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BARIUM-SOLUBLE SALTS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Heavy metals and related compounds.

Specific Substances

    A) CONSTITUENTS OF THE GROUP
    1) Barium acetate
    2) Barium carbonate
    3) Barium chloride
    4) Barium fluoride
    5) Barium hydroxide
    6) Barium nitrate
    7) Barium styphenate
    8) Barium sulfide
    1.2.1) MOLECULAR FORMULA
    1) Ba

Available Forms Sources

    A) FORMS
    1) All water or acid soluble barium salts are highly toxic. The most commonly involved in poisoning (accidental or intentional) are as follows:
    1) Barium carbonate, a white powder
    2) Barium fluoride
    3) Barium sulfide, an ingredient of various depilatories
    4) Barium oxide, a white to yellowish powder
    5) Barium chloride
    6) Barium acetate
    7) Barium styphenate, a 2,4,6-trinitroresorcinol salt, is made from styphnic acid (Jacobs et al, 2002)
    8) Barium sulfate
    2) Refer to "BARIUM SULFATE" management for further information.
    3) Isolated case reports indicate that intoxication may be possible after repeated radiological examinations (Savry et al, 1999) or as a result of direct transfer of barium from the gastrointestinal tract into the vascular system during radiological examination (Pelissier-Alicot et al, 1999).
    4) BARIUM CHLORATE: A 35-year-old man, with severe mental retardation, developed barium toxicity, including dysrhythmias and severe hypokalemia, after ingesting 16 small fireworks, identified as "color snakes" and "black snakes" and believed to contain barium chlorate, that he had mistaken as chewing gum. A serum barium concentration, obtained approximately 15 hours postingestion, was 20,200 mcg/L (reference range less than 200 mcg/L). With supportive therapy, the patient recovered and was discharged 12 days postingestion (Rhyee & Heard, 2009).
    B) USES
    1) Barium carbonate, used as a rodenticide and frequently mistaken for flour; used in some welding fluxes;
    2) Barium fluoride, used in some welding fluxes;
    3) Barium sulfide, an ingredient of various depilatories;
    4) Barium oxide, used in the manufacture of glass;
    5) Barium chloride and barium acetate, used as agents in dyeing textiles;
    6) Barium styphenate, a 2,4,6-trinitroresorcinol salt, is made from styphnic acid and used in the manufacture of explosive detonators (Jacobs et al, 2002).
    7) Barium sulfate, used as an opaque contrast media for gastrointestinal studies, is insoluble and not well absorbed. Refer to "BARIUM SULFATE" management for further information.

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Soluble barium salts are used in some rodenticides, in welding fluxes and some depilatories, in glass manufacture, in textile dyeing, in explosive detonators and fireworks (sparklers).
    B) TOXICOLOGY: Rapid onset, severe hypokalemia is caused by sequestration of potassium in skeletal muscle cells, secondary to barium blocking potassium efflux via the sodium-potassium pump in those cells.
    C) EPIDEMIOLOGY: Poisoning is rare, and most often occurs when barium carbonate, a white powder, is mistaken for flour, or after deliberate ingestion. Toxicity from dermal exposure to intact skin or inhalation has not been reported. One case describes systemic toxicity after an explosion, with presumed barium absorption through wounds and burns.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE POISONING: Nausea, vomiting, colicky abdominal pain and diarrhea, paresthesias, increased salivation, onset usually within one hour. Chronic inhalation can produce a pneumoconiosis (baritosis). Barium oxide and barium hydroxides are alkaline in contact with water, can cause burns.
    2) SEVERE POISONING: Profound hypokalemia, tremors, seizures, vertigo, severe muscle weakness, mydriasis, hypertension, chest pain, bradycardia, ventricular dysrhythmias, respiratory failure, shock, and cardiac arrest.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Hypertension may occur.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no reproductive studies were found for barium in humans.

Laboratory Monitoring

    A) Institute continuous cardiac monitoring and obtain an ECG (evaluate for evidence of hypokalemia including T wave flattening and prominent U waves).
    B) Monitor vital signs, with particular attention to evidence of respiratory insufficiency. Perform serial neurologic exams to evaluate for muscle weakness.
    C) Determine potassium levels frequently (every 1 to 2 hours until stabilized). Monitor serum phosphorus, magnesium CK and renal function in symptomatic patients.
    D) Serum barium concentrations are not readily available or useful in guiding therapy.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Monitor serum potassium and correct as necessary. Administer intravenous fluids to maintain urine.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Profound hypokalemia may develop rapidly, causing profound weakness, respiratory insufficiency, and dysrhythmias. Monitor for weakness and respiratory insufficiency, manage airway early. Monitor serial serum potassium and correct aggressively. Dysrhythmias are usually secondary to hypokalemia and generally respond to potassium administration. Administer intravenous fluids to maintain adequate urine output. Hemodialysis should be performed in patients with severe hypokalemia, severe weakness, or ventricular dysrhythmias that are not responding to potassium supplementation.
    C) DECONTAMINATION
    1) Activated charcoal likely ineffective in adsorbing barium. Consider insertion of a nasogastric tube to aspirate gastric contents, or gastric lavage, in patients with recent ingestion who can protect their airway or who are intubated.
    2) Wash exposed skin with soap and water. Remove contaminated clothing.
    D) AIRWAY MANAGEMENT
    1) Severe hypokalemia may result in respiratory muscle weakness and respiratory failure. Monitor adequacy of respirations, and manage airway early if necessary.
    E) MAGNESIUM SULFATE
    1) Magnesium sulfate when given orally results in the formation of nonabsorbable barium sulfate within the gastrointestinal tract. Dose: 250 mg/kg for children and 30 g for adults. Sodium sulfate is an alternative. ADULT: 30 g in 250 ml water orally.
    F) HYPOKALEMIA
    1) Profound hypokalemia can develop rapidly. Aggressive supplementation, both orally and intravenously, is the mainstay of therapy.
    G) DYSRHYTHMIAS
    1) Dysrhythmias are usually secondary to hypokalemia. Aggressive intravenous and oral potassium supplementation is the mainstay of treatment. Antidysrhythmics such as lidocaine or amiodarone may be used, but efficacy may be limited in patients with persistent hypokalemia.
    H) HEMODIALYSIS
    1) Hemodialysis is effective (corrects hypokalemia, and associated weakness and dysrhythmias, enhances barium elimination) in patients with severe poisoning. It should be considered early in patients with hypokalemia, severe weakness or dysrhythmias that are not responding to potassium supplementation.
    I) PATIENT DISPOSITION
    1) OBSERVATION CRITERIA: All patients who have ingested a soluble barium salt should be sent to a healthcare facility for evaluation and treatment. Patients should be observed for 6 to 8 hours with ECG monitoring, serial serum potassium concentrations, and evaluation for weakness. Patients who are asymptomatic with normal serum potassium during 6 to 8 hours of observation may be discharged.
    2) ADMISSION CRITERIA: Patients with hypokalemia, weakness or dysrhythmias should be admitted to an intensive care setting for cardiac, respiratory and neurologic monitoring and aggressive potassium replacement.
    3) CONSULT CRITERIA: Consult a medical toxicologist and/or poison center for any patient with significant barium poisoning or in whom the diagnosis is unclear. Consult a nephrologist for emergent dialysis in any patients with severe poisoning.
    J) PITFALLS
    1) Inadequate monitoring for weakness, respiratory insufficiency, hypokalemia, dysrhythmias.
    2) Since barium does not decrease total body potassium, but rather shifts it intracellularly; hyperkalemia may develop once barium toxicity has resolved.
    K) TOXICOKINETICS
    1) Rapidly absorbed, primarily fecal elimination. Half life 18 hours (based on single case report).
    L) DIFFERENTIAL DIAGNOSIS
    1) Toluene toxicity, renal tubular acidosis, hypokalemic periodic paralysis.

