Poison of the month, June: THALLIUM

[greenban]

Dear Gentle Readers:

Thallium poisoning has long been one of my favorites. Until very recently there were no effective treatments, thus it was a slow and painful death, often heralded by hair loss and a horribly painful burning sensation in the hands and feet. Only a very suspicious Doctor would think to test for thallium, and again, until recently their was no effective treatment.

The Mensa Murderer used Thallium, and it was a favorite of Dame Agatha Christie (along with strictnine).

And now, without further ado.......

Thallium Poisoning:

[AFMom]

Ahhhhh - yes - I remember that one from Agatha Christie...... such a morbid thread to brighten up my cruddy Monday!:crackedup

[greenban]

From Wikipedia:

Famous uses as a poison:
In 1953, Australian Caroline Grills was sentenced to life in prison after three family members and a close family friend died. Authorities found thallium in tea that she had given to two additional family members.

In 1957, Nikolai Khokhlov, a former KGB assassin, was poisoned with thallium. Khokhlov fell ill with stomach cramps and nausea and within days his hair had fallen out and he was covered with marks on his skin. He fled the Soviet Union to Germany where doctors suspected thallium poisoning and tried every known antidote without success. Khokhlov was then taken to the US hospital and treated with hydrocortisone, steroids, and blood and plasma transfusions and he eventually recovered.

In 1971, thallium was the main poison that Graham Frederick Young used to poison around 70 people in the English village of Bovingdon, Hertfordshire, of which 2 died.

Zhu Ling (1973) the victim of an unsolved 1995 thallium poisoning case in Beijing, China. In 1994, Zhu Ling was a sophomore in Class Wuhua2 (Physical Chemistry) at Tsinghua University in Beijing. She began to show strange and debilitating symptoms at the end of 1994, when she reported experiencing acute stomach pain, along with extensive hair loss ultimately she was diagnosed on Usenet with poisoning by thallium. To this date speculation of the true poisoner is still discussed by many Chinese expatriates overseas.

In 1988, members of the Carr family from Alturas, Polk County, Florida fell ill from what appeared to be thallium poisoning. Peggy Carr, the mother, died slowly and painfully from the poison. Her son and stepson were critically ill but eventually recovered. The Carr's neighbor, George J. Trepal, a chemist and member of Mensa, was convicted of murdering Mrs. Carr and attempting to murder her family and sentenced to death. The thallium was slipped into bottles of Coca-Cola at the Carr's home and Trepal's.

Corroded thallium rod in June 2004, 25 Russian soldiers earned Honorable Mention Darwin Awards after becoming ill from thallium exposure when they found a can of mysterious white powder in a rubbish dump on their base at Khabarovsk in the Russian Far East. Oblivious to the danger of misusing an unidentified white powder from a military dump site, the conscripts added it to tobacco, and used it as a substitute for talcum powder on their feet.

In 2005, a 17 year old girl in Numazu, Shizuoka, Japan, admitted to attempting to murder her mother by lacing her tea with thallium, causing a national scandal.

In February 2007, two Americans, Marina and Yana Kovalevsky, a mother and daughter, visiting Russia were hospitalized due to thallium poisoning. Both had emigrated from the Soviet Union to the United States in 1989 and had made several trips to Russia since then.

In February 2008, members of Iraqi air force club and some of their children were poisoned by cake laced with thallium. Two of the children died.

In fiction:
Agatha Christie, who worked as a pharmacist, used thallium as the agent of murder in her detective fiction novel The Pale Horse — the first clue to the murder method coming from the hair loss of the victims.

In Nigel Williams' 1990 novel The Wimbledon Poisoner, Henry Far uses thallium to baste a roast chicken in a failed attempt to murder his wife.

Thallium figures prominently in the 1995 film The Young Poisoner's Handbook, a dark comedy loosely based on the life of Graham Frederick Young.

"Concentrated thallium" is used as the poison of choice of the Wyoming Widow in the 2006 comedy Big Nothing

Thallium (pronounced /ˈθæliəm/) is a chemical element with the symbol Tl and atomic number 81. This soft gray malleable poor metal resembles tin but discolors when exposed to air. Approximately 60-70% of thallium production is used in the electronics industry, and the rest is used in the pharmaceutical industry and in glass manufacturing. It is also used in infrared detectors. Thallium is highly toxic and is used in rat poisons and insecticides, and its use has been cut back or eliminated in many countries. It is used in murders and has the nicknames "The Poisoner's Poison" and "Inheritance powder" (alongside arsenic).

