Barium poisonings are uncommon and usually result from accidental contamination of food sources, suicidal ingestion, or occupational inhalation exposure. Accidental mass poisoning has occurred from the addition of barium carbonate to flour and the contamination of table salt. The incidence of barium poisoning in developing countries is much higher than in developed countries.

Barium is a dense alkaline earth metal that exists in nature as a divalent cation in combination with other elements. The water-soluble barium salts (acetate, chloride, fluoride, hydroxide, nitrate, and sulfide) are highly toxic. The solubility of barium carbonate is low at physiologic pH, but increases considerably as the pH is lowered (such as in the presence of gastric acid). Soluble barium salts are found in depilatories, ceramic glazes, and rodenticides and are used in the manufacture of glass and in dyeing textiles. Barium chlorate used to be a common ingredient in fireworks, producing a green color on ignition, however it has been replaced by the more stable barium nitrate and barium carbonate. Barium sulfide and polysulfide may also produce hydrogen sulfide toxicity. Barium may also enter the air during mining and refining processes, the burning of coal and gas, and the production of barium compounds. The oil and gas industries use barium compounds to make drilling mud, which lubricates the drill while it passes through rocks.

The insoluble salts, such as barium sulfate, are poorly absorbed. However, intravasation from a radiologic study has occurred, where barium sulfate administered under pressure leaked into the peritoneal cavity or portal venous system. Cardiovascular collapse has been reported, although it is unclear if this was directly from the barium or from overwhelming sepsis.

1. Systemic barium poisoning is characterized by profound hypokalemia, leading to weakness, and in severe cases respiratory or cardiac arrest. Barium competitively blocks potassium channels, interfering with the efflux of intracellular potassium out of the cell. Barium ions may also have a direct effect on either skeletal muscle or neuromuscular transmission. In the GI tract, barium stimulates acid and histamine secretion and peristalsis.
2. Inhalation of insoluble inorganic barium salts can cause baritosis, a benign pneumoconiosis. One death resulted from barium peroxide inhalation. Detonation of barium styphnate caused severe poisoning from inhalation and dermal absorption.
3. Pharmacokinetics. After ingestion, soluble barium salts are rapidly absorbed by the digestive mucosa. A rapid redistribution phase is followed by a slow decrease in barium levels, with a half-life ranging from 18 hours to 3.6 days. The predominant route of elimination is the feces, with renal elimination accounting for 10-28%. Barium is irreversibly stored in bone.

The minimum oral toxic dose of soluble barium salts is undetermined but may be as low as 200 mg. Lethal doses range from 1 to 30 g for various barium salts because absorption is influenced by gastric pH and foods high in sulfate. Patients have survived ingestions of 129 and 421 g of barium sulfide. The US Environmental Protection agency (EPA) has set an oral reference dose for barium of 0.07 mg/kg/d. A level of 50 mg/m³ may be immediately dangerous to life and health (IDLH).

Acute intoxication manifests within 10-60 minutes with severe gastrointestinal symptoms, such as vomiting, epigastric discomfort, and profuse watery diarrhea. This is soon followed by skeletal muscle weakness due to profound hypokalemia, that progresses to flaccid paralysis, areflexia, and respiratory failure. Ventricular arrhythmias, hypophosphatemia, mydriasis, impaired visual accommodation, myoclonus, salivation, hypertension, convulsions, rhabdomyolysis, acute renal failure, and coagulopathy may also occur. Profound lactic acidosis and CNS depression may be present. More often, patients remain conscious even when severely poisoned.

Is based on a history of exposure, accompanied by rapidly progressive hypokalemia and muscle weakness. A plain abdominal radiograph may detect radiopaque material, but the sensitivity and specificity of radiography have not been determined for barium ingestions.

1. Specific levels. Serum barium levels are not readily available. They can be measured by a variety of techniques, and levels greater than 0.2 mg/L are considered abnormal.
2. Other useful laboratory studies include electrolytes, BUN, creatinine, phosphorus, arterial blood gases or pulse oximetry, and continuous ECG monitoring. Measure serum potassium levels frequently.

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary.
   2. Treat fluid losses from gastroenteritis with IV crystalloids.
   3. Attach a cardiac monitor and observe the patient closely for at least 6-8 hours after ingestion.
2. Specific drugs and antidotes. Administer potassium chloride to treat symptomatic or severe hypokalemia. Large doses of potassium may be necessary (doses as high as 420 mEq over 24 hours have been given). Use potassium phosphate if the patient has hypophosphatemia. Serum potassium levels should be followed closely as rebound hyperkalemia has been reported.
3. Decontamination
   1. Activated charcoal does not bind barium and is not recommended unless other agents are suspected or have been ingested.
   2. Consider gastric lavage for a large recent ingestion.
   3. Magnesium sulfate or sodium sulfate (adults, 30 g; children, 250 mg/kg) should be administered orally to precipitate ingested barium as the insoluble sulfate salt. IV magnesium sulfate or sodium sulfate is not advised as it may result in the precipitation of barium in the renal tubules, leading to renal failure.
4. Enhanced elimination. Hemodialysis has been associated with rapid clinical improvement and a faster reduction in barium plasma half-life in several case reports. In one case report, continuous venovenous hemodialfiltration (CVVHD) was successfully used, reducing the serum barium half-life by a factor of 3, with resulting complete neurologic recovery within 24 hours. Either method of enhanced elimination should be considered in any severely poisoned patient who does not respond to correction of hypokalemia.