Range Of Toxicity

    A) There are insufficient data in the literature to accurately characterize the acute toxicity of barium salts. Ingestions on the order of 0.8 to 1 g have been reported as potentially lethal. With aggressive intensive care, adults have recovered from severe toxicity after ingesting as much as 30 grams of barium carbonate.

Clinical Effects

Summary Of Exposure

    A) USES: Soluble barium salts are used in some rodenticides, in welding fluxes and some depilatories, in glass manufacture, in textile dyeing, in explosive detonators and fireworks (sparklers).
    B) TOXICOLOGY: Rapid onset, severe hypokalemia is caused by sequestration of potassium in skeletal muscle cells, secondary to barium blocking potassium efflux via the sodium-potassium pump in those cells.
    C) EPIDEMIOLOGY: Poisoning is rare, and most often occurs when barium carbonate, a white powder, is mistaken for flour, or after deliberate ingestion. Toxicity from dermal exposure to intact skin or inhalation has not been reported. One case describes systemic toxicity after an explosion, with presumed barium absorption through wounds and burns.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE POISONING: Nausea, vomiting, colicky abdominal pain and diarrhea, paresthesias, increased salivation, onset usually within one hour. Chronic inhalation can produce a pneumoconiosis (baritosis). Barium oxide and barium hydroxides are alkaline in contact with water, can cause burns.
    2) SEVERE POISONING: Profound hypokalemia, tremors, seizures, vertigo, severe muscle weakness, mydriasis, hypertension, chest pain, bradycardia, ventricular dysrhythmias, respiratory failure, shock, and cardiac arrest.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hypertension may occur.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) HYPOTHERMIA: Body temperature is usually normal or below normal.
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Hypertension may occur (Jacobs et al, 2002; Diengott et al, 1964; Gould et al, 1973; Roza & Berman, 1971; Wetherill et al, 1981; Johnson & VanTassell, 1991).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) MYDRIASIS: Early in the course, the pupils are dilated and not always responsive to light (Jourdan et al, 2001; Morton, 1945).
    2) IRRITATION: Alkaline barium compounds (barium hydroxide, barium oxide, barium carbonate) may cause local irritation of eyes (Sittig, 1991).
    3) BURNS: Strongly alkaline solutions (barium hydroxide, barium oxide) may cause severe burns of the eyes (ACGIH, 1991; Hathaway et al, 1996).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypertension has been reported with acute barium intoxication (Ananda et al, 2013; Jacobs et al, 2002; Wells & Wood, 2001; Jourdan et al, 2001; Downs et al, 1995; Diengott et al, 1964; Gould et al, 1973; Roza & Berman, 1971; Wetherill et al, 1981; Johnson & VanTassell, 1991).
    B) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Dysrhythmias may occur (Jacobs et al, 2002; Jourdan et al, 2001; Diengott et al, 1964) Mattila et al, 1986; Roza, 1981; (Tenenbein, 1985). These include premature ventricular complexes, ventricular tachycardia, bradycardia and ventricular fibrillation (Talwar et al, 2007; Jourdan et al, 2001; Thomas et al, 1998; Janssen et al, 1992; Schorn et al, 1991; Aks et al, 1991; Deng et al, 1991; Johnson & VanTassell, 1991)
    b) CASE REPORT: A 52-year-old woman developed progressive widening of the QRS complex, followed by torsades de pointes approximately 2 hours after intentionally ingesting 70 mg of amlodipine, 280 mg of fluoxetine, and an unknown amount of barium carbonate. Lab analysis showed a serum potassium level of 1.1 mEq/L. The patient stabilized following decontamination with activated charcoal and potassium supplementation (Koch et al, 2003).
    c) CASE REPORT: Tachycardia (160 beats/min) accompanied by a widened QRS complex (0.35 sec) occurred in a 30-year-old man who ingested the entire contents of a bottle of barium chloride. The patient was also profoundly hypokalemic (serum potassium level of 1.7 mEq/L). The QRS complex normalized after intravenous administration of 240 mEq of potassium (Wells & Wood, 2001).
    d) CASE REPORT: Wide complex ventricular tachycardia occurred in a 39-year-old man following a suicidal ingestion of a depilatory containing barium sulfide. Cardiac arrest occurred and the patient died approximately 7 hours post-ingestion. Premortem lab results, that were unavailable prior to the patient's death, showed a potassium level of 0.9 mEq/L. The cause of death was certified as cardiac dysrhythmia due to hypokalemia and barium toxicity as a result of barium sulfide ingestion (Downs et al, 1995).
    e) CASE REPORT: A 22-year-old man developed atrial fibrillation and torsade de pointes after intentionally ingesting an unknown amount of barium nitrate. His serum potassium concentration was 1.5 mmol/L. With supportive therapy, including hemodialysis, the patient completely recovered (Bahlmann et al, 2005a).
    f) BARIUM CHLORATE: Wide complex ventricular tachycardia and severe hypokalemia occurred in a 35-year-old man following ingestion of 16 small fireworks, identified as "color snakes" and "black snakes" and believed to contain barium chlorate. Serum and urine barium concentrations, obtained approximately 15 hours post-ingestion, were 20,200 mcg/L (reference range less than 200 mcg/L) and 5,600 mcg/L (reference range less than 20 mcg/L), respectively. With supportive therapy, the patient recovered and was discharged approximately 12 days post-ingestion (Rhyee & Heard, 2009).
    g) CASE REPORT: A 16-year-old boy presented with acute quadriparesis and respiratory failure, and subsequent development of ventricular tachycardia, all of which were secondary to severe hypokalemia, following ingestion of fireworks. With supportive treatment, including ventilation and rapid potassium infusion, the patient recovered. Suspecting barium poisoning, toxicologic analysis of blood confirmed the presence of barium (98.5 mcg/dL) (Deepthiraju & Varma, 2012).
    C) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) ECG changes associated with barium intoxication and hypokalemia include T wave flattening and U waves (Torka et al, 2009; Johnson & VanTassell, 1991; Deng et al, 1991).
    b) CASE REPORT: A 52-year-old woman developed progressive widening of the QRS complex, followed by torsades de pointes approximately 2 hours after intentionally ingesting 70 mg of amlodipine, 280 mg of fluoxetine, and an unknown amount of barium carbonate. Lab analysis showed a serum potassium level of 1.1 mEq/L. The patient stabilized following decontamination with activated charcoal and potassium supplementation (Koch et al, 2003).
    D) CHEST PAIN
    1) WITH POISONING/EXPOSURE
    a) Chest pain may occur with acute intoxication and usually occurs within 10 to 60 minutes of exposure (Jourdan et al, 2001; Sigue et al, 2000).
    b) CASE REPORT: A prisoner developed chest pain and hypokalemia after ingesting approximately 128 grams of hair remover (Sigue et al, 2000).
