(1338) The Price of Salt: A Rare Case of Accidental Sodium Chlorite Ingestion

Introduction: Sodium chlorite is a mass produced odorless flaky salt. Its strong oxidizing properties lend its use in many industries that process paper, drinking water, leather, and textiles. Human ingestion of sodium chlorite is rare and usually occurs intentionally. Toxicity presents as a cascade of oxidative cellular injury to red blood cells (RBC) and kidneys.

Description: A 72-year-old man working on his home water purification system drinks from an unmarked water bottle accidentally ingesting 4oz of 28% sodium chlorite. He develops intractable coffee ground emesis which prompts an ED visit. He is cyanotic with refractory hypoxemia on supplemental oxygen. His chocolate brown-colored blood is diagnosed as methemoglobinemia with a level of 23.9%. Methylene blue is administered and his MetHb level improves to 8%. However, the patient has persistent hypoxemia, lactic acidosis, worsening renal function, and early signs of RBC hemolysis. He is transferred to a tertiary hospital for ICU level management. Serum Hb count falls from 16 mg/dl to 10.1 mg/dL. A high serum LDH of 2234 U/L and indirect bilirubin of 2.5 mg/dL are consistent with intravascular hemolysis. On admission day 2, he is initiated on continuous renal replacement therapy resolving his hypoxemia by day 4. The following day, he transitions to intermittent hemodialysis (iHD). He receives multiple blood transfusions till day 10 for persistent anemia. The patient’s Hemoglobin, liver enzymes and LDH finally stabilize by hospital day 11. The patient is discharged home on iHD and makes a full renal recovery after 4 weeks.

Discussion: The chlorite ion is the oxidative agent formed on dissolution of sodium chlorite salt. While the data pertaining to human ingestion of chlorite salt is limited to case reports, we know it is highly water soluble, and follows a predictable pattern of injury. Chlorite contact with lipid coated red blood cells manifests as methemoglobinemia. RBC hemolysis follows due to a shortened cell half-life, and compromised cell integrity. Oxidation also induces acute renal tubular necrosis. This reaction seems dose dependent. Methylene blue and RBC transfusions can temporize organ dysfunction, but the oxidative cascade is terminated by early dialysis which removes chlorate ions from circulation before further harm ensues.