Notable characteristics:

1 gram of ThalliumThallium is very soft and malleable and can be cut with a knife. It has a metallic luster, but when exposed to air, it quickly tarnishes with a bluish-gray tinge that resembles lead. (It is preserved by keeping it under oil). A heavy layer of oxide builds up on thallium if left in air. In the presence of water, thallium hydroxide is formed.

Occurrence and production:
Thallium occurs naturally in the minerals crookesite, lorandite, hutchinsonite, and pyrites

Thallium metal is obtained as a by-product in the production of sulfuric acid by roasting of pyrites, and also in the smelting of lead and zinc ores.

Applications:
The odorless and tasteless thallium sulfate was once widely used as rat poison and ant killer. Since 1975, this use in the United States and many other countries is prohibited due to safety concerns. Other uses:

thallium sulfide's electrical conductivity changes with exposure to infrared light therefore making this compound useful in photocells.

Thallium(III) salts, as thallium trinitrate or triacetate, are useful reagents in organic synthesis performing different transformations in aromatics, ketones, olefins, among others.

thallium bromide-iodide crystals have been used as infrared optical materials, because they are harder than other common infrared optics, and because they have transmission at significantly longer wavelengths. The trade name KRS-5 refers to this material.

thallium oxide has been used to manufacture glasses that have a high index of refraction.

used in semiconductor materials for selenium rectifiers,

used as a dopant for sodium iodide crystals in gamma radiation detection equipment, such as scintillation counters,

high-density liquid used for sink-float separation of minerals,

used in the treatment of ringworm and other skin infections. However this use has been limited due to the narrow margin that exists between toxicity and therapeutic benefit.

radioactive thallium-201 (half-life of 73 hours) is used for diagnostic purposes in nuclear medicine, particularly in stress tests used for risk stratification in patients with coronary artery disease A(CAD).[4][5] This isotope of thallium can be generated using a transportable generator which is similar to the technetium cow. The generator contains lead-201 (half life 9.33 hours) which decays by electron capture to the thallium-201. The lead-201 can be produced in a cyclotron by the bombardment of thallium with protons or deuterons by the (p,3n) and (d,4n) reactions.

combined with sulfur or selenium and arsenic, thallium has been used in the production of high-density glasses that have low melting points in the range of 125 and 150 °C. These glasses have room temperature properties that are similar to ordinary glasses and are durable, insoluble in water and have unique refractive indices.

an 8.5% thallium amalgam is used in thermometers and switches for use in low temperatures, because it freezes at -58 °C (pure mercury freezes at -38 °C).

thallium is used in the electrodes in dissolved oxygen analyzers.

thallium is a constituent of the alloy in the anode plates in magnesium seawater batteries.

In addition, research activity with thallium is ongoing to develop high-temperature superconducting materials for such applications as magnetic resonance imaging, storage of magnetic energy, magnetic propulsion, and electric power generation and transmission.

History:

Thallium (Greek θαλλός, thallos, meaning "a green shoot or twig")[8] was discovered by Sir William Crookes in 1861 in England while he was making spectroscopic determinations for tellurium on residues from a sulfuric acid plant. The name comes from Thallium's bright green spectral emission lines. In 1862 Crookes and Claude-Auguste Lamy isolated the metal independently of each other.


Occurrence:

Although the metal is reasonably abundant in the Earth's crust at a concentration estimated to be about 0.7 mg/kg, mostly in association with potassium minerals in clays, soils, and granites, it is not generally considered to be commercially recoverable from those forms. The major source of commercial thallium is the trace amounts found in copper, lead, zinc, and other sulfide ores.

Thallium is found in the minerals crookesite TlCu7Se4, hutchinsonite TlPbAs5S9, and lorandite TlAsS2. It also occurs as trace in pyrites and extracted as a by-product of roasting this ore for sulfuric acid production. The metal can be obtained from the smelting of lead and zinc rich ores. Manganese nodules found on the ocean floor also contain thallium, but nodule extraction is prohibitively expensive and potentially environmentally destructive. In addition, several other thallium minerals, containing 16% to 60% thallium, occur in nature as sulfide or selenide complexes with antimony, arsenic, copper, lead, and silver, but are rare, and have no commercial importance as sources of this element.