    E) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 49-year-old male pharmacist with a history of depression developed cardiorespiratory arrest following a suicidal barium chloride ingestion. He died following unsuccessful resuscitation attempts. Autopsy revealed hemorrhagic gastritis and the following barium levels: blood 9.9 mg/L, bile 8.8 mg/L, urine 6.3 mg/L, gastric 10 g/L (Jourdan et al, 2001).
    b) CASE REPORT: Wide complex ventricular tachycardia occurred in a 39-year-old man following a suicidal ingestion of a depilatory containing barium sulfide. Cardiac arrest occurred and the patient died approximately 7 hours post-ingestion. Premortem lab results, that were unavailable prior to the patient's death, showed a potassium level of 0.9 mEq/L. The cause of death was certified as cardiac dysrhythmia due to hypokalemia and barium toxicity as a result of barium sulfide ingestion (Downs et al, 1995).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) WITH POISONING/EXPOSURE
    a) Patients with profound hypokalemia with resultant muscle weakness may develop respiratory failure (Ananda et al, 2013; Torka et al, 2009; Talwar et al, 2007; Jacobs et al, 2002; Sigue et al, 2000; Thomas et al, 1998; Gould et al, 1973; Deng et al, 1991; Johnson & VanTassell, 1991). Dyspnea and cyanosis may occur with acute intoxication and usually occurs within 10 to 60 minutes of exposure. Shallow breathing, tachypnea and respiratory arrest may also occur after 2 to 3 hours (Jourdan et al, 2001).
    b) CASE SERIES: In a series of patients with suspected barium poisoning secondary to contaminated radiocontrast solution, 14 (34%) of 41 developed dyspnea (CDC, 2003).
    c) CASE REPORT: A 16-year-old boy presented with acute quadriparesis and respiratory failure, and subsequent development of ventricular tachycardia, all of which were secondary to severe hypokalemia, following ingestion of fireworks. With supportive treatment, including ventilation and rapid potassium infusion, the patient recovered. Suspecting barium poisoning, toxicologic analysis of blood confirmed the presence of barium (98.5 mcg/dL) (Deepthiraju & Varma, 2012).
    B) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) Bronchoconstriction may result from inhaling fumes from barium-containing fluxes (Hicks et al, 1986).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Initial symptoms of barium intoxication often consist of transient feelings of numbness and tingling around the mouth and sometimes the face, neck and extremities (Lewi & Bar-Khayim, 1964; Morton, 1945; Deng et al, 1991; Johnson & VanTassell, 1991).
    B) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) Muscle weakness may progress to paralysis (Jacobs et al, 2002; Jourdan et al, 2001; Deng et al, 1991; Johnson & VanTassell, 1991). It usually begins in the limbs (usually arms before legs) and may progress to the muscles involved in respiration (Talwar et al, 2007). Speech is often lost or impaired as the tongue and pharynx are affected.
    b) The patient generally remains conscious and alert throughout the course of intoxication (Talwar et al, 2007; Agarwal et al, 1986; Berning, 1975; Diengott et al, 1964; Lewi & Bar-Khayim, 1964; Morton, 1945; McNally, 1925).
    c) CASE REPORT - A 52-year-old woman developed severe hypokalemia (initial serum potassium level of 1.1 mEq/L) followed by flaccid quadriplegia after a suicidal ingestion of 70 mg of amlodipine, 280 mg of fluoxetine, and an unknown amount of barium carbonate. Continuous veno-venous hemodiafiltration (CVVHDF) was initiated, and within 24 hours, the patient's paralysis rapidly improved (Koch et al, 2003).
    d) CASE REPORT - A 32-year-old woman presented with severe hypokalemia (serum potassium 1.1 mmol/L), hypotension, and facial twitching approximately 4 hours after ingesting a potter's glaze containing 62% barium sulfide. Over the next 3 hours, she developed generalized weakness that progressed to flaccid paralysis and respiratory failure, necessitating mechanical ventilation. Initial serum barium concentration was 200 mcmol/L. Her paralysis persisted despite saline diuresis and intravenous potassium supplementation. Hemodialysis was initiated on hospital day 3 using a dialysate potassium concentration of 4 mmol/L. After 4 hours of hemodialysis, the patient's paralysis gradually resolved and she completely recovered without neurologic sequelae (Thomas et al, 1998).
    e) CASE REPORT - A 20-year-old man presented to the emergency department with quadriparesis approximately 6 hours following ingestion of an unknown amount of a rodenticide containing barium carbonate. At the time, the patient was also experiencing vomiting, abdominal pain, and a perioral tingling followed by heaviness of his extremities. A neurologic exam demonstrated generalized hypotonia with motor weakness (power of 3/5) in all four extremities, diminished deep tendon reflexes, and flexor plantar responses. Initial laboratory data indicated severe hypokalemia with a serum potassium concentration of 1.1 mEq/L, resulting in a diagnosis of hypokalemic paralysis. Despite initial supplementation with oral and intravenous potassium, within 1 hour, the patient developed difficulty in breathing and the power in his extremities decreased to 1/5. Arterial blood gas analysis revealed respiratory failure, necessitating intubation. With continued potassium supplementation, the patient's serum potassium concentration normalized, power in his extremities increased to 4/5, and he was extubated. He was discharged 72 hours post-admission without neurologic sequelae (Torka et al, 2009).
    f) CASE REPORT: A 16-year-old boy presented with acute quadriparesis and respiratory failure, and subsequent development of ventricular tachycardia, all of which were secondary to severe hypokalemia, following ingestion of fireworks. With supportive treatment, including ventilation and rapid potassium infusion, the patient recovered. Suspecting barium poisoning, toxicologic analysis of blood confirmed the presence of barium (98.5 mcg/dL) (Deepthiraju & Varma, 2012).
    C) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Dizziness is frequently reported following ingestion of barium salts (Deng et al, 1991). Syncope may occur (Johnson & VanTassell, 1991). Vertigo may occur with acute intoxication and usually occurs within 10 to 60 minutes of exposure (Jourdan et al, 2001).
    D) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) After 2 to 3 hours, tremors and seizures may occur with acute barium intoxication (Jourdan et al, 2001).
    b) Small amounts of barium in cerebrospinal fluid result in convulsions (Zenz, 1994).
    E) PSYCHOMOTOR AGITATION
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a series of patients with suspected barium poisoning secondary to contaminated radiocontrast material, 11 (27%) of 40 developed agitation (CDC, 2003).
    F) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Headache was reported in 14 (37%) of 38 patients in a series of cases of suspected barium poisoning due to contaminated radiocontrast material (CDC, 2003).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) DRUG-INDUCED GASTROINTESTINAL DISTURBANCE
    1) WITH POISONING/EXPOSURE
