Arsenic toxicity may be mistaken for Guillain-Barre syndrome, as it presents with paresthesias and numbness in a symmetric stocking-glove distribution and muscle weakness. Arsenic-induced neuropathy may persist after exposure stops, but long-term exposure may present with a sensory neuropathy that resembles alcoholic neuropathy. Burning paresthesias in glove and stocking distribution, early loss of stretch reflexes, and later weakness are also seen. In severe cases, flaccid paralysis may appear in the lower extremities and then the upper extremities, again resembling Guillain-Barre syndrome (27-29).
A 24-hour urine specimen should be obtained for measurement of arsenic levels, as well as a CBC with peripheral smear. Analysis of hair and fingernail clippings is less useful as there is a significant risk of environmental contamination (27-29).
Chelation therapy with BAL, DMSA, or d-penicillamine is the primary treatment of arsenic toxicity. Removal of the offending agent and aggressive gastric decontamination aids in reducing ongoing absorption of arsenic. Hemodialysis may be beneficial in patients with acute renal failure (16,27-29).
Was this article helpful?