[greenban]

From www.emedicine.com


Thallium Toxicology:

Thallium can be absorbed from the skin as well as by inhalation and ingestion. When thallium enters the body, in the first few hours it distributes throughout the vascular space. After about 48 hours in the body, it starts entering the CNS and other tissues. As thallium is a heavy metal, its method of action is to bind to sulphydryl groups in the body, which upsets many biochemical processes. It resembles potassium in size and charge, so it has a wide distribution volume. The body tries to excrete the thallium by secreting about 2/3rds of it into the intestine (much of which is reabsorbed), and the remaining 1/3rd is excreted in the urine. Thallium has a half life in the body of up to 30 days, but this may be reduced to as little as 2 days with treatment.

Clinical features
The clinical features of acute thallium poisoning are shown below:

12-48 hours after exposure: Nausea, vomiting, diarrhoea, gastritis, duodenitis, pancreatic and parotid damage.

2-5 days: Paraesthesiae, hyperaesthesia, headaches, respiratory depression, nystagmus (scanning movement of the eyes when they should be still), optic neuropathy (damage to optic nerves) and atrophy, myalgia (muscle pain), myopathy (muscle wasting), severe pain, loss of reflexes, convulsions, coma, delirium, acute motor neuropathy , dementia and psychosis.

2-3 weeks Characteristic changes at the bases of hair shafts, followed by loss of hair.

> 3 weeks Cardiac arrhythmias may occur for up to 2 months (due to damage to the controlling autonomic nerves or direct toxicity. However, if there is sinus tachycardia, this is probably due to increased catecholamine production.) Skin rash as in riboflavin deficiency.

Thallium poisoning by ingestion may be diagnosed by x-ray as thallium is radio-opaque. Severe poisoning occurs if more than 1g or 8 mg per kg of body weight has been ingested.

Chronic exposure to thallium causes effects on the nervous system, and patients experience numbness of fingers and toes. After around 2-3 weeks, they also will loose their hair, and this is a characteristic feature of thallium poisoning.

Treatment
If the patient is seen within 6 hours of ingestion of the thallium, gastric lavage and induced emesis may be useful to try to stop the absorption of thallium into the body. Thallium can be succesfully treated as a specific antidote exists and this is known as potassium ferrihexacyanoferrate, or Prussian blue or Berlin blue. This works by sequestering the ions in the intestine, preventing their absorbtion and readsorption. Unlike other forms of metal poisoning, activated charcoal is useful, and can help reduce the severity of the poisoning by disrupting the enterohepatic circualtion. Other treatments that may be tried include forced diuresis, treatment with potassium chloride (this promotes the renal excretion of thallium), and peritoneal dialysis.

Additional information:
Thallium is a soft and pliable metal. It melts at 303.5°C and boils at 1482°C. It is colorless, odorless, and tasteless.

In the past, thallium was used as a therapeutic agent to treat syphilis, gonorrhea, tuberculosis, and ringworm, and it was also used as a depilatory for excess hair. However, reports of poisoning and death were noted, and these uses have been discontinued. Thallium was successfully used in killing rats, prairie dogs, and other unwanted pests. Its use as a household rodenticide was banned in the United States in 1965 after multiple unintentional poisonings. Commercial use was banned a decade later. Unfortunately, unintentional poisonings are still reported in other countries where thallium is used as a rodenticide and ant killer.

It is used in the manufacture of electronic components, optical lenses, semiconductor materials, alloys, gamma radiation detection equipment, imitation jewelry, artist's paints, low temperature thermometers, and green fireworks. Trace amounts of thallium are used as a contrast agent in the visualization of cardiac function and tumors. Thallium exposure may occur at smelters in the maintenance and cleaning of ducts and flues and through contamination of cocaine, heroin, and herbal products. Criminal and unintentional thallium poisonings are still reported, some leading to death.

Pathophysiology:
Thallium poisoning may occur via oral ingestion, inhalation of contaminated dust, or dermal absorption. The exact mechanism of thallium toxicity is unclear; however, it may impede the proper functioning of sodium-potassium ATPase for which thallium has a significantly greater affinity than potassium. Because of its similarity in charge and ionic radius to potassium, thallium is able to enter cells, inhibit Na-K-ATPase, and interfere with energy production at essential steps in glycolysis, the Krebs cycle, and oxidative phosphorylation. In addition, thallium may interfere with formation of disulfide bonds due to a high affinity for sulfhydryl groups. Furthermore, its similarity to potassium allows it to accumulate in areas rich in potassium, including muscular, hepatic, and nervous tissue. Its accumulation in muscular tissue is the basis for the use of radioactive thallium in cardiac imaging studies.

A further possible toxic mechanism of thallium is interference in riboflavin homeostasis. Thallium forms insoluble complexes with riboflavin resulting in its intracellular sequestration. Indeed, deficiency of this vitamin results in dermatitis, alopecia, and neuropathy, which are the hallmarks of thallium poisoning.

