesias of the finger and lips, and a brief blackout. Shortly after admission, he became drowsy and had a brief seizure, followed by progressive weakness and paresthesias. Severe calf pain required epidural analgesia. Neurologic impairment progressed to include dysarthria, difficult swallowing, and paralytic ileus. Cardiac manifestations included sinus tachycardia, mild hypertension, and transient ST and T wave changes, followed by an episode of ventricular fibrillation. He was treated simultaneously with Prussian blue, forced diuresis, potassium, hemodialysis, hemofiltration, and diethyldithiocarbamate. Each dose of diethyldithiocarbamate was followed by an increase in serum thallium and clinical deterioration, including ventilatory failure, necessitating artificial ventilation. The initial serum concentration was 5,750 mcg/L, with a urine level of 60,000 mcg/L. Residual sequelae after one year included flaccid paraparesis, cerebellar ataxia, contractures, memory impairment, and decreased performance on IQ testing (Wainwright et al, 1988).

1) ROUTE UNKNOWN

a) Four members from a family of 6 in Granada, Spain, experienced thallium toxicosis from an unidentified source. Clinical signs seen in the father, mother, and two of their daughters included: severe abdominal and spinal pain; paresthesias; vomiting; weakness in the legs; diplopia; headache; dysphagia; gastrointestinal and genitourinary hemorrhage; and hair loss. Poisoning due to thallium is rarely diagnosed in Spain (Villnueva et al, 1990).

1) A 39-year-old man became acutely ill with generalized body pain and tingling after returning from a holiday. He developed hair loss, nystagmus, bilateral lower motor neuron weakness, and flaccid paralysis with absent reflexes in his legs. Serum thallium at 30 days postadmission was 1000 nanomoles/liter. Following complications including septicemia, tachycardias, and psychosis, the patient required 96 days of assisted ventilation and a total of 224 days of hospitalization. Visual handicaps, lack of fine finger function, and inability to walk more than a few steps persisted 500 days after the initial insult. The source of his exposure to thallium remains unknown (Chandler et al, 1990).

1) A 50-year-old woman experienced nearly complete neurological recovery by 18 months following diagnosis of thallotoxicosis. She required mechanical ventilation for more than 2 months. Treatment consisted of forced diuresis, administration of Prussian blue 150 mg/kg/day dissolved in mannitol for 3 weeks, and intensive physiotherapy (Vergauwe et al, 1990).

Range Of Toxicity

Serum Plasma Blood Concentrations

7.5.2)

A) TOXIC CONCENTRATION LEVELS

1) CASE SERIES

a) Ten cases of acute thallium poisoning occurred in 2 families that consumed a cake from a local bakery that was contaminated with thallium (the source was unknown). Approximately 5 to 7 days after transfer to a higher level of care, thallium was detected in blood and urine samples in all cases. The median thallium level was 323.5 mcg/L (range: 53 to 1700 mcg/L) and the median urine level of 9 cases was 1959 mcg/L (range: 452 to 2909 mcg/L). Thallium was detected in the cake sample. Serial levels showed a marked decrease in blood thallium concentration (median concentration 10.5 mcg/L; range: 5 to 46 mcg/L) 2 weeks after initiating therapy; the median urine concentration was 79 mcg/L (range: 27 to 150 mcg/L) (Al Hammouri et al, 2011).
b) Blood thallium concentrations ranged from 0.5 to 11 mg/L in 5 adults who died within 4 to 15 days after ingestion of up to 17 g thallium (Grunfeld & Hinostroza, 1964; Smith & Doherty, 1964; Baselt, 2000).