    a) Paresthesias are often accompanied by severe nausea, vomiting, pyrosis, increased salivation, and abdominal pain (Jacobs et al, 2002; Jourdan et al, 2001; Sigue et al, 2000; Diengott et al, 1964; Gould et al, 1973; McNally, 1925; Morton, 1945; Wetherill et al, 1981; Aks et al, 1991; Deng et al, 1991; Johnson & VanTassell, 1991; Hathaway et al, 1996).
    b) Severe colicky, watery diarrhea may also develop (Koch et al, 2003; Jacobs et al, 2002; Jourdan et al, 2001; Diengott et al, 1964; Lewi & Bar-Khayim, 1964; McNally, 1925; Morton, 1945; Deng et al, 1991; Johnson & VanTassell, 1991).
    c) CASE SERIES: Two prisoners developed nausea, vomiting, abdominal pain after ingesting depilatories containing barium sulfide (approximately 420 grams and 129 grams, respectively) (Sigue et al, 2000).
    d) CASE SERIES: In a series of patients with suspected barium toxicity after exposure to contaminated radiographic contrast media, 40 (93%) of 43 had nausea, 38 (88%) of 43 had abdominal pain, 35 (80%) of 44 had diarrhea, and 29 (67%) of 43 had vomiting (CDC, 2003).
    e) BARIUM CHLORIDE: Nausea, vomiting, diarrhea, and abdominal pain were reported in several patients following barium chloride poisoning (Ananda et al, 2013).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) WITH POISONING/EXPOSURE
    a) BARIUM DEPOSITION: Venous intravasation of barium may result in deposition of barium in the reticuloendothelial system, measured by increased density in the liver, spleen, and bones on plain radiographs (Chan et al, 1987).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Oliguric renal insufficiency may result (Phelan et al, 1984; Wetherill et al, 1981; Shankle & Keane, 1988).
    b) Acute renal failure may occur (Goldfrank, 1998).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) RESPIRATORY ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) A profound respiratory acidosis may result as the paralysis affects the muscles involved in respiration (Berning, 1975; Gould et al, 1973).
    b) CASE REPORTS: Mixed metabolic and respiratory acidosis (pH 7.1, pCO2 60 mmHg, HCO3 17 mmol/L) was reported in a 32-year-old woman who ingested a potter's glaze containing 62% barium sulfide (Thomas et al, 1998).
    c) BARIUM CHLORATE: Mixed metabolic and respiratory acidosis (pH 7.03; pCO2 57 mmHg; pO2 109 mmHg; HCO3 15 mmol/L; base excess 16.8 mmol/L) occurred in a 35-year-old man who ingested 16 small fireworks, identified as "color snakes" and "black snakes" and believed to contain barium chlorate (Rhyee & Heard, 2009).
    B) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Metabolic acidosis may develop in patients with recurrent dysrhythmias (Johnson & VanTassell, 1991; Jacobs et al, 2002).
    b) CASE REPORT: Severe metabolic acidosis (pH 7.1, PO2 151, PCO2 45, Base Excess -17.7) was reported in a patient who developed seizures and broad complex ventricular tachycardia as well as complete quadriplegia after unintentionally ingesting a tea containing a barium salt. Toxicology screen of his blood indicated the presence of barium at a level of 5.7 mg/L (normal 0.08 to 0.4 mg/L). The patient recovered following supportive treatment (Talwar et al, 2007).
    c) CASE REPORTS: Mixed metabolic and respiratory acidosis (pH 7.1, CO2 60 mmHg, HCO3 17 mmol/L) was reported in a 32-year-old woman who ingested a potter's glaze containing 62% barium sulfide (Thomas et al, 1998).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Alkaline barium compounds (barium hydroxide, barium oxide) cause irritation of the skin (ACGIH, 1991; Hathaway et al, 1996).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) Weakness and paralysis frequently develop in patients with severe hypokalemia from barium salt poisoning (Ananda et al, 2013; Deepthiraju & Varma, 2012; Talwar et al, 2007; Koch et al, 2003; Jacobs et al, 2002; Sigue et al, 2000; Johnson & VanTassell, 1991; Lewis, 2000; Thomas et al, 1998; Deng et al, 1991) .
    B) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 30-year-old man intentionally ingested the entire contents of a bottle of barium chloride and, 30 minutes later, became areflexic with severe muscle weakness. His only movement was confined to his facial muscles and to his fingertips. The patient required endotracheal intubation and hemodialysis was started. Within 2 hours after beginning hemodialysis, the patient showed strong movement in all extremities, and was subsequently extubated (Wells & Wood, 2001).
    b) CASE REPORT: A 22-year-old man presented to an outpatient clinic with abdominal pain and increasing weakness in his arms and legs. At the clinic, the patient became hypertensive (140/96 mmHg) and cyanotic, and he developed generalized areflexic muscle weakness and increased salivation. Despite supportive care, the patient's condition deteriorated and he died. Post-mortem toxicologic analysis of his tissues indicated the presence of barium. Interview of his parents revealed that the patient had inadvertently used barium chloride in soup that he had consumed instead of cooking salt (Ananda et al, 2013).
    C) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Rhabdomyolysis has developed in patients with severe barium carbonate or barium sulfide poisonings (Sigue et al, 2000; Johnson & VanTassell, 1991). The effect may have been secondary to severe hypokalemia.
    D) DISORDER OF BONE
    1) WITH POISONING/EXPOSURE
    a) BARIUM DEPOSITION: Venous intravasation of barium may result in deposition of barium in the reticuloendothelial system, measured by increased density in the liver, spleen, and bones on plain radiographs (Chan et al, 1987).
    E) ABNORMALLY INCREASED MUSCLE CONTRACTION
    1) WITH POISONING/EXPOSURE
    a) When ingested, soluble, ionized barium compounds increase muscle contractility, especially that of smooth muscle (Sittig, 1991).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no reproductive studies were found for barium in humans.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) There is little information about reproductive hazards of barium compounds. The chloride produced curled toes in chickens when injected into the yolk sac (Ridgway & Karnofsky, 1952), and the fluoride did not cause birth defects in rats (Popova & Peretolchina, 1976).
    2) Oral barium chloride dihydrate in male and female rats or mice prior to and during mating was not associated with anatomic defects in the offspring even at doses associated with maternal toxicity (Dietz et al, 1992).
    3) There were no anatomical effects seen in the offspring of Fischer 344/N rats and B6C3F1 mice exposed to barium chloride at levels up to 4000 ppm, but a marginal reduction in the pup weight in the high dose rats was seen. Rat and mice reproductive indices were not affected (Bingham et al, 2001) Hathaway et al, 2001).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7440-39-3 (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
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Bronchogenic carcinomas are reported in rats injected intra-tracheally with insoluble barium sulfate (Bingham et al, 2001).
    B) LACK OF EFFECT
    1) A 2-year NTP study of barium chloride in water using rat and mouse reported no evidence of carcinogenicity (Bingham et al, 2001).