The lethal dose of thallium is approximately 15-20 mg/kg; however, significant toxicity and death may occur with smaller amounts. Thallium poisoning more commonly occurs after oral ingestion. Thallium is rapidly distributed intracellularly throughout all body tissues, with a large volume of distribution estimated to be about 3.6 L/kg.

Thallium follows a 3-phase toxicokinetics: first intravascular distribution, then CNS distribution, and finally elimination. In the first 4 hours following exposure, thallium is rapidly distributed to the blood and to well-perfused organs such as the kidney, liver, and muscle. Over the next 4-48 hours, thallium is distributed into the CNS. The elimination phase begins about 24 hours after ingestion. Thallium is primarily eliminated through excretion into the feces (51.4%) and the urine (26.4%). The high concentrations of thallium found in the kidney (>5.5 times more than other tissues) result from renal filtration with approximately 50% reabsorbed in the kidney tubules. Elimination is slow with an elimination half-life of 3-30 days, varying with the dose and chronicity of the exposure. Because of this prolonged elimination phase, thallium may act as a cumulative poison.

Frequency:
United States
Few data exist related to recent thallium intoxication cases in the United States.

Mortality/Morbidity:
The mortality rate for acute thallium toxicity has been reported as 6-15%; among survivors, 33-50% have neurologic or ocular sequelae.


Thallium can be lethal to humans. The lethal dose for humans is 15-20 mg/kg (around 1 g for a 70-kg person). Nonfatal effects occur below this dose. However, it is conceivable that even smaller doses can still cause fatality (minimal reported dose was 8 mg/kg). In addition, some of the treated patients survived exposure up to 28 mg/kg.

Race:
No scientific data substantiate any differences in thallium toxicity that are attributable to race.

Sex:
No scientific data substantiate any differences in thallium toxicity that are attributable to sex.

Age:
No scientific data substantiate any differences in thallium toxicity that are attributable to age.




Next Month.....Ricin Poisoning (The San Fransisco Treat!)

[greenban]

Annoyingly detailed Medical Info:

Medical History:
The clinical presentation of thallium toxicity can vary depending on the type, severity, and timeframe of the exposure. Acute thallium poisoning is primarily characterized by gastrointestinal symptoms, while neurologic findings predominate with chronic exposure. The neurologic manifestations tend to progress, even despite decreasing blood thallium levels. Thallium toxicity is characterized by a painful ascending peripheral neuropathy and alopecia; this clinical manifestation presents 2-3 weeks after an acute poisoning.

Gastrointestinal symptoms:
These symptoms predominate early, usually within the first 3-4 hours, and the most common symptom is severe, paroxysmal abdominal pain. Nausea, vomiting, constipation, and diarrhea are reported. The vomitus and stools are often bloody.
Neurologic symptoms: These symptoms usually appear 2-5 days postexposure and include severely painful, rapidly progressive, ascending peripheral neuropathies. Pain and paresthesias of the hands and the lower extremities, especially the soles of the feet, also predominate. Distal motor weakness occurs, with the lower limbs more affected than the upper limbs. Ataxia, tremor, athetosis, cranial nerve palsies, headache, seizures, insomnia, coma, and death may also occur.

Neuropsychological manifestations may include anxiety, confusion, delirium, hallucinations, and psychosis. Acute agitation and aggression, personality changes, depression, apathy, and confabulation have been observed in both adults and children. Psychosis and associated symptoms can occur with or without a psychiatric history.

Ocular symptoms:
Diplopia, abnormal color vision, and impairment of visual acuity may develop.

Other manifestations may include loss of the lateral half of the eyebrows, skin lesions on the lids, ptosis, seventh nerve palsy, internal and external ophthalmoplegia, and nystagmus. Noninflammatory keratitis, lens opacities, and optic atrophy due to toxic optic neuropathy also may occur.

Dermatologic symptoms:
The first cutaneous signs are not specific and include scaling of the palms and soles and acnelike lesions of the face. During week 2-3, a sudden onset of hair loss quickly progresses to diffuse alopecia. The hair loss primarily affects the scalp, temporal parts of the eyebrows, the eyelashes, and the limbs. Less often, the axillary regions are affected. One month after the poisoning, Mees lines (transverse white lines on the nails) appear in the nail plate. Other dermatologic findings include crusted eczematous lesions, hypohidrosis, anhidrosis, palmar erythema, painful glossitis with redness of the tip of the tongue, stomatitis, and hair discoloration.