2) CASE REPORTS

a) ADULT

1) A 40-year-old man was intentionally poisoned with thallium nitrate (amount unknown). His initial blood thallium level was 3764 ng/mL (reference value, less than 0.1 ng/mL). Following aggressive care, including hemoperfusion and continuous veno-venous hemodiafiltration, his symptoms, including limb pain and numbness, improved significantly. The patient recovered without neurologic deficits (Huang et al, 2014).
2) A 25-year-old woman was found to have a blood thallium concentration of 2.9 mcg/dL and a urine thallium concentration of 120 mcg/dL following 2 ingestions, separated by several months, of thallium containing rodenticide (Alarcon-Segovia et al, 1989). The exact time of ingestions in relation to reported level was not stated.
3) A 19-year-old man had a urine thallium concentration of 1 mcg/dL approximately one month following an ingestion of thallium-containing rodenticide in a suicide attempt (Alarcon-Segovia et al, 1989).
4) A 20-year-old man with an initial serum concentration of 5,750 mcg/L and urine concentration of 60,000 mcg/L survived with severe neurological sequelae (Wainwright et al, 1988).
5) A 50-year-old woman with an initial urine thallium concentration of 7.1 mg/L had nearly complete neurologic recovery by 18 months after diagnosis (Vergauwe et al, 1990). Source of subacute thallium poisoning was not determined.
6) A 38-year-old woman with an initial serum thallium concentration of 5,240 mcg/L and urine thallium concentration of 69,600 mcg/L had nearly complete neurologic recovery by 10 weeks after the poisoning (Malbrain et al, 1997).
7) Laboratory analysis of blood, hair, and urine, performed 21 days following a 15-day consumption, by a 26-year-old woman, of wheat contaminated with thallium, showed thallium levels of 0.1206 ppm, 0.0459 ppm, and 30 ppb, respectively. The recommended normal levels for thallium are less than 2 ppb, 5 to 10 ppb, and less than 5 ppb, respectively (Saha et al, 2004).
8) Paired serum and spinal fluid thallium concentrations, following thallium intoxication of a 48-year-old man, were 8700 microns/liter (normal is less than 2 microns/liter) and 1200 microns/liter, respectively, on hospital day 1; however, on hospital day 3, the paired serum and spinal fluid thallium levels were 7200 microns/liter and 2100 microns/liter, respectively, indicating that thallium distributes more slowly into the CNS than in blood which may account for the progression of neurotoxicity despite a decrease in thallium serum concentrations (Sharma et al, 2004).
9) The thallium serum level of a 49-year-old man was 440 mcg/L following ingestion of 50 g of a rat poison containing thallium sulfate. It was determined, using a volume of distribution of 30 L/kg, that the total amount of thallium present in the body was 990 mg (Kielstein et al, 2004).
10) CASE REPORT: A 48-year-old woman presented with acute peripheral neuritis and progressive alopecia. Laboratory studies revealed a blood thallium concentration of 97 mcg/L (normal 0.9 mcg/L), indicating acute thallotoxicosis. Following five treatments of double-filtration plasmapheresis (one treatment every 2 days), the patient gradually recovered and was discharged 21 days later (Tian et al, 2005).
11) Five days postingestion, the blood thallium concentrations of two patients, who drank 750 mL and 500 mL of water containing thallium at a concentration of 3,124 mg/L, were 2,056 mcg/L and 950 mcg/L, respectively (Tsai et al, 2006).
12) An adult had an initial blood thallium level of 40,980 mcg/mL and a urine level of 608 mcg/mL following homicidal thallium poisoning. Treatment included hemodialysis, potassium, laxatives and high-dose multivitamins. The patient gradually recovered from peripheral neuropathy both clinically and neurophysiologically, but had persistent visual impairment (vision 6/60 bilaterally) (Kalita & Misra, 2006).
13) Postmortem thallium concentrations of a 48-year-old man following thallium intoxication are as follows (Sharma et al, 2004):

TISSUE/FLUID	THALLIUM LEVELS (MCG/L)
Femoral blood	620
Heart blood	580
Brain	66
Cecum	27
Descending Colon	25
Duodenum	31
Ileum	29
Jejunum	26
Heart muscle	72
Kidney, medulla, cortex	50
Liver	32
Lung	27
Skeletal muscle	33
Head hair, full length	68

Workplace Standards

1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

a) Adopted Value

1) Thallium

a) TLV:

1) TLV-TWA: 0.02 mg/m(3)
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: I, Skin
3) Definitions:

a) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
b) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.

