Introduction Arsine gas intoxication generates enzymatic changes on glutathione in erythrocytes, leading to massive hemolysis, which manifests as altered consciousness, hematuria, jaundice, and renal failure. Its importance lies in the early diagnosis for the limitation of its sequelae.
Methods 26-year-old worker, operator in the area of polymetals, who in June 2016, after adding zinc in a mixing tank, starts with ocular ardour, upper respiratory tract irritation, nausea and vomiting. Initially treated as gastroenteritis, whithout response to treatment. Evaluated by internal medicine diagnosing hemolytic uremic syndrome and liver failure requiring hospitalisation. Presenting later short-term memory loss, vertigo, pain and weakness in pelvic limbs. Evaluated by neurology granting symptomatic management and requesting electromyography of pelvic limbs, which reported segmental demyelinating polyneuropathy. Valorated by the occupational health division, where a specific study was carried out observing the inconsistent use of personal protective equipment, as well as the inadequate manipulation of the zinc as causative factors of intoxication, determining neuropathy as a sequel.
Result Laboratory: arsenic: in urine 715.0 µg/L, in blood 95 µg/L; Hb 7.1 g/dl, Hct 28%, creatinine 3.2 mg/dl, urea 149 mg/dl, urinalysis: nitrites +, proteins 500 mg/dl, haematuria. Physical examination: paraesthesia and dysaesthesias of pelvic limbs, muscle strength 3/5 bilateral, electromyography of pelvic limbs: motor polyneuropathy of the type of segmental demyelination.
Discussion Exposure to arsine gas without adequate personal protective equipment can lead to severe intoxication, develop of sequelae and even death. In the present case the process by which arsine gas is produced in the workplace is compatible with the symptoms and sequelae presented by the worker, demonstrating the cause-effect work-injury relationship.
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