Genotoxicity

    A) Limited genotoxicity tests with barium salts have been largely negative.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Institute continuous cardiac monitoring and obtain an ECG (evaluate for evidence of hypokalemia including T wave flattening and prominent U waves).
    B) Monitor vital signs, with particular attention to evidence of respiratory insufficiency. Perform serial neurologic exams to evaluate for muscle weakness.
    C) Determine potassium levels frequently (every 1 to 2 hours until stabilized). Monitor serum phosphorus, magnesium CK and renal function in symptomatic patients.
    D) Serum barium concentrations are not readily available or useful in guiding therapy.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Serum potassium levels are helpful to diagnose and monitor hypokalemia and its concomitant paralysis.
    2) Serum creatinine and blood urea nitrogen levels may aid in diagnosing and monitoring for possible renal injury.
    B) ACID/BASE
    1) Arterial blood gas measurements aid in the treatment of respiratory acidosis caused by the paralysis of the muscles involved in respiration.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Continuous EKG monitoring for hypokalemia and dysrhythmias.

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) Jacobs et al (2002) described a 50-year-old male patient who sustained burns, multiple traumatic injuries and severe acute barium toxicity from an explosion of barium styphnate propellant. Spectrometric analysis of the serum and urine for barium revealed concentrations roughly 20 to 80 times higher than normal (serum and urine concentrations of 370 mcg/mL and 1600 mcg/L, respectively; abnormal serum barium level >20 mcg/dL) (Jacobs et al, 2002).
    B) OTHER
    1) Serum barium concentrations are not available in routine hospital service laboratories and do not contribute to the management of this poisoning.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with hypokalemia, weakness or dysrhythmias should be admitted to an intensive care setting for cardiac, respiratory and neurologic monitoring and aggressive potassium replacement.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist and/or poison center for any patient with significant barium poisoning or in whom the diagnosis is unclear. Consult a nephrologist for emergent dialysis in any patients with severe poisoning.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) All patients who have ingested a soluble barium salt should be sent to a healthcare facility for evaluation and treatment. Patients should be observed for 6 to 8 hours with ECG monitoring, serial serum potassium concentrations, and evaluation for weakness. Patients who are asymptomatic with normal serum potassium during 6 to 8 hours of observation may be discharged.