Pulmonary symptoms:
Some patients can experience pleuritic chest pain or tightness upon exposure. The mechanism for this particular symptom is unclear.

Physical:
Focus the physical examination primarily on the organ systems most commonly affected.

Perform careful abdominal and rectal examinations, including stool guaiac tests. Abdominal tenderness, hyperactive bowel sounds, mild guarding, and guaiac-positive stools can be found as early findings in thallium intoxication.
Perform a detailed neurologic examination, including a complete cranial nerve and visual field assessment.

All cranial nerves can be affected by thallium. Nystagmus (fourth and sixth CN involvement) and ptosis (third CN) may be present.

Decreased lower extremity strength with the lower limbs more affected than the upper limbs, hyperesthesia (especially of the soles of the feet), and decreased sensation to pinprick, touch, temperature, vibration, and proprioception in the fingers and toes may be present.

Perform a slit lamp examination and funduscopic examination, and carefully document visual acuity and color perception.

Decreased visual acuity with impairment of contrast sensitivity and tritanomaly (blue color vision defect) may be observed.

In the early stages of thallium toxicity, funduscopic examination may reveal signs of an optic neuritis characterized by a red and poorly defined papilla. Continued thallium exposure causes atrophy of the optic nerve, which results in the development of a pale or white papilla.

Noninflammatory keratitis and lens opacities have also been described.

Perform a skin and scalp examination.

Early skin findings include scaling of the palms and soles and acnelike lesions of the face. Scalp alopecia, which is one of the most characteristic manifestations of thallium toxicity and is related to atrophy of the hair follicles, usually occurs 10-21 days postexposure. In addition to the scalp, hair loss also occurs in the lateral eyebrows, the eyelashes, the limbs, and occasionally the axillary regions.
Dark brown or black pigment, the result of thallium deposits, may be visualized in the hair roots. With chronic exposure, these deposits appear zebralike, demonstrating multiple thallium exposures.

Approximately 1 month after thallium exposure, Mees lines (transverse white lines on the nails) appear in the nail plate.

Other dermatologic findings include well-demarcated hyperkeratosis of the palms and soles, crusted eczematous lesions, hypohidrosis, anhidrosis, palmar erythema, crusted perioral dermatitis, painful glossitis with redness of the tip of the tongue, stomatitis, and hair discoloration.

Causes:
Because it is odorless and tasteless, thallium has successfully been used worldwide as a rat poison and ant killer. It was restricted for household use in the United States in 1965 and banned commercially in 1975. Thallium is still commonly used as a rodenticide and insecticide in other countries resulting in severe unintentional poisoning. This is despite the World Health Organization recommendation against its use in 1973.

Thallium has been used as a pesticide in other countries, such as Africa, causing poisoning through contaminated foods. It has been discovered as a contaminant in some Chinese herbal medications.

According to the 2002 American Association of Poison Control Centers Annual Report for toxic exposures, unintentional thallium poisoning accounts for the majority of reported cases. However, homicide and suicide represent a significant percentage of cases in the United States.

Thallium is toxic by cumulative intake; it can be absorbed through the skin, respiratory, and GI tracts. Therefore, besides oral ingestion, inhalation of contaminated dust during manufacture, sniffing what was thought to be cocaine, and skin absorption through protective gloves have all been reported as causes of thallium toxicity. In addition, cases of thallium intoxication by intravenous injection of contaminated heroin have been reported.

Because chronic thallium exposure mimics other disease, many cases of industrial thallium exposure most likely go unnoticed. On the other hand, accidental poisoning caused by direct contact with and careless handling of thallium-containing materials occurs more frequently.

Thallium is used most often in the semiconductor and optical industries. In addition, it is used in some industries for the production of photoelectric cells, scintillation counters, chemical catalysts, green-emitting fire-works, cement plants, and imitation jewelry.

Trace amounts of thallium are used as a radioactive contrast agent (thallium-201) to visualize cardiac function. The amount of carrier thallium used for this purpose is 4000 times less than the dose at which some toxic effects first appear in humans.

