• Barium Carbonate (Rodenticide)
• Barium styphnate (propellant)
• Barium chloride
• Barium Sulphate
• Barium Sulfide
• Barium nitrate
• Barium acetate

Although poisoning by barium salts is rare these salts are widely used in industry and therefore represents a substantial risk for human exposure. Barium salts typically produces a rapid onset of symptoms and can produce life threatening toxicity. In addition to good supportive care the mainstay of treatment is rapid correction of hypokalemia.

Patients may present with gastrointestinal symptoms :abdominal pain, nausea, vomiting, and diarrhea to severe cardiac arrhythmias and hypertension. Within hours profound flaccid muscle weakness and respiratory failure may follow. Major hypokalemia is a key feature of barium intoxication.

Repeated profound hypokalemia, cardiac arrhythmias, respiratory failure, prolonged gastrointestinal dysfunction, paralysis, myoclonus, hypertension, and profound lactic acidosis transfusion related

Barium is a soft metallic element with an atomic weight of 137.327. The metal oxidizes easily when exposed to water or alcohol and has a melting point of 727 °C (1341 °F) and a boiling point of 1870 °C (3398 °F). Elemental barium is not found in nature; it normally occurs as an oxide, dioxide, sulphate (barite) or carbonate (witherite). .While some salts are naturally occurring, most salts commercially used are purposes are produced from barium carbonate or oxides.

Barium salts may be either water soluble or insoluble. The solubility of all barium salts increases as pH is lowered. The soluble salts: acetate, chloride, hydroxide, oxide, nitrate and (poly)sulfide are the most commonly associated with toxicity. Barium (poly)sulfide may also produce toxicity through the formation of hydrogen sulfide when it combines with the acid normally present in the stomach. The solubility of barium carbonate is low at a normal pH, but increase significantly when the pH is lowered. In addition, in gastric acid conversion to barium chloride occurs, which is high soluble.

Insoluble salts such as arsenate, carbonate, chromate, fluoride, oxalate, and sulfate are rarely associated with toxicity. Toxicity has occurred in the unusual situation of intravasation (see below).

At a cellular level barium induces hypokalemia by two synergistic mechanisms.

Barium is a competitive blocker of the potassium rectifier channel which is responsible for the efflux of intracellular potassium out of the cell. It may also directly increase cell membrane permeability to sodium. This causes a secondary increase Na+-K+ pump electrogenesis leading to a shift of extracellular potassium into the cell.

Intracellular trapping of potassium leads to depolarization and paralysis. (14) Additionally, the inhibition of potassium channels increases vascular resistance and reduces blood flow (2)(4) and is the likely mechanism for hypertension and lactic acidosis (see below).

While severe hypokalemia is a major contributor to paralysis some authors have found that muscle weakness is better correlated with barium concentration than with potassium concentration. (18;22) This suggests a possible direct effect of barium on either skeletal muscle or neuromuscular transmission.

Toxicity from ingestion of as little as 200 mg of barium salt , oral lethal doses are reported to range from 1-30 g barium salt. In ambient air, inhaled concentrations greater than 250 mg/m3 are considered dangerous.

Following ingestion, 5 to 10% of soluble barium salts are absorbed(14), with the rate of absorption dependent upon the degree of water solubility of the salt. The time to peak serum concentrations is 2 hours(12).

Toxicokinetics are characterized by a rapid redistribution phase, followed by a slow decrease of plasma barium levels with a reported half-life ranging between 18 hours and 3.6 days.(12;20) Renal elimination of the absorbed dose accounts for 10 to 28% of total barium excretion, with the feces being the predominant route of elimination is through the gastrointestinal tract.

Deaths are most commonly reported following ingestion, but have also occurred from inhalation, intraperitoneal exposure, vaginal exposure or by extravasation(13) Death from an ingestion with barium chloride was associated with the following barium levels at autopsy: blood, 9.9 mg/L; bile, 8.8 mg/L; urine, 6.3 mg/L; and gastric contents, 10 gm/L.(13)

Barium poisoning is rare only 24 (13 symptomatic) exposures were reported to the TESS database (n=2.4 million reports) in 2003.(23) Toxicity has been reported for most forms of barium. While it is most commonly reported following the intentional ingestion of soluble salts found in rodenticides(7) insecticides, or depilatories.(8) Toxicity has also followed occupational exposure to barium salts through ingestion or inhalation. An explosion of the propellant barium styphnate caused extensive burns and trauma in a 50 year old man who developed significant barium toxicity within 2 hours of exposure with persistent toxicity for at least 4 days (11). Barium carbonate has an appearance that is similar to flour and has been responsible for most unintentional barium poisonings. Despite the fact that barium sulfate being insoluble, rare cases of unintentional toxicity have been reported during radiographic procedures and include complications associated with oral(17) and rectal administration(10;15;19). Toxicity and death occurred when soluble barium salts unintentionally contaminated contrast solution.(21) and flour (6).

