Black plasma resulting from inhalation of arsine gas

Abstract

A 46-year-old man was accidentally exposed to arsine gas while observing an industrial procedure. Within hours he developed fatigue, sore throat, nausea and vomiting, and tingling in his extremities and voided dark urine. After initial treatment in a local hospital he was transferred to our tertiary-care center. He soon developed renal failure secondary to acute arsine toxicity (arsine level, 1250 mg/L). Laboratory findings were: Hct 24.9 percent, BUN/Cr 84/5.5 mg per dL, bilirubin 9.1 mg per dL, indirect bilirubin 6.8 mg per dL, haptoglobin <6 (normal, 30-200), and LDH 10,413 units per L (normal, 265-580). An emergent (2 days after arsine exposure) 1-vol RBC exchange transfusion revealed black, grossly hemolyzed plasma (see figure). Daily hemodialysis was begun and two additional RBC and plasma exchanges were performed at 24-hour intervals (Days 3 and 4 after arsine exposure). Serial arsenic levels declined post exchanges. The patient was not treated with chelators (controversial therapy for arsenic poisoning) and completely recovered over 1 month. He remains in good health. Acute arsine poisoning due to inhalation of arsine gas (AsH 3 ) is now quite rare but has no known antidote. It is the most acutely toxic form of arsenic causing rapid and severe hemolysis immediately on exposure. The mechanisms of hemolysis are not completely understood; however, studies have shown that arsine causes disruption of ion gradients causing cell membrane instability, and RBC membrane sulfhydryl groups are probable targets of arsine toxicity as is hemoglobin. The resulting renal failure with acute tubular necrosis occurs by the direct toxic effect of arsine on renal tissue and/or heme-pigment nephropathy. Arsine has a short half-life and is converted to various arsenic derivatives following a three-phase model of half-lives varying from 27 to 96 hours. Before hemodialysis, all cases of arsineinduced renal failure were fatal.

L’arsine : un toxique chimique industriel peu connu

“…Arsenic hematotoxicity from Biswas et al [10] d'hémolyse tels que l'élévation de l'activité enzymatique de la lactate déshydrogénase (LDH), de la bilirubine non conjuguée et de la kaliémie. Conséquence de l'hémolyse, le plasma des patients intoxiqués est de couleur noire [15]. Le test de Coombs est négatif, le test de fragilité osmotique des hématies normal.…”