c) TLV Basis - Critical Effect(s): GI dam; peripheral neuropathy
d) Molecular Weight: 204.37

1) For gases and vapors, to convert the TLV from ppm to mg/m(3):

a) [(TLV in ppm)(gram molecular weight of substance)]/24.45

2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:

a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

e) Additional information:

b) Adopted Value

1) Thallium and compounds, as TI

a) TLV:

1) TLV-TWA: 0.02 mg/m(3)
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: I, Skin
3) Definitions:

c) TLV Basis - Critical Effect(s): GI dam; peripheral neuropathy
d) Molecular Weight: Varies

1) For gases and vapors, to convert the TLV from ppm to mg/m(3):

a) [(TLV in ppm)(gram molecular weight of substance)]/24.45

2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:

a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

e) Additional information:

B) ACGIH TLV Values for CAS563-68-8 (American Conference of Governmental Industrial Hygienists, 2010):

1) Not Listed

C) NIOSH REL and IDLH Values for CAS7440-28-0 (National Institute for Occupational Safety and Health, 2007):

1) Listed as: Thallium (soluble compounds, as Tl)
2) REL:

a) TWA: 0.1 mg/m(3)
b) STEL:
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: [skin]

1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.

f) Note(s):

3) IDLH:

a) IDLH: 15 mg Tl/m3
b) Note(s): Not Listed

D) NIOSH REL and IDLH Values for CAS563-68-8 (National Institute for Occupational Safety and Health, 2007):

1) Not Listed

E) Carcinogenicity Ratings for CAS7440-28-0 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Thallium
2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Thallium and compounds, as TI
3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
4) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Thallium (soluble compounds, as Tl)
6) MAK (DFG, 2002): Not Listed
7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

F) Carcinogenicity Ratings for CAS563-68-8 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
2) EPA (U.S. Environmental Protection Agency, 2011): Inadequate information to assess carcinogenic potential. ; Listed as: Thallium acetate
3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
5) MAK (DFG, 2002): Not Listed
6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

G) OSHA PEL Values for CAS7440-28-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Listed as: Thallium, soluble compounds (as Tl)
2) Table Z-1 for Thallium, soluble compounds (as Tl):

a) 8-hour TWA:

1) ppm:

a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

2) mg/m3: 0.1

a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

3) Ceiling Value:
4) Skin Designation: Yes
5) Notation(s): Not Listed

H) OSHA PEL Values for CAS563-68-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Not Listed

Summary

Minimum Lethal Exposure

1) ADULT

a) Death has been reported after ingestion of 3.2 g of thallium sulfate (Grunfeld & Hinostroza, 1964), and 5 to 10 g of thallium nitrate (Davis et al, 1981), 10 g of thallous malonate (8 g thallium) (Aoyama et al, 1986).
b) The reported adult fatal dose is approximately 1 g of absorbed thallium based on extrapolation from studies in dogs.
c) Administration of 930 mg of thallous acetate in 2 adults resulted in death; a coworker given 310 mg survived (Cavanagh et al, 1974).

2) PEDIATRIC

a) CASE REPORTS: Three children, aged 5, 7, and 10 years, who were inadvertently given 85 to 89 mg/kg of thallium acetate and subsequently died within 24 hours (Lynch et al, 1930).

Maximum Tolerated Exposure

1) The more water-soluble forms (sulfate, acetate, malonate, and carbonate) are more toxic than the less water-soluble forms (sulfide and iodide) (Saddique & Peterson, 1983).
2) Thallium acetate, 8 mg/kg as a single dose, was formerly used as a depilatory to treat ringworm in children. This resulted in an incidence of thallotoxicosis in about 6% and fatality in 0.1% (Munch, 1934).