Abdominal pain, nausea, vomiting, and diarrhea commonly occur within 1 hour of ingestion. Esophageal injury(1) and hemorrhagic gastritis are also reported (13).

Severe hypokalemia is the cardinal feature of barium toxicity and can occur within 2 hours following oral or parenteral exposure. Hypokalemia may be exacerbated by blood transfusions, suggesting that fresh red blood cells provide a new reservoir for K+ sequestration.(11)Progressive hypokalemia is associated with severe ventricular dysrhythmias, hypertension, profound flaccid muscle weakness and respiratory failure.

Other effects less commonly reported effects include lactic acidosis, hypophosphatemia and rhabdomyolysis (12). Altered level of consciousness and seizures(5) and basal ganglia manifestations are reported (9). It is unclear whether these later findings are due to direct toxicity or secondary to tissue ischemia.

Barium can be measured by a variety of techniques. Mass spectrometry can quantiate barium in blood and urine. Graphite furnace atomic absorption spectrometry (GF-AAS) is also been used(14) Serum barium levels are not readily available, but values greater than 0.2 mg/L are considered abnormal.(3)
Following acute exposures, patients should have serum electrolytes (particularly potassium and phosphate measured) measured hourly while performing continuous ECG monitoring. CPK and acid base status and renal function should also be measured. A plain abdominal radiograph may show barium, but the sensitivity and specificity of radiography has never been determined for barium poisoning.(14)

Other causes of acute hypokalemia associated with paralysis such as periodic hypokalemic paralysis, toluene toxicity, and diuretic use should be considered if there is no history or laboratory confirmation of barium exposure. Likewise, toxicological etiologies for flaccid paralysis such as hypermagnesemia, botulism and the administration of neuromuscular blockers should also be considered.

Patients should be admitted to a monitored bed with the facilities for respiratory support readily available. Patients who are asymptomatic at 6 hours with normal potassium concentrations can be discharged.

Activated charcoal is unlikely to be effective. Orogastric lavage should be considered in patients who present early after ingestion, but is unlikely to provide extra benefit in patients who are already symptomatic or who have had spontaneous emesis. Oral sodium sulfate administration may prevent absorption by precipitating unabsorbed barium ions to insoluble, nontoxic barium sulfate. Oral magnesium sulfate has also been used with success.(16) The oral dose of magnesium sulfate is 250 mg/kg for children and 30 gm for adults. Intravenous magnesium sulfate or sodium sulfate is not advised as may lead to renal failure due to precipitation of barium in the renal tubules. (18;25)

Patients in respiratory failure should receive assisted ventilation. Aggressive correction of hypokalemia is important to minimize the risk or to treat cardiac dysrhythmias. Large doses of potassium replacement (400 mEq in 24 hours) are reported to be required to correct serum potassium but may still not improve muscle strength(14). As hypokalemia is due to intracellular sequestration of potassium, potassium supplementation increases the total body potassium load. In this situation, rebound hyperkalemia may occur when barium is eliminated, especially in the setting of a patient with impaired renal function and observation should be anticipatory.

Correction of hypokalemia alone may not reverse weakness and would not be expected to completely restore the resting membrane potential. In this, setting hemodialysis can be considered. Hemodialysis for the management of severe barium intoxication has been reported in three cases (20;24) Additionally, in a case report, CVVHDF tripled the measured barium elimination, reduced serum barium half-life by a factor of three, stabilized serum potassium levels, and rapidly improved motor strength, with complete neurological recovery within 24 h.(14) Either method of enhanced elimination should be considered in any severely symptomatic patient who does not respond to correction of hypokalemia.

• in g/litre at 20 °C; where the solubility was not measured at 20 °C, the temperature used is shown in parentheses.(26)

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Ref Type: Electronic Citation

Based on a chapter submitted by the Author to Goldfranks Toxicology 2007

Agency for Toxic Substance & Disease Registry (ATSDR)

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