Monitoring

    A) Institute continuous cardiac monitoring and obtain an ECG (evaluate for evidence of hypokalemia including T wave flattening and prominent U waves).
    B) Monitor vital signs, with particular attention to evidence of respiratory insufficiency. Perform serial neurologic exams to evaluate for muscle weakness.
    C) Determine potassium levels frequently (every 1 to 2 hours until stabilized). Monitor serum phosphorus, magnesium CK and renal function in symptomatic patients.
    D) Serum barium concentrations are not readily available or useful in guiding therapy.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL/ NOT RECOMMENDED
    1) Charcoal administration is not advised since ionic barium would likely not be adsorbed by charcoal. Spontaneous vomiting and risk of loss of airway protection both due to the barium puts the patient at risk for charcoal aspiration.
    B) DERMAL EXPOSURE
    1) Wash exposed skin with soap and water. Remove contaminated clothing.
    6.5.2) PREVENTION OF ABSORPTION
    A) GASTRIC LAVAGE
    1) Gastric lavage or insertion of a nasogastric tube to aspirate gastric contents may be considered in patients with a recent ingestion who can protect their airway or in whom airway is protected.
    B) ACTIVATED CHARCOAL
    1) Charcoal administration is not advised since ionic barium would likely not be adsorbed by charcoal. The spontaneous vomiting and risk of loss of airway protection due to the barium puts the patient at risk for charcoal aspiration.
    C) MAGNESIUM SULFATE
    1) Administration of magnesium sulfate to a patient who ingested barium carbonate was felt to result in barium sulfate precipitation in the gastrointestinal tract, preventing further barium absorption (Mills & Kunkel, 1993).
    2) Magnesium sulfate when given orally results in the formation of nonabsorbable barium sulfate within the gastrointestinal tract. Dose: 250 milligrams/kilogram for children and 30 grams for adults.
    6.5.3) TREATMENT
    A) DIURESIS
    1) Administer sufficient intravenous fluids to maintain brisk urine output. Routine administration of diuretics has not been shown to be beneficial.
    B) HYPOKALEMIA
    1) Treat hypokalemia by infusing potassium (KCl) intravenously (up to 250 milliequivalents administered over 24 hours has been used) (Jourdan et al, 2001; Agarwal et al, 1986; Berning, 1975; Diengott et al, 1964; Gould et al, 1973; Wetherill et al, 1981). Oral supplementation may also be used in patients who are alert or in whom airway is protected.
    2) PLASMA POTASSIUM CONCENTRATIONS should be monitored frequently for hypokalemia.
    3) SKELETAL MUSCLE PARALYSIS, cardiac arrhythmias, and diarrhea appear to respond to potassium therapy, but no effect is seen on barium-induced hypertension (Roza & Berman, 1971; Smith & Gosselin, 1976).
    4) Administration of potassium should be effective in the treatment of paralysis (Diengott et al, 1964; Gould et al, 1973; Roza & Berman, 1971).
    5) CASE REPORT: A 16-year-old boy presented with acute quadriparesis and respiratory failure, and subsequent development of ventricular tachycardia, all of which were secondary to severe hypokalemia, following ingestion of fireworks. With supportive treatment, including ventilation and rapid potassium infusion (a total of 360 mEq of potassium was administered in the first 20 hours post-presentation), the patient recovered. Suspecting barium poisoning, toxicologic analysis of blood confirmed the presence of barium (98.5 mcg/dL) (Deepthiraju & Varma, 2012).
    C) MONITORING OF PATIENT
    1) Institute continuous cardiac monitoring and perform serial ECGs to evaluate for evidence of hypokalemia (T wave flattening and prominent U waves) and dysrhythmias. Monitor vital signs, with particular attention to evidence of respiratory insufficiency. Perform serial neurologic exams to evaluate for muscle weakness. Determine potassium levels frequently (every 1 to 2 hours until stabilized). Monitor serum phosphorus, magnesium CK and renal function in symptomatic patients.
    D) VENTRICULAR ARRHYTHMIA
    1) POTASSIUM
    a) Cardiac dysrhythmias appear to respond to potassium therapy (Roza & Berman, 1971; Smith & Gosselin, 1976). Correction of hypokalemia is the preferred treatment of ventricular tachycardia associated with barium poisoning.
    b) Traditional antidysrhythmics (lidocaine, amiodarone) may be used but efficacy may be limited in patients with persistent hypokalemia.
    c) Sustained ventricular tachycardia refractory to intravenous lidocaine boluses of 100 and 50 milligrams was reported in a 48-year-old man secondary to barium intoxication (Johnson & VanTassell, 1991). Resolution of ventricular dysrhythmias in this patient was associated with correction of hypokalemia.
    2) VENTRICULAR DYSRHYTHMIAS SUMMARY
    a) Obtain an ECG, institute continuous cardiac monitoring and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders (particularly hypokalemia, hypocalcemia, and hypomagnesemia). Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Amiodarone should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require immediate cardioversion.
    3) LIDOCAINE
    a) LIDOCAINE/INDICATIONS
    1) Ventricular tachycardia or ventricular fibrillation (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010; Vanden Hoek et al, 2010).
    b) LIDOCAINE/DOSE
    1) ADULT: 1 to 1.5 milligrams/kilogram via intravenous push. For refractory VT/VF an additional bolus of 0.5 to 0.75 milligram/kilogram can be given at 5 to 10 minute intervals to a maximum dose of 3 milligrams/kilogram (Neumar et al, 2010). Only bolus therapy is recommended during cardiac arrest.
    a) Once circulation has been restored begin a maintenance infusion of 1 to 4 milligrams per minute. If dysrhythmias recur during infusion repeat 0.5 milligram/kilogram bolus and increase the infusion rate incrementally (maximal infusion rate is 4 milligrams/minute) (Neumar et al, 2010).
    2) CHILD: 1 milligram/kilogram initial bolus IV/IO; followed by a continuous infusion of 20 to 50 micrograms/kilogram/minute (de Caen et al, 2015).
    c) LIDOCAINE/MAJOR ADVERSE REACTIONS
    1) Paresthesias; muscle twitching; confusion; slurred speech; seizures; respiratory depression or arrest; bradycardia; coma. May cause significant AV block or worsen pre-existing block. Prophylactic pacemaker may be required in the face of bifascicular, second degree, or third degree heart block (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010).
    d) LIDOCAINE/MONITORING PARAMETERS
    1) Monitor ECG continuously; plasma concentrations as indicated (Prod Info Lidocaine HCl intravenous injection solution, 2006).
    4) AMIODARONE
    a) AMIODARONE/INDICATIONS
    1) Effective for the control of hemodynamically stable monomorphic ventricular tachycardia. Also recommended for pulseless ventricular tachycardia or ventricular fibrillation in cardiac arrest unresponsive to CPR, defibrillation and vasopressor therapy (Link et al, 2015; Neumar et al, 2010). It should be used with caution when the ingestion involves agents known to cause QTc prolongation, such as fluoroquinolones, macrolide antibiotics or azoles, and when ECG reveals QT prolongation suspected to be secondary to overdose (Prod Info Cordarone(R) oral tablets, 2015).
    b) AMIODARONE/ADULT DOSE
    1) For ventricular fibrillation or pulseless VT unresponsive to CPR, defibrillation, and a vasopressor therapy give an initial dose of 300 mg IV followed by 1 dose of 150 mg IV. For stable ventricular tachycardias: Infuse 150 milligrams over 10 minutes, and repeat if necessary. Follow by a 1 milligram/minute infusion for 6 hours, then a 0.5 milligram/minute. Maximum total dose over 24 hours is 2.2 grams (Neumar et al, 2010).
    c) AMIODARONE/PEDIATRIC DOSE
    1) Infuse 5 milligrams/kilogram as a bolus for pulseless ventricular tachycardia or ventricular fibrillation; may repeat twice up to 15 mg/kg. Infuse 5 milligrams/kilogram over 20 to 60 minutes for perfusing tachycardias. Maximum single dose is 300 mg. Routine use with other drugs that prolong the QT interval is NOT recommended (Kleinman et al, 2010).
    d) ADVERSE EFFECTS
    1) Hypotension and bradycardia are the most common adverse effects (Neumar et al, 2010).
    5) PROCAINAMIDE
    a) PROCAINAMIDE/INDICATIONS
    1) An alternative drug in the treatment of PVCs or recurrent ventricular tachycardia when lidocaine is contraindicated or not effective. It should be avoided when the ingestion involves agents with quinidine-like effects (e.g. tricyclic antidepressants, phenothiazines, chloroquine, antidysrhythmics) and when the ECG reveals QRS widening or QT prolongation suspected to be secondary to overdose(Neumar et al, 2010; Vanden Hoek,TLet al,null).
    b) PROCAINAMIDE/ADULT LOADING DOSE
    1) 20 to 50 milligrams/minute IV until dysrhythmia is suppressed or toxicity develops from procainamide (hypotension develops or the QRS is widened by 50%), or a total dose of 17 milligrams/kilogram is given (1.2 grams for a 70 kilogram person) (Neumar et al, 2010).
    2) ALTERNATIVE DOSING: 100 mg every 5 minutes until dysrhythmia is controlled, or toxicity develops from procainamide (hypotension develops or the QRS is widened by 50%) or 17 mg/kg have been given (Neumar et al, 2010).
    3) MAXIMUM DOSE: 17 milligrams/kilogram (Neumar et al, 2010).
    c) PROCAINAMIDE/CONTROLLED INFUSION
    1) In conscious patients, procainamide should be administered as a controlled infusion (20 milligrams/minute) because of the risk of QT prolongation and its hypotensive effects (Link et al, 2015)
    d) PROCAINAMIDE/ADULT MAINTENANCE DOSE
    1) 1 to 4 milligrams/minute via an intravenous infusion (Neumar et al, 2010).
    e) PROCAINAMIDE/PEDIATRIC LOADING DOSE
    1) 15 milligrams/kilogram IV/Intraosseously over 30 to 60 minutes; discontinue if hypotension develops or the QRS widens by 50% (Kleinman et al, 2010).
    f) PROCAINAMIDE/PEDIATRIC MAINTENANCE DOSE
    1) Initiate at 20 mcg/kg/minute and increase in 10 mcg/kg/minute increments every 15 to 30 minutes until desired effect is achieved; up to 80 mcg/kg/minute (Bouhouch et al, 2008; Ratnasamy et al, 2008; Mandapati et al, 2000; Luedtke et al, 1997; Walsh et al, 1997).
    g) PROCAINAMIDE/PEDIATRIC MAXIMUM DOSE
    1) 2 grams/day (Bouhouch et al, 2008; Ratnasamy et al, 2008; Mandapati et al, 2000; Luedtke et al, 1997; Walsh et al, 1997).
    h) MONITORING PARAMETERS
    1) ECG, blood pressure, and blood concentrations (Prod Info procainamide HCl IV, IM injection solution, 2011). Procainamide can produce hypotension and QT prolongation (Link et al, 2015).
    i) AVOID
    1) Avoid in patients with QT prolongation and CHF (Neumar et al, 2010).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    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.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: 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, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) Dermal exposure only requires treatment if associated with a burn. Rapid irrigation and burn debridement are important to decrease the absorption of barium (Stewart & Hummel, 1984). X-rays may be helpful in the judgement of the effectiveness of dermal decontamination.