Differential Diagnosis:
Guillain-Barré Syndrome
Systemic Lupus Erythematosus
Toxicity, Arsenic
Toxicity, Carbon Monoxide
Toxicity, Heavy Metals
Toxicity, Hydrocarbons
Toxicity, Isoniazid
Toxicity, Lead
Toxicity, Mercury
Toxicity, Organophosphate and Carbamate

Other Problems to be Considered

Acute intermittent porphyria
Diabetic polyneuritis
Thiamine deficiency
Poliomyelitis
Colchicine toxicity
Hydralazine toxicity
Selenium toxicity
Vasculitis
Botulism

Lab Studies:
Because laboratory studies are generally nonspecific, any unexplained peripheral neuropathy, especially accompanied by alopecia, should raise clinical suspicion for thallium toxicity. In consultation with the medical toxicologist, initiate treatment for patients with high suspicion of thallium toxicity while awaiting laboratory confirmation.

The definitive clinical diagnosis of thallium poisoning can only be established by demonstrating elevated thallium levels. Thallium can be recovered in the hair, nails, feces, saliva, blood, and urine.

A 24-hour urine thallium concentration is the standard toxicologic method and is assayed by atomic absorption photospectrometry. The normal level is less than 5 mcg/L.

A urine spot test can deliver faster results. However, it often gives false-positive results, and it requires the use of 20% nitric acid, which can be dangerous and is usually not readily available.

Because it is rapidly eliminated from the body, measurements of blood thallium reflect only recent exposures. Thus, it is not generally considered to be a reliable means of identifying or monitoring exposure to thallium.

A CBC with differential can identify anemia, leukocytosis, eosinophilia, and thrombocytopenia, which have all been reported in cases of thallium exposure. Anemia most likely occurs secondary to GI hemorrhage.

Electrolytes, calcium, glucose, BUN, creatinine, and LFTs should be obtained. Thallium exposure can lead to electrolyte and glucose abnormalities, hypocalcemia, and impair renal and hepatic dysfunction.

A pregnancy test should be considered for all women of childbearing age.

[greenban]

Even More Annoyingly detailed Medical Info:

Imaging Studies:
Thallium is radiopaque; therefore, an abdominal radiograph should be obtained. This may reveal thallium metal after an acute ingestion. Radiographs of suspected exposure sources may be useful for confirming the presence of a heavy metal.

Other Tests:
Nerve conduction studies (NCS) may reveal findings consistent with an axonal sensorimotor peripheral neuropathy, with nerves innervating the feet most significantly involved. NCS may be useful in both diagnosing and monitoring patients with thallium exposure. The severity of abnormalities on NCS has been shown to correlate with the severity of other symptoms and findings.

An EEG may show nonspecific slow-wave activity in severe cases.

Microscopic inspection of scalp hair reveals dark black and brown pigment in the hair roots in approximately 95% of poisoned patients. However, this may be difficult to visualize by the untrained observer. Darkening of the hair root can occur as early as 4 days postexposure and is thought to represent the accumulation of thallium within the hair root, resulting in the appearance of a black band.

Electroretinographic (ERG) examination reveals a delayed visual evoked response. These ERG changes tend to occur before development of clinical symptoms in thallium intoxication. ERG may be useful when persons with known thallium exposure receive follow-up examinations.

An ECG should be obtained to identify tachycardia and cardiac arrhythmias.

Prehospital Care:
The prehospital treatment should focus on 4 areas: (1) stabilizing acute life-threatening conditions, (2) initiating supportive therapy, (3) identifying the time and route of exposure, and (4) beginning the decontamination process.

Establish ABCs.
Administer oxygen as needed.

Obtain intravenous access.

Remove contaminated clothing as soon as possible. Avoid self-exposure and wear protective clothing that is appropriate to the type and degree of contamination. Wear air-purifying or supplied-air respiratory equipment as necessary.

Vomiting may be induced with ipecac syrup if initiated within 30 minutes of ingestion.

Emergency Department Care:
The goals of treating a patient with thallium toxicity are initial stabilization, prevention of absorption, and enhanced elimination. Following the initial assessment and stabilization of the ABCs, and after decontamination of the patient, aggressive gastrointestinal decontamination should be instituted.

Institute proper decontamination procedures. If not performed in the prehospital setting, remove contaminated clothing while avoiding self-exposure. With dermal exposure, thoroughly wash exposed skin with soap and water. For eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Be sure to wear protective clothing appropriate to the type and degree of contamination, and wear air-purifying or supplied-air respiratory equipment as necessary.

Gastrointestinal decontamination, activated charcoal, and Prussian blue (potassium ferric hexacyanoferrate) are recommended in thallium ingestions.

Ipecac-induced emesis may be useful for initial treatment if the ingestion occurred within minutes of presentation.

