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Barium poisonings are uncommon and usually result from accidental contamination of food sources, suicidal ingestion, or occupational inhalation exposure. Accidental mass poisoning has occurred owing to the addition of barium carbonate to flour and the contamination of table salt.

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, carbonate, chloride, fluoride, hydroxide, nitrate, and sulfide) are highly toxic, whereas the insoluble salt, barium sulfate, is nontoxic because it is poorly absorbed. Soluble barium salts are found in depilatories, fireworks, ceramic glazes, and rodenticides and are used in the manufacture of glass and in dyeing textiles. Barium sulfide and polysulfide may also produce hydrogen sulfide toxicity (See Hydrogen Sulfide). 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. Drilling mud lubricates the drill while it passes through rocks.

  1. Mechanism of toxicity

    1. Systemic barium poisoning is characterized by profound hypokalemia, leading to respiratory and cardiac arrest. Barium is a competitive blocker of 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–3.6 days. The predominant route of elimination is the feces, with renal elimination accounting for 10–28%. Barium is irreversibly stored in bone.

  2. Toxic dose. The minimum oral toxic dose of soluble barium salts is undetermined but may be as low as 200 mg. Lethal doses range from 1–30 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).

  3. Clinical presentation. Acute intoxication manifests within 10–60 minutes with a variety of symptoms including vomiting, epigastric discomfort, severe watery diarrhea, salivation, and weakness. This is soon followed by profound hypokalemia and skeletal muscle weakness that progresses to flaccid paralysis of the limbs and respiratory muscles and areflexia. Ventricular arrhythmias, hypophosphatemia, mydriasis, impaired visual accommodation, myoclonus, 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 intoxicated.

  4. Diagnosis is ...

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