SODIUM CHLORITE POISONING – A CASE OF SEVERE METHAEMOGLOBINAEMIA AND DIALYSIS-REQUIRING ACUTE KIDNEY INJURY

M TUNBRIDGE1,4,  N ISBEL2,4,  D JEGATHEESAN2,4,  I MCNEILL3,4,  K ISOARDI3,4,  A VIECELLI2,4

1Nephrology Department, Royal Brisbane And Women’s Hospital, Brisbane, Australia, 2Nephrology Department, Princess Alexandra Hospital, Brisbane, Australia, 3Clinical Toxicology Department, Princess Alexandra Hospital, Brisbane, Australia, 4Faculty of Medicine, University of Queensland, Brisbane, Australia

Background:Sodium chlorite is an industrial solvent, ingestion of which leads to oxidative injury with methaemoglobinaemia, haemolysis, coagulopathy, and acute kidney injury (AKI).
Case Report: A 29-year-old male was brought to the Emergency Department after ingesting 90g sodium chlorite in a suicide attempt. He had a previous suicide attempt but otherwise no co-morbidities or regular medications. Within 1 hour of ingestion the patient was hypoxic, tachycardic and experiencing profuse diarrhoea. Arterial blood gas demonstrated methaemoglobinaemia 40.5% with a haemoglobin of 158 g/L. He was oliguric with creatinine rising from 94 to 355 µmol/L within 24 hours, evidence of oxidative haemolysis and coagulopathy. Methylene blue was administered (2mg/kg, first dose immediately then at 30 minutes) with methaemoglobinaemia improving to 4.9% by 2 hours while diarrhoea was managed with intravenous fluid resuscitation. Daily intermittent haemodialysis was initiated anticipating worsening AKI and to remove circulating sodium chlorite and/or metabolites. On day 3, haemoglobin dropped to 57 g/L while the coagulation profile normalised. N-acetylcysteine was added but 9 units of packed red blood cells were required between day 3–7. Intermittent haemodialysis was required for 23 days, but over 5 months there was complete recovery.
Conclusions:The mechanism of kidney injury is unclear but likely a combination of ischaemic insult and direct tubular toxicity. This is the highest reported dose of sodium chlorite poisoning, and severity of AKI appears to be dose dependent. Early administration with methylene blue reduces methaemoglobin to haemoglobin. Haemodialysis may remove chlorite from the circulation. Later management is supportive, with blood transfusions for haemolytic anaemia and ongoing haemodialysis for AKI. Longer-term prognosis of sodium chlorite ingestion appears favourable with complete recovery in most reported cases.


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