Consider orogastric lavage in patients presenting within 1 hour postingestion if they have not vomited or if thallium is observed in the stomach on radiographs in patients who have vomited. In addition, whole-bowel irrigation with polyethylene glycol electrolyte lavage solution may be useful, especially when radiopaque material is visualized on an abdominal radiograph.

Although both Prussian blue and activated charcoal absorb thallium, it appears that Prussian blue has absorptive superiority. In addition, because it has a far better safety profile than other proposed therapies, Prussian blue should be considered the drug of choice in acute thallium poisoning.

Prussian blue is a crystal blue lattice of potassium ferric ferrocyanide and acts by forming a nonabsorbable complex with thallium. This use as a chelator interrupts its enterohepatic recirculation and increases its excretion. Prussian blue (Radiogardase) was approved by the Food and Drug Administration (FDA) in 2003 but is still difficult to obtain for pharmaceutical use in the United States. However, it has been obtained from The Oak Ridge Institute for Science and Education and the Radiation Emergency Assistance Center (REAC) in Oak Ridge, Tennessee. In addition, successful therapy using the laboratory reagent of Prussian blue has been documented in the United States.

In patients in whom Prussian blue cannot be obtained and thallium poisoning is suspected, multidose activated charcoal may be effective. Because thallium undergoes enterohepatic and enteroenteric recirculation, repeated charcoal administration (0.25-0.5 g/kg q2-4h) may enhance fecal elimination.

Forced diuresis with potassium loading was previously recommended to increase the renal clearance of thallium, but this may exacerbate the neurologic and cardiovascular symptoms and is no longer advised.

Chelating agents such as EDTA, dimercaprol, and D-penicillamine have not been shown to be effective and should be avoided.

The usefulness of hemodialysis and hemoperfusion is controversial, but they may be useful during early thallium poisoning before extensive distribution within the body tissues has occurred.

Further Inpatient Care:
Admit all patients with significant signs and symptoms of thallium toxicity.

Initially measure thallium concentrations in the urine 3 times per week to confirm a decreasing trend. Prussian blue treatment should be continued until the 24-hour urine thallium concentration returns to the reference range (0-5 mcg/d).

Thallotoxicosis also is associated with a severe form of stomatitis; thus, monitor mouth hygiene closely. Shaving the patient's head may reduce the stress induced by hair loss and improve the patient's morale.

Physical therapy may be instituted to prevent development of muscle contractures.

Further Outpatient Care:
Patients with unintentional intoxication who are asymptomatic with a minimal increase in urine thallium level may be discharged with close follow-up care.

Patients with intentional ingestions should have a psychiatric evaluation before discharge from the hospital.

Transfer:
Consider transferring patients with severe symptomatology if a medical toxicologist is not readily available.

Deterrence/Prevention:
Regular follow-up care is recommended for persons with known thallium exposure.

Complications:
Prolonged neurologic damage may persist if detoxification therapy is delayed.

Cases of persistent agitation, aggression, personality changes, depression, and other psychiatric symptoms have been reported following thallium exposure.

Prognosis:
If recognized and treated early, thallium intoxication carries a favorable prognosis; however, the course of recovery may be lengthy.

Patient Education:
For excellent patient education resources, visit eMedicine's Poisoning Center and Poisoning - First Aid and Emergency Center. Also, see eMedicine's patient education articles Poisoning and Activated Charcoal.

[JimP]

Tony,

When are you going to report on the "It's a Small World" song poison?

/Jim

[greenban]

Tony,

When are you going to report on the "It's a Small World" song poison?

/Jim

I've got mercury posioning and it is always fatal.

Jim, I am a big fan of IASW(AA) and love the song. I have stayed on for 10 rides in a row one magical late night visit in CA.

Poison, never!

-Tony

[AZDVC]

Thanks, GB! Good info to know!:scary:
Patsy

[greenban]

Bump!

This is good stuff people, good stuff. :idontgeti :idontgeti

-Tony

[TikiTwinsDad]

I figure you've done enough for us with your info and insight (albeit frogcentric & distorted), that I could return the favor by bumping your thallium poisoning post.

[greenban]

You, Sir, Rock in a very MODly way, and your tickers are now working!

-Tony

[djgrab]

that was a great post Tony! Will there be one for July?

I saw you will be at WDW same time as us. Maybe we'll past each other.

[tammymacb]

Why use poison when you can just give somebody a big bear hug.........and turn off their scuba tank! :woohoodan

Tammy ( who tries to avoid pesky chemicals )

[greenban]

that was a great post Tony! Will there be one for July?

I saw you will be at WDW same time as us. Maybe we'll past each other.

