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Sodium chlorite poisoning: a case of severe methaemoglobinaemia and dialysis‐requiring kidney injury

A 29-year-old Caucasian man was brought to the Emergency Department after ingesting 113 g sodium chlorite dissolved in water in an impulsive suicide attempt. He had had a previous suicide attempt, but otherwise no comorbidities or regular medications. He arrived within 1 h of ingestion, vomiting and peripherally cyanosed with oxygen saturations 70% on 15 L/min oxygen delivered by non-rebreather mask, heart rate 100 b.p.m. and blood pressure 133/86 mmHg. He quickly developed profuse watery diarrhoea. Arterial blood gas demonstrated methaemoglobinaemia at 40.5% with haemoglobin 158 g/L and serum lactate 3.9 mmol/L. By 10 h he developed oxidative haemolysis (blister cells, haemoglobin drop to 136 g/L, neutrophilia 20.8 10/L, lactate dehydrogenase (LDH) 3630 U/L, total bilirubin 34 μmol/L) and mild coagulopathy (international normalised ratio 1.4). He was oliguric, and creatinine rose from 94 to 355 μmol/L within 24 h. Methylene blue was administered (2 mg/kg, two doses) for methaemoglobinaemia, and diarrhoea was managed with intravenous fluid resuscitation (5 L normal saline over 12 h). Daily intermittent haemodialysis was initiated in anticipation of worsening acute kidney injury (AKI) and to remove any circulating sodium chlorite and/or metabolites (Fig. 1). On Day 3, haemoglobin dropped to 57 g/L, although the coagulation profile had normalised. N-acetylcysteine was added as adjunctive therapy, but with ongoing haemolysis (haptoglobin 0.05 g/L, bilirubin 44 μmol/L, LDH 1750 U/L), nine units of packed red blood cells were required between Days 3 and 7. Upper endoscopy excluded bleeding, but revealed mild gastritis. The patient required intermittent haemodialysis for 23 days. Over the following 5 months he had complete recovery of kidney function and haemolysis. Sodium chlorite is available as an industrial solvent commonly used in water treatment. In vitro sodium chlorite causes oxidation of Fe in the haem ring of haemoglobin leading to formation of methaemoglobin, reactive oxygen species that lead to erythrocyte membrane fragility, and haemolysis. The mechanism of AKI is unclear, but is likely a combination of ischaemic insult and direct tubular toxicity leading to severe tubulointerstitial inflammation and injury. This is the highest dose of sodium chlorite poisoning reported. Severity of AKI appears to be dose dependent with dialysisrequiring AKI only reported in cases involving >10 g. Early management is focussed on minimising oxidative insult. Methylene blue reduces methaemoglobin back to haemoglobin using nicotinamide adenine dinucleotide phosphate in a redox reaction. Response is variable and appears reliant on a functional glutathione reduction system that may be irreversibly altered by the presence of chlorite. In the present case, methaemoglobinaemia swiftly improved with methylene blue, and this may relate to the short times since ingestion. Nacetylcysteine may replenish endogenous glutathione and