Symptoms Mimicking Those of Hypokalemic Periodic Paralysis Induced by Soluble Barium Poisoning

Case Presentation

A male veteran aged 45 years when treated by the authors was well until moving into a new rural home when he began to experience acute episodes of variable perioral numbness, diarrhea, paresthesias, abdominal cramping, and weakness, which ranged from mild, self-terminating extremity weakness to 3 episodes of respiratory failure that required intubation and mechanical ventilation.

All episodes were accompanied by hypokalemia in the range of 2 to 3 mEq/L, but levels varied erratically during admissions from severe hypokalemia to normo- and hyperkalemia. Over 3 years, the patient was admitted to the hospital 19 times, underwent extensive workup, and was referred to endocrinology services at Duke University, Vanderbilt University, and the Cleveland Clinic. Diagnostic efforts centered on establishing whether he had a latepresenting variant of familial HPP.

Genetic evaluations could not identify known single-nucleotide polymorphisms associated with that condition. The consensus was that he had a potassium leak somewhere between his kidneys and bladder. Recommended management was a high baseline oral potassium supplementation and spironolactone. He had a brief period of improvement after moving to a different house, but the episodes returned once he moved back to his old house despite adherence to recommended treatment. In December 2012, he experienced his worst episode, with potassium 1.8 mEq/L on admission, resulting in admission to the intensive care unit (ICU).

Following a precipitous clinical decline, the patient was intubated and mechanically ventilated. Nephrology was consulted and given the recurrent life-threatening pattern, an intensive chart review was undertaken. It was noted that a urine arsenic level that had been normal several admissions previously at 18 μg/L was elevated during a subsequent admission at 59 μg/L, and several weeks later during a later admission the level had fallen to 15 μg/L. Urine lead was undetectable on 3 occasions, and urine mercury was within normal limits.

Arsenic toxicity did not match the patient’s clinical syndrome, but the pattern seemed to be consistent with the possibility of unexplained toxic exposure and subsequent clearance. Therefore, an intensive literature search for syndromes of environmental exposure or poisoning resembling HPP was undertaken. The search revealed several references in the literature to paralysis similar to HPP that involved ingestion of hair-removing soap and rat poison containing barium sulfide and carbonate. References also pointed to the similarity of the symptoms to Guillain-Barre syndrome.

As a result of that literature search, a blood barium level was collected in the ICU that revealed 14,550 ng/mL. A scalp hair sample showed 6.1 μg barium per gram of hair (reference, 0.53 μg/g to 2 μg/g). Neither the patient nor his wife reported being involved in painting, ceramic work, decorating glassware or fabric with dyes, working with stained glass, smelting, metal welding, or use of vermicides.

A U.S. Environmental Protection Agency team was sent to the house, and a detailed toxic survey of the house and the surrounding grounds was conducted with no excess barium found. Barium levels were checked by a private physician on the wife and 2 minor children. The wife’s barium levels came back undetectable in a blood sample and elevated in a hair sample. One child had a very low detected level in her blood and slightly elevated in her hair, and the other child had a low level in her blood and her hair. Because the circumstances of the wife’s and children’s exposure could not be explained environmentally nor could the veteran’s exposure source be identified, the VA Police Service contacted the Tennessee Bureau of Investigation, and they questioned the veteran and his wife.