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis is effective (corrects hypokalemia, and associated weakness and dysrhythmias, enhances barium elimination) in patients with severe poisoning. In most case reports the dialysate used has contained greater than normal quantities of potassium (in the range of 4 to 7 mMol/L). Emergent hemodialysis should be considered early in patients with hypokalemia, severe weakness, or dysrhythmias that are not responding to potassium supplementation.
    2) Several case reports indicate considerable improvement after hemodialysis (Bahlmann et al, 2005; Wells & Wood, 2001; Thomas et al, 1998; Schorn et al, 1991). While several of these cases document rapid declines in serum barium concentration during hemodialysis, and it is possible that some of this improvement was due to correction of hypokalemia.
    3) The use of hemodialysis with a sodium bicarbonate/potassium dialysate allowed safe infusion of 400 millimoles of potassium over one day in a 22-year-old man who ingested 5 to 10 grams of barium carbonate. Barium elimination seemed to have been accelerated by the procedure, with a barium half life of 1.9 hours during hemodialysis and a half life of 18 hours after dialysis. The total amount of barium removed was not calculated (Schorn et al, 1991).
    4) CASE REPORT: A 17-year-old boy became unresponsive, requiring cardiac resuscitation, following ingestion of 7 grams of barium nitrate in a suicide attempt. His initial plasma potassium concentration was 1.3 to 1.7 mM/L that did not respond to administration of IV fluids. Hemodialysis was initiated with dialyzing fluid containing 7 mM/L (approximately twice the usual concentration), resulting in an increase in his plasma potassium concentration to 3.7 mM/L after 45 minutes. The patient regained consciousness and hemodialysis was continued for a total of 6 hours with dialyzing fluid of normal potassium concentration. The patient then recovered uneventfully (Szajewski, 2004).
    B) HEMODIAFILTRATION
    1) Continuous veno-venous hemodiafiltration (CVVHDF) was initiated in a 52-year-old woman who developed severe hypokalemia and persistent flaccid paralysis after intentionally ingesting amlodipine, fluoxetine, and an unknown amount of barium carbonate. A total of approximately 125 mg of barium was eliminated 14 hours after initiation of CVVHDF, and a total of 152 mg of barium was eliminated 42 hours after CVVHDF initiation. Barium half life was 6 hours during CVVHD(Koch et al, 2003; Koch et al, 2003).

Abstracts

Case Reports

    A) ADULT
    1) ROUTE OF EXPOSURE
    a) INHALATION
    1) Inhalation of barium carbonate powder resulted in abdominal cramps, nausea, and vomiting one hour later, followed by diaphoresis, salivation, and rapidly progressive weakness. Six hours after exposure extremity and neck paralysis, absent deep tendon reflexes, hematuria, renal dysfunction, and hypokalemia (0.2 mmoL/L) were noted. A barium level was 250 mEq/L. Complete remission occurred within 5 days after administration of intravenous potassium (Shankle & Keane, 1988).
    2) Inhalation of dust from several days exposure to barium peroxide crushing operations by a worker in the mid-1920s led to abdominal pain, vomiting, dyspnea, cyanosis, tachycardia, and paralysis of the right leg and arm, followed by death on the third day (Harbison, 1998).
    b) DERMAL
    1) Percutaneous absorption occurred after a burn from molten barium chloride to 20% of the body. At four hours after the burn, serum potassium was 2.2 mEq/L and intravenous potassium supplementation was administered. Peak plasma barium concentration was 12.4 mg/L and no weakness or paralysis was noted (Stewart & Hummel, 1984).
    c) INGESTION
    1) Ingestion of an unknown amount of barium acetate by a 15-year-old girl resulted in a life threatening ventricular arrhythmia, arterial hypertension, vomiting, paresthesias, muscular weakness, and profound hypokalemia. These occurred within one hour of ingestion. Treatment included intravenous lidocaine and potassium (Tenenbein, 1985).
    2) A 22-year-old man ingested about 5 to 10 grams of barium carbonate dissolved in hydrochloric acid, which forms barium chloride. Abdominal pain and generalized muscle weakness developed 20 minutes later.
    a) On admission to the emergency department 1.5 hours postingestion salivation, cyanosis, hypertension (180/110 mmHg), diarrhea, and an irregular pulse were noted. Laboratory values showed respiratory acidosis and hypokalemia (2.1 mmol/L). Respiratory insufficiency developed, requiring intubation and mechanical ventilation. Ventricular fibrillation occurred during intubation.
    b) Hemodialysis was begun 7 hours postingestion using sodium bicarbonate and potassium in the dialysate fluid. At the end of dialysis, the serum potassium level was 3.4 mmol/L, and muscle strength had started to return. Barium levels fell during hemodialysis with a half-life of 1.9 hours, and more slowly afterwards with a half-life of 18 hours. He recovered with no adverse neurological sequelae (Schorn et al, 1991).
    3) Seven members of a family (ages 2 to 48 years) were poisoned following accidental ingestion of fried fish prepared with a breading containing 35.5% barium carbonate by weight (Johnson & VanTassell, 1991).
    a) Three of the patients demonstrated classic signs of barium toxicity. A 48-year-old man developed rhabdomyolysis, respiratory failure, and hypophosphatemia in addition to the classic signs of barium toxicity.
    b) The five patients less than 20 years old presented with gastrointestinal symptoms consistent with gastroenteritis; four of these patients ate quantities of the fish similar to those ingested by the 48-year-old man described above, indicating that perhaps children and adolescents experience minimal toxicity from barium ingestion. All patients recovered completely from this toxic insult.
    4) A 45-year-old woman developed nausea, vomiting, diarrhea, hypokalemia, ventricular arrhythmia, and ascending flaccid paralysis associated with an ingestion of a tablespoon of barium carbonate powder in a suicide attempt (Janssen et al, 1992). GI complaints were present by 4 hours postingestion. She recovered uneventfully following symptomatic and supportive treatment.
    5) A 33-year-old woman ingested 16 veterinary capsules filled with barium carbonate and within 2 hours experienced profuse repetitive vomiting, watery diarrhea, and abdominal cramps. Three hours post ingestion gastric lavage was performed and 30 grams of magnesium sulfate was administered through an NG tube.
    a) IV fluids with potassium were given. Hypokalemia and muscle weakness did not occur. A KUB X-ray revealed a large amount of radiopaque material in the duodenum, believed to be barium sulfate. Twelve hours later a repeat KUB X-ray showed the radiopaque material in the colon. During this 12 hour period the patient remained asymptomatic.
    b) Nine hours after ingestion a whole-blood barium level was 552 mcg/L. Twenty-four hours after hospital admission the patient was discharged. It is believed that administration of magnesium sulfate precipitated the barium and prevented absorption of toxic barium (Mills & Konkel, 1993).
    6) Aks et al (1991) reported a series of five suicide attempts within a prison population, utilizing depilatory products containing barium sulfide. One of five suicide attempts resulted in death; postmortem revealed a serum barium concentration of less than 20 mcg/mL and 14,300 mcg/L in the bile. Three prisoners exhibited esophageal injury (Aks et al, 1991).
    7) Several case reports indicate that barium toxicity may occur after repeated radiological examinations using oral barium sulfate (Savry et al, 1999) or as a result of direct transfer of barium from the gastrointestinal tract into the vascular system during radiological examination (Pelissier-Alicot et al, 1999).
    8) A barium concentration of 1.9 was found in the blood of an adult who died only hours after ingesting 11.5 grams of barium sulfide (Baselt, 2000).
    2) SPECIFIC AGENT
    a) BARIUM STYPHENATE: An explosives worker was working with approximately 1 pound of dry barium styphenate powder, ammonia, and acetone when the compounds exploded and became aerosolized. The man was thrown several feet by the explosion and was found unconscious with severe trauma and third degree burns. The man needed treatment with potassium chloride and potassium phosphate to correct electrolyte abnormalities. Serum barium was 370 mcg/dL with urinary levels of 1600 mcg/L (Hung et al, 1998).
    b) Jacobs et al (2002) described a 50-year-old man who sustained burns and multiple traumatic injuries in addition to acute barium toxicity from an explosion of barium styphenate propellant. In addition to critical injuries, the patient experienced repeated profound hypokalemia, profuse diarrhea, severe muscular weakness, cardiac dysrhythmias, respiratory failure, prolonged gastrointestinal dysfunction, paralysis, myoclonus, hypertension, and profound lactic acidosis. Spectrometric analysis of the serum and urine for barium revealed concentrations roughly 20 to 80 times higher than normal (serum and urine concentrations of 370 mcg/mL and 1600 mcg/L, respectively; abnormal serum barium level >20 mcg/dL) (Jacobs et al, 2002).

