Page 18 - ANZCP Gazette November 2021

It is felt by the team that initially treated the patient that the combined drug intake probably preceded the ingestion of the sodium nitrite in the BAU. This combination alone may have been fatal without the sodium nitrite, however, there are suggestions that this particular combination of the non-prescribed drugs was taken to facilitate the actions of the sodium nitrite and to depress the body’s natural reaction to excrete the compound through vomiting.
The findings of the coroner are presumed cause of death by sodium nitrite poisoning upon review of the CCTV footage.
Discussion
Sodium nitrite is a yellowish/white powder and is used as a food additive, in dyes and also pesticides. It is also the antidote for cyanide poisoning. Accidental ingestion is often related to affected water wells and pipes (it is used as an anti-corrosive agent) although, as this case has shown, it can also be intentionally ingested to cause harm and in the worst case, death. The lethal oral dose reported for sodium nitrite is 0.7–6.0 g, but we are unsure of the amount our patient consumed. Nitrites are known to be potent vasodilators which can lead to coronary ischaemia and stroke due to hypotension. When ingested, there is an increase in oxidative stress when erythrocytes are exposed to nitrites; this is an indirect reaction which reduces the oxygen to the free radical and thus in turn leads to an increase in production of methaemoglobin.
In the acute setting a decision was taken to try and stabilise the patient based on age and unknown substance abuse. We have found no other reports of ECMO support for sodium nitrite poisoning. ELSO data reported in January 2017 shows a survival rate of 39% for adult ECPR. However, having the resource of an ECMO service and a young patient in cardiac arrest it was not unreasonable to try to resuscitate and support this patient on ECMO. The [darker] natural pigmentation of the patient’s skin hid the characteristic ‘blueish hue’ seen with methaemoglobinaemia which has been mentioned previously (Harvey 2010). It was also noted that the MetHb is not reported on venous blood gas print outs in ED and therefore the high levels of MetHb were not noted until in the operating theatre once CPB had commenced and an arterial blood gas done. This has now changed and all ABG samples taken and processed in ED include a MetHb value.
Partial pressures of oxygen are all reported within normal ranges (75–100 mmHg) in cases such as these. Given our exposure to this case we would find it reasonable to assess the oxygenator with an arterial side blood gas and if there was a high PO2 assume that the membrane was functioning after all preliminary checks had been completed.
References
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Chui, J.S.W. et al. Nitrite-induced methaemoglobinaemia – aetiology, diagnosis and treatment. Anaesthesia, 2005; 60: 496–500.
Curry, S. Continuous Methylene Blue Infusions for Treating Recurrent Methemoglobinemia. Tox and Hound. https://emcrit. org/toxhound/refractory-methemoglobinemia/ [accessed 19-09-21]
ELSO – ECLS Registry Report: International Summary 2017.
Falkenhahn, M. et al. Unexplained acute severe methaemoglobinaemia in a young adult. British Journal of Anaesthesia, 2001; 86: 278–280.
Harvey, M. et al. Fatal methaemoglobinaemia induced by self- poisoning with sodium nitrite. Emergency Medicine Australasia, 2010; 22: 463–465.
Hunter, L. et al. Methaemoglobinaemia associated with the use of cocaine and volatile nitrites as recreational drugs: a review. British Journal of Clinical Pharmocology, 2011; 72:1:18–26.
Katabami, K. et al. Case Report: Severe Methemoglobinemia due to Sodium Nitrite Poisoning. Case Reports in Emergency Medicine, 2016; Article ID 9013816.
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Wright, R.O. et al. Methemoglobinemia: Etiology, Pharmacology, Clinical Management. Annals of Emergency Medicine, 1999; 34:5: 646–656.
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