1) ADULT

a) Ingestion of 650 mg of thallium sulfate by four adults has been associated with survival (Grunfeld & Hinostroza, 1964), as has 2 g of thallium sulfate (Pedersen et al, 1978), 1.3 g of thallium sulfate (Grunfeld & Hinostroza, 1964), 9 g thallium sulfate in an adult (Malbrain et al, 1997), 1 g of thallium sulfate (15 mg/kg of thallium) (Richelmi et al, 1980), and 20 g of thallium iodide (12 g thallium) (Koshy & Lovejoy, 1981).
b) Two adults survived ingestions of an estimated thallium dosage of 2.3 g and 1.5 g, respectively. Neurologic symptoms slowly resolved over a one year period (Lu et al, 2007).

Pharmacology Toxicology

Toxicologic Mechanism

Physicochemical

Molecular Weight

Animal Toxicology

Clinical Effects

11.1.3)

A) ACUTE POISONING -

1) Gastroenteritis (anorexia, vomiting, diarrhea, abdominal sensitivity) is often observed. Motor parlysis, conjunctivitis, bronchitis, pneumonia, and some alopecia may occur. Cardiovascular collapse, sialosis, and stomatitis have been reported (Ruhr & Andries, 1985).

B) CHRONIC POISONING -

1) Dermatological lesions may be the primary manifestation. Skin hyperkeratosis, parakeratosis, hyperemia, and hyaline changes may be noted (VPB, 1984). Lesions are usually near mucocutaneous junctions, inner surface of the pinna, axillae, and inguinal regions. Alopecia and secondary infection may be present. Fever is usually absent (Ruhr & Andries, 1985).

11.1.6)

A) ACUTE POISONING -

1) Acute gastroenteritis, bloody diarrhea, vomiting, and fever may occur abruptly, followed by depression, anorexia, and dehydration. Bone marrow depression (leukopenia, anemia), and liver and kidney damage may develop as the disease progresses. Skin findings may be absent (Zook et al, 1968).

B) CHRONIC POISONING -

1) Cats may present with apathy, anorexia, and occasionally vomiting. Skin changes ensue shortly thereafter, usually beginning with reddened, swollen, and crusting at the lips and nasal cleft. Lesions progress to the chin and face. Eyelids may be contracted, and blepharitis, conjunctivitis, and ocular discharge may be present.
2) Hair loss begins as skin lesions evolve, leaving oozing areas of raw skin. Eventually foot pads, toes, limbs, neck, axillae, flank, ventral abdomen, and perineum are involved.
3) Other signs noted include ataxia, episodes of trembling, falling, or rolling and hindlimb paresis or paralysis (Zook et al, 1968).

Treatment

11.2.2)

A) GENERAL

1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.

11.2.4)

A) GASTRIC DECONTAMINATION

1) RODENT

a) Activated charcoal 0.5 g/kg/day, given twice daily resulted in increased elimination of thallium in the feces in rats. In this study activated charcoal was more effective than Prussian blue (Lehman & Favare, 1984).

11.2.5)

A) GENERAL TREATMENT

1) Treatment is primarily supportive. Forced diuresis or hemodialysis may be helpful in long-term management (Ruhr & Andries, 1985). Blood transfusions may be needed, particularly in cats.

Range Of Toxicity

11.3.2)

A) CAT

1) 10 mg/kg: 1 of 2 cats died (Zook et al, 1968).
2) 20 mg/kg or more: all 5 cats died (Zook et al, 1968).

Continuing Care

11.4.2)

11.4.2.2) GASTRIC DECONTAMINATION

A) GASTRIC DECONTAMINATION

1) RODENT

References

General Bibliography

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THALLIUM

Classification | Detailed evidence-based information

Therapeutic Toxic Class

Specific Substances

Available Forms Sources

Life Support

Clinical Effects

Laboratory Monitoring

Treatment Overview

Range Of Toxicity

Summary Of Exposure

Vital Signs

Heent

Cardiovascular

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Monitoring Parameters Levels

Radiographic Studies

Methods

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Enhanced Elimination

Case Reports

Serum Plasma Blood Concentrations

Workplace Standards

Summary

Minimum Lethal Exposure

Maximum Tolerated Exposure

Toxicologic Mechanism

Molecular Weight

Clinical Effects

Treatment

Range Of Toxicity

Continuing Care

General Bibliography