Range Of Toxicity

Summary

    A) There are insufficient data in the literature to accurately characterize the acute toxicity of barium salts. Ingestions on the order of 0.8 to 1 g have been reported as potentially lethal. With aggressive intensive care, adults have recovered from severe toxicity after ingesting as much as 30 grams of barium carbonate.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The toxic dose of barium salts may be as low as 0.2 gram and the lethal dose as low as 3 grams. It has been reported that the LD50 for barium ingestion is 1 gram (Jacobs et al, 2002; Hathaway et al, 1996) Kunkel, 1993).

Maximum Tolerated Exposure

    A) SPECIFIC SUBSTANCE
    1) BARIUM CARBONATE - Adults have recovered after ingesting as much as 30 grams of barium carbonate and it is thought that much depends on the food ingested (food high in sulfate may precipitate barium as barium sulfate and, thus detoxify some of the ingested barium), and on medical attention and supportive care received.
    2) BARIUM SULFIDE - Ingestion of 15.8 grams of barium sulfide was associated with survival in a 26-year-old man (Gould et al, 1973).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) SPECIFIC SUBSTANCE
    a) BARIUM CARBONATE
    1) Inhalation of barium carbonate powder resulted in severe hypokalemia and paralysis within 6 hours, with a barium level of 250 milliequivalents/liter (Shankle & Keane, 1988).
    2) Ingestion of barium carbonate resulted in quadriparesis within 10 hours and a peak barium level of 150 milliequivalents/liter (Phelan et al, 1984).
    b) BARIUM SULFIDE
    1) Ingestion of an unknown amount of a depilatory product containing barium sulfide resulted in death. Postmortem revealed a serum barium concentration of less than 20 micrograms/milliliter and a bile concentration of 14,300 micrograms/liter (Aks et al, 1991).
    2) A 25-year-old man developed a profound hypokalemia (skeletal muscle weakness, respiratory arrest, rhabdomyolysis), as well as life-threatening hyperkalemia after ingesting a depilatory containing barium sulfide (Magic Shave; Carson Products Co, Savannah, GA). The urinary barium level was 1750 mcg/dL (Sigue et al, 2000).
    3) CASE REPORT - Wide complex ventricular tachycardia occurred in a 39-year-old man following a suicidal ingestion of a depilatory containing barium sulfide. Cardiac arrest occurred and the patient died approximately 7 hours postingestion. Postmortem barium concentrations were as follows (Downs et al, 1995):
    Sample (units) Barium concentration
    Brain (mcg/g)1.6
    Kidney (mcg/g) 9.1
    Liver (mcg/g) 3.8
    Vitreous (mcg/g) 26
    Blood (mcg/dL) 216
    Bile (mcg/dL) 220
    Gastric (mcg/g) 6,700

    c) BARIUM CHLORIDE
    1) Cardiorespiratory arrest developed in a 49-year-old man following a suicidal barium chloride ingestion. He died following unsuccessful resuscitation attempts. Autopsy revealed the following barium levels: blood 9.9 mg/L, bile 8.8 mg/L, urine 6.3 mg/L, gastric 10 g/L (Jourdan et al, 2001). The authors believe that the lethal dose of ingested barium is probably 0.8 to 0.9 gram (or approximately 11 milligrams/kilogram).
    d) BARIUM CHLORATE
    1) A 35-year-old man, with severe mental retardation, developed barium toxicity, including dysrhythmias and severe hypokalemia, after ingesting 16 small fireworks, identified as "color snakes" and "black snakes" and believed to contain barium chlorate, that he had mistaken as chewing gum. A serum barium concentration, obtained approximately 15 hours postingestion, was 20,200 mcg/L (reference range less than 200 mcg/L). With supportive therapy, the patient recovered and was discharged 12 days postingestion (Rhyee & Heard, 2009).

Workplace Standards

    A) ACGIH TLV Values for CAS7440-39-3 (American Conference of Governmental Industrial Hygienists, 2010):
    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) Barium and soluble compounds, as Ba
    a) TLV:
    1) TLV-TWA: 0.5 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Not Listed
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) TLV Basis - Critical Effect(s): Eye, skin and GI irr; muscular stim
    d) Molecular Weight: 137.3
    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) NIOSH REL and IDLH Values for CAS7440-39-3 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Barium (soluble compounds, as Ba)
    2) REL:
    a) TWA: 0.5 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): [*Note: The REL also applies to other soluble barium compounds (as Ba) except Barium sulfate.]
    3) IDLH:
    a) IDLH: 50 mg Ba/m3 (as Ba)
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7440-39-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Barium and soluble compounds, as Ba
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Barium and Compounds
    a) D : Not classifiable as to human carcinogenicity.
    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 ; Listed as: Barium (soluble compounds, as Ba)
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7440-39-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Barium, soluble compounds (as Ba)
    2) Table Z-1 for Barium, soluble compounds (as Ba):
    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: 0.5
    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: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) BARIUM ACETATE: (Values are from Bingham et al, 2001)
    B) BARIUM CHLORIDE: (Values are from Bingham et al, 2001)
    1) LD50- (ORAL)RAT:
    a) weanling, 220 mg/kg
    b) adult, 220 mg/kg
    C) BARIUM ZIRCONATE: (Values are from Bingham et al, 2001)
    1) LD50- (ORAL)RAT:
    a) >1980 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) The rapid onset of the marked hypokalemia so characteristic of barium intoxication is due to sequestering of potassium by muscle cells. Barium clogs the exit channel for potassium ions in skeletal muscle cells (Knochel, 1987). The rapidity of the fall in serum potassium suggests potassium migrates into tissue cells (Knochel, 1987; Roza & Berman, 1971; Smith & Gosselin, 1976).
    B) Barium-induced hypokalemia is not characterized by an increased excretion of potassium and is also apparently not due to barium-induced stimulation of adrenergic receptors since agents such as propranolol and phentolamine are ineffective in preventing the development of hypokalemia in barium poisoning (Schott & McArdle, 1974).
    C) Barium stimulates striated, smooth and cardiac muscle resulting in violent peristalsis, arterial hypertension and arrhythmias (Roza & Berman, 1971; Smith & Gosselin, 1976).

Physicochemical

Physical Characteristics

    A) Note: values refer to barium metal, unless noted otherwise.

Molecular Weight

    A) Elemental barium: 137.33

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