July will be ricin (an all natural 'organic' food additive (poison) for tammymacb who doesn't pesky chemicals!)

I'd love a meet at WDW if we can arrainge it.

Sadly no GV's are available for a margarita meet!

-Tony

[Colorado Belle]

Did someone mention MARGARITAS?????
so the next poison will be organic?
hmmmmmm.......since the crooked judge is retiring, I might be able to try organics on one of the jolly roger crew that banes my life....will read will high interest, Froggie!

[minniekissedme]

Did someone mention MARGARITAS?????
so the next poison will be organic?
hmmmmmm.......since the crooked judge is retiring, I might be able to try organics on one of the jolly roger crew that banes my life....will read will high interest, Froggie!

mind if I join you??? It's been one of those 24 hours to forget!

[TikiTwinsDad]

Seems like my little bump has gotten some great play. I didn't realize you were taking request DJ GB! If so, how about batrachotoxins? <http://en.wikipedia.org/wiki/Batrachotoxin>

[tomandrobin]

<http://en.wikipedia.org/wiki/Batrachotoxin>

Poison darts are prepared by the Chocó Indians by first impaling a frog on a piece of wood. By some accounts, the frog is then held over or roasted alive over a fire until it cries in pain. Bubbles of poison form as the frog's skin begins to blister. The dart tips are prepared by touching them to the toxin, or the toxin can be caught in a container and allowed to ferment.

Other accounts say that a stick siurukida ("bamboo tooth") is put through the mouth of the frog and passed out through one of its hind legs. This causes the frog to perspire profusely on its back, which becomes covered with a white froth. The darts are dipped or rolled in the froth, preserving its lethal power for up to a year.

:holymoly::holymoly::holymoly::holymoly: Run Tony, Run..........

[djgrab]

Our MO frog does not give off such toxins. He is of better pedigree.
You will have to go to other boards to find such low life Amphibians.
Got your back Tony.:ROTFL:

[greenban]

Our MO frog does not give off such toxins. He is of better pedigree.
You will have to go to other boards to find such low life Amphibians.
Got your back Tony.:ROTFL:

And I owe ya one, anytime, anyplace, just ask!

Many Thanks,

-Tony

[greenban]

Poison darts are prepared by the Chocó Indians by first impaling a frog on a piece of wood. By some accounts, the frog is then held over or roasted alive over a fire until it cries in pain. Bubbles of poison form as the frog's skin begins to blister. The dart tips are prepared by touching them to the toxin, or the toxin can be caught in a container and allowed to ferment.

Other accounts say that a stick siurukida ("bamboo tooth") is put through the mouth of the frog and passed out through one of its hind legs. This causes the frog to perspire profusely on its back, which becomes covered with a white froth. The darts are dipped or rolled in the froth, preserving its lethal power for up to a year.

:holymoly::holymoly::holymoly::holymoly: Run Tony, Run..........

Sick and getting sicker people!

I'm speechless :tapedshut

Thanks for the heads up Thomas!

-Tony

Again, let me point out, yet another reason to not mess with the frog!

http://www.be.wednet.edu/Acts/S.%20Olson/Images/frog51.jpg

Can you find the Hidden Mickey on this Poison Dart Frog?

http://i50.photobucket.com/albums/f312/snarfer1/blue20frog353.jpg

[bababear]

Quick story
one of my grade three students --on a field trip to Butterfly conservatory(last week) (stole) pinched a rather large frog,,stuffed him in a bag and kept him on the bus for two hours. :faint:Well Mrs **** blew a gasket ......WHAT were you Thinking?????? How would you like it if someone stole you and put you in a bag???? This child has a problem with stealing but I never thought she'd take a living thing,,,,,,,after I calmed down and phoned the parent we took the Frog to the river and let it go. Did I mention I only have one more sleep till summer break??????
Next years trip ----grade fours --ZOO:holymoly::holymoly: lions and tigers and bears --Oh My!!

HUGS Mr Frog
Mel

[JimP]

Quick story
one of my grade three students --on a field trip to Butterfly conservatory(last week)

Did you go to the butterly conservatory near Buchart Gardens?

/Jim

[bababear]

Hi Jim

We went to

http://www.wingsofparadise.com/

it's in Cambridge Ontario Canada

beautiful place with a wonderful school programe

Hugs Mel

[JimP]

Hi Jim

We went to

http://www.wingsofparadise.com/

it's in Cambridge Ontario Canada

beautiful place with a wonderful school programe

Hugs Mel

Oh.. my mistake, I thought